PERIODONTICS PERIODONTICS
A. PERIODONTIUM: The functional unit of tissue supporting the tooth. Four components: 1. Gingiva 2. Periodontal Ligament 1
3. 4.
Cementum Alveolar Bone
(Fedi Perio Syl)
1. GINGIVA from gingival margin to MGJ that increases in width with age. Has stratified squamous epith and lamina propria (dense, fibrous CT predominantly collagen fibers) a. Marginal (Free) Gingiva - 1.0-1.5 mm on facial and lingual. The unattached sleevelike portion of the gingiva surrounding the neck of tooth, not directly attached to the tooth forming the soft tissue wall of the sulcus. From the free gingival margin to the FG Grove * Free gingival groove - A fine grove running parallel to the gingival margin dividing the free gingival from the attached gingiva, present in 30-40% teeth. Often corresponds to the location of the bottom of the gingival sulcus. b. Attached Gingiva - Located from free gingival groove to MGJ Tightly bound to tooth and bone by epithelium and CT or just tooth with dehiscence. Attached gingiva is normally covered by keratinized or parakeratinized epith that has marked rete ridges Keratinized, width = 0+ to 10 mm Facially narrowest over the bicuspids, Mandibular lingual is narrowest at incisors * Interdental groove - vertical groove parallel to long axis of adjacent teeth in interdental area of attached gingiva c. Interdental Papillae - gingiva that fills the interproximal space between adjacent teeth. Concave faciolingually (saddle-like) depression called col (nonkeratinized, more susceptible to bacterial breakdown) d. Gingival Sulcus - space between tooth and free gingiva with Juntional Epithelium at base, 0.0-0.5 mm histologic depth, 0.5-3.0 mm clinical depth depending on probe penetration e. Junctional Epithelium - Approximately 1 mm in health Nonkeratinized, attached to enamel in the normal situation by basement lamina and hemidesmosomes, apical to sulcus, usually at CEJ. Proline/hydroxyproline secreted by epithelial cells bind JE to enamel or cementum. f. Connective Tissue - Approximately 1 mm between CEJ and crest of bone Composed of lamina propria without submucosa Primary cell is the fibroblast g. Alveolar Mucosa - thin, nonkeratinized epithelium lacking rete ridges CT consisting of thin lamina propria and vascular submucosa Predominantly elastic fibers, so is loosely bound h. Gingival Fibers – stabilize the attached gingiva to alveolar process and to the tooth, important in postorthodontic relapse: 1) Alveologingival – from the bone of the alveolar crest into the lamina propria of the free and attached gingiva. 2) Circular – fibers within the gingiva that encircles the tooth in a ring like fashion 3) Dentogingival – from cervical cementum to CT of free and attached gingiva. 4) Dentoperiosteal – from cementum to the outer cortical plates of the alveolar process where they insert into the alveolar process or muscle * Gingival apparatus maintains the free gingiva & JE in close approximation to tooth i. Types of Oral Mucosa: 1. Masticatory - Gingiva and mucosal covering of hard palate 2. Specialized mucosa - Dorsum of tongue 3. Lining mucosa - Alveolar and floor of mouth j. Clinical Health: 1. Color – “Coral Pink” Varies according to: Degree of Vascularity Keratinization Pigmentation Thickness of Epithelium 2. Contours – thin, knife edge margins, papillae fills space when teeth contact. 3. Consistency - firm, tightly anchored 4. Texture - Keratinized with stippling in ~30-40%. 5. Tendency of Bleeding on Probing - Healthy gingival will display no bleeding k. Vasculature of Gingiva Abundant from alveolar bone, PDL, & supraperiosteal vessels. Mainly from supraperiosteal branch of internal maxillary artery.
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2. PDL: White collagenous CT fiber that surrounds the root of tooth attached to bone. -
0.25 mm in width (0.10 to 0.25 mm) depending on age & function. "hour glass" shape – narrowest at mid-root. Fibers course mainly in apicocoronal direction from cementum to bone inserting as Sharpey's fibers Blood supply from apical area, interdental alveolar process, gingiva Functions - sensory, formative, regenerative, nutritive, supportive
Fiber groups by location & direction: 1. Alveolar Crest – From cementum (just apical to CEJ to rim of alveolus) 2. Apical – From cementum at apex of tooth to bone forming the base of the alveolus 3. Horizontal – Located just apical to alveolar crest and run perpendicular to the long axis of the tooth from cementum to bone. 4. Interradicular – found between roots of multi-rooted teeth running from cementum into the crestal bone of the interradicular septum. 5. Oblique (Most Numerous) – Run from cementum outwardly and coronally to insert into the bone. 6. Transseptal – From one tooth to another. 3. CEMENTUM: a. Continuing depostion throughout life b. Relationship to CEJ 1. 60-65% Overlaps with Enamel 2. 30% Butt Joint 3. 5-10% Exposed Dentin c. Cellular in apical 1/3 forms after tooth erupted d. Primary Cementum – Acellular forms with root formation and eruption (cementoid). e. Secondary Cementum – Cellular forms after eruption. f. Functions 1. Anchors tooth to bone 2. Compensates for loss of tooth structure through wear by growth 3. Allows mesial drif 4. Allows PDL fiber rearrangement 4. ALVEOLAR BONE: a. Components are: 1. Alveolar bone proper - cribriform plate lines each socket 2. Supporting bone - cortical plates & cancellous bone b. Relationship to teeth - Should be 2 mm apical to the CEJ to be WNL - CEJ to CEJ but varies with tooth position & angulation, root form, crown form, stage of eruption, & distance between roots - Tooth position in the arch may have thick or thin alveolar process, dehiscence and fenestrations. Dehiscence – More common in the Mandible (usually bilateral) Do not Scl x RP. Leave Sharpey’s fibers alone if healthy area. Fenestration – More common in the Maxilla. *Biologic width - 3 clinical entities are: 1. Connective fibers 1 mm 2. Junctional epithelium 1 mm 3. Sulcus 1 mm The potential minimum sum = 3 mm Ref: Nevins & Skurow Int F Perio Rest Dent 4(3)31-47, 1984. II. INFLAMMATION: 1. Gingivitis: - inflammation of gingiva soft tissues (onset any age). - gingival bleeding, color change to red or purple
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- gingival pseudopockets may develop, - may or may not progress to periodontitis - reversible generally present with periodontitis 2. Periodontitis: - inflammation of deeper structures plus destruction of periodontium, i.e. loss of CT attachment to root surface. - loss of bone adjacent to that area. - then replacement of CT attaches to root surf by JE. - apical migration of JE. - coronal aspect of JE breaks down resulting in pocket formation. - degeneration of CT attachment occurs before pocket formation. Page and Schroeder model of pathogenesis of inflammatory periodontal disease: - 1976. Histologic progression: 1. Periodontal health: - G+ cocci, few spirochetes & motile forms - no vasculitis present - PMN's and lymphocytes are present as a normal feature - Serum proteins and fibrin are contained within the blood vessels - the junctional epithelium uniformly joins the CT with rete ridges, the CT is dense and highly organized into tissue fiber bundles 2. Initial lesion (subclinical gingivitis): - Starts with health and take away oral hygiene. In 2-4 days get perivascular infiltrate of PMN's in JE. vasculitis of vessels subjacent to JE - exudation of fluid from the gingival sulcus - increased migration of PMN's into the JE and gingival sulcus - loss of perivascular collagen (5-10% of CT may be involved) - no visible change. 3. Early lesion (clinically detectable gingivitis): - the early lesion appears within 4 - 7 days following the beginning of plaque accumulation - lymphoid cells make up 75% of total infiltrate - fibroblasts show cytopathic changes possibly associated with interactions with lymphoid cells - no apical migration of JE. - localized loss of collagen fiber (60 - 70% of collagen fibers are lost in the inflamed area) 4. Established lesion (severe gingivitis): - develops within 2-3 weeks - may still be reversible as gingivitis - acute inflammation - may progress to advanced lesion but more often appear not to progress. - lesion dominated by plasma cells. - May/ may not have gingival pocket - coronal part of JE breaks down. - apical part of JE intact. - continued loss of collagen and CT substance - no appreciable bone loss. 5. Advanced lesion (periodontitis): - develops in years to decades - formation of periodontal pockets. - plasma cells dominate lesion. - continued loss of collagen subjacent to the pocket epithelium - extension of the lesion into alveolar bone and PDL with significant bone loss - permanent destruction of deeper structures.
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loss of attachment – formation of periodontal pockets periods of quiescence and exacerbation < 50% of population progress to advanced lesion. periodontitis.
Histologic evidence of gingivitis after 2-4 days after stopping OH. Clinical evidence of gingivitis 21 days post OH, Loe 1955. - since then other studies say 7-21 days. III. DIAGNOSIS: Based on disease activity and rate of attachment loss a. Three Models of Periodontitis 1. Continuous paradigm (traditional concept) Plaque-induced, slowly progressive disease. - continuous deepening of pockets. - gradual loss of attachment. 2. Random burst (newer concept) - bacteria induced disease. - destruction of attachment apparatus progresses by recurrent acute episodic bursts of activity. 3. Asynchronous multiple burst - destruction occurred during a defined time - disease goes into remission for an indefinite time - Studies trying to observe attach loss: - most sites showed no change. - 3-4% of sites experienced attachment loss. - 5-6% sites experienced attachment gain. - done over short time. - need to observe 2-4 mm of loss before calling it loss. b. Overall definition of periodontitis: - bacteria induced, slowly progressive disease with episodes of rapid attachment loss activity brought on by alterations in host/parasite relationship. c. Health vs disease: 3 stages: 1. periodontal health. 2. periodontitis inactive: inflammation but no attachment loss. 3. periodontitis active: inflammation with attachment loss. d. When probing attach level need fixed reference, CEJ. e. Host/parasite equilibrium factors affecting: - alterations in environment: - overhang, food impaction, restoration contours. - major/minor illnesses (diabetes. - altered emotional state; stress, depression. IV. CLASSIFICATION OF PERIODONTAL DISEASES (WWP 1989): a. GINGIVITIS 1. Plaque associated gingivitis - Most common periodontal disease - Clinically characterized by redness, gingival bleeding, edema and enlargement - Overgrowth of gram positive plaque 2. Acute narcotizing ulcerative gingivitis -Acute, recurrent, necrosis of gingival papillae, spontaneous bleeding, pain, and fetor ors. Invasion by spirochetes & fusiforms (Bacteroides intermedius) 3) Steroid hormone-influenced gingivitis -Manifested by puberty, pregnancy, steroid therapy and BCPs -Bacteroides enhances with elevated with elevated hormones 4) Medication-influenced gingival overgrowth -phenytoin (seizure control), cyclosporin (immunosuppressive therapy, and
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nifedipine 5) Desquamative gingivitis -desquamation or sloughing of the epithelium leaving an intensely red surface -oral manifestations of dermatoses-erosive lichen planus, benign mucous membrane pemphigoid, and pemphigus vulgaris - Can be caused by allergic reactions 6) Miscellaneous gingivitis -blood disorders, nutritional deficiencies, tumors, genetic factors, mouthbreathing, diffuse bacterial and viral infections. b. PERIODONTITIS: 1) Adult periodontitis: - most common form, plaque & calculus -related. - onset in adolescence and continues for the life of individual. - prevalence and severity increases with age, with no sex predilection - usually horizontal bone loss. - blood cell defects not commonly found. - Bacteria vary (attached) Actinomyces israelii, A. naeslundii, and A. viscosus - Unattached portion of subgingival plaque is spirochetes & gram (-) rods 2) Early Onset Periodontitis A. Rapidly progressive periodontitis: - Type A = younger, little plaque, neutrophil problems - severe gingival inflammation & rapid CTA & alveolar bone support. - onset = young adults puberty to age 35. - 66% have depressed neutrophils chemotaxis response and monocytes. - Type B = 26-35 yo, significant plaque & calculus, OK neutrophils - Acute phase may have associated malaise, weight loss and depression. - Can respond well to scaling and antibiotic therapy - RPP related to: diabetes mellitus type I, Down’s syndrome, Papillon-Lefevre, AIDS - Bacteria = Bacteriodes gingivalis & B. intermedius, Wolinella recta. B. Juvenile periodontitis, JP: - characterized by severe angular bone loss in the first molar in otherwise healthy adolescents. Lesions are often bilaterally symmetrical. (3-5X adult rate of loss) - permanent 1st molars and sometimes incisors, usually bilaterally symmetrical - My have genetic basis, and be inherited as an X-linked dominant trait. - lack of plaque & clinical inflammation - females 3:1, blacks > whites - good response to curettage and antibiotic treatment. - tetracycline 1gram/day 14-21 days (Slots). before meals and at bedtime. - Bacteria: Haemophilus (Actinobacillus) actinomycetemcomitans, B intermedius - A.A.- gram (-) rod, non-motile, inhibits PMN chemotaxis. - capnocytophaga- gram (-) rod. - Prevotella- gram (-) rod, non-motile. Localized, LJP: - vertical bone loss 1st molars. - horizontal bone loss incisors. - mirror image defects 75% bilateral symmetry, furcations intact. - peripheral PMN's defective 75% of cases. - generalized, GJP: - horizontal bone loss. - may be same as rapidly progressive p. - post juvenile periodontitis: - dramatic decrease in rate of destruction - affected sites clinically similar to adult p. C. Pre-pubertal periodontitis: rare condition generalized or localized form
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- onset after eruption of primary teeth. - prevalence unknown. - localized form: - little or no gingival inflammation. - age 4 or before. - functional defects in either neutrophils or monocytes but not both. - no hx of frequent infections. - generalized form: - acute, red, proliferative gingival inflammation. - rapid destruction. - peripheral WBC's increased. - PMN defects, absent from gingival tissues. - frequent infections, otitis media, skin, URI. - refractory to antibiotic therapy. - primary & secondary teeth affected. 3) Refractory periodontitis: - disease in multiple sites with patients demonstrate attachment. - any form of periodontitis which does not respond to treatment. - probably an inadequate diagnosis resulting in inadequate therapy. - same organisms as adult perio 4) Periodontitis associated with systemic disease - HIV associated periodontitis - rapid onset and progressive p. - 6-12 mm bone loss in months. - interproximal necrosis and cratering. - marked edema and intense erythema of gingiva. - acute pain and spontaneous bleeding. - treatment: - betadine lavage. - scale and root plane. - OHI. - peridex. - metronidazole 250 mg x 2-3 days (7 days). Systemic diseases predispose to periodontitis: - insulin dependent diabetes mellitus, IDDM. - Down's syndrome. - Papillon-Lefevre syndrome: - early in life, doubtful infective origin, mimics JP. - includes hyperkeratosis of palms and soles. - teeth sparsity of cementum middle and coronal 1/3's. - Crohn's disease - neutropenia - agranulocytosis - leukemia - Chediak - Higashi Syndrome - all have in common defective neutrophil counts and/or function. 5) Necrotizing Ulcerative Periodontitis: - progression of ANUG to include the attachment apparatus V. EXAMINATION 1. Considerations in diagnosis of periodontal disease: Active or inactive. Sulcus vs pocket: - sulcus, healthy attachment, plaque < threshold.
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- pocket, diseased attachment, plaque > threshold. 2. Assessment methods: - clinical = BOP, suppuration, color changes, probing depth changes, attachment level changes, gingival crevicular fluid flow, temperature probe - histological = difficult, invasive, multiple sites. - microbiological = culture and sensitivity (where to sample?), ($70 per culture), DNA probe (species specific DNA, limited to 3 species; AA, P. gingivalis & P.intermedius, phase contrast microscopy (spirochetes & motile), Gram stain (morphology) - immunological = PMNs, lymphocytes, antibody titers, complement fractions, lymphokines - enzyme analysis 3. Organisms associated with different tissue conditions: - healthy sulcus, gram (+) predominate. - gingivitis, shift to gram (-). - adult periodontitis, gram (-) anaerobic rods, 30-50% motile rods and spirochetes. - JP, G (-) A.A., P. gingivalis, capnocytophaga, P. melaninogenicus & Porphyromonas 4. Clinical methods of direct observation: - subgingival plaque and calculus. - gingival inflammation. - bleeding on probing (BOP). - suppuration. - loss of form. - gingival retraction. - pocket depth/probing depths. CEJ-FGM = recession FGM = Free Gingival Margin CEJ-BP = attachment loss BP = Bottom of the pocket FGM-BP = Pocket depth CEJ = Cementum Enamel Junction 5. Variables in measuring pocket depth: - accurate probe gradations. - diameter of probe, angle and force. - degree of inflammation. 6. Histologic vs clinical pocket depth: - histologic, probe coronal of JE. - clinical, probe passes into JE and possibly CT. 7. Bleeding on probing: - best clinical indicator of inflammation. - Lange study: - absence of BOP 100% predictability of health. - BOP had 30% chance of losing 2 mm attachment. - pockets 5 mm or more had high incidence of BOP. What about PSR? Periodontal Screening And Recording Code 0: Probes < 3.5 mm, no BOP Code 1: Probes < 3.5mm, BOP Code 2: Probes < 3.5mm, BOP, with calculus or defective margins Code 3: Probing between 3.5mm and 5.5mm Code 4: Probing > 5.5mm Meaning of PSR Score: Indicated Care Code 0: Preventive Care Indicated Code 1: OHI and professional plaque removal Code 2: above plus scaling, and correction of defective margins Code 3: comprehensive periodontal examination and charting of affected sextants, or mouth, further tx Code 4: comprehensive perio exam, including XRs, and charting to determine treatment plan
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8. Radiographic evaluation: - vertical bitewings good screening. - width PDL, calculus, root proximity, over hangs. - in health alveolar bone parallels CEJ. - adequate radiographs. - non-overlapping proximal contact. - cusptips superimposition. - furcations (furcation arrow – Gher study). -max molar ML furc is closest to sulcus (Oct80 DCNA) -distal of molars access is most difficult VI. TREATMENT PLAN: 1. Diagnosis of disease: a. mild, moderate, severe. b. AAP Classifications Type I – gingivitis with bleeding on probing (BOP) Type II – early periodontitis, BOP, with PD 3-4 mm Type III – moderate periodontitis, BOP, with PD 4-6 mm, furcation involvement, class I mobility, angular bony defects, bone loss < 1/3 of root length Type IV – Severe Periodontitis, BOP, with PD >6 mm, bone loss > 1/3 root length, vertical or angular bony defects, class II/II tooth mobility c. causative factors: - primary, only and always bacteria. - secondary: overhang, root proximity, caries, anatomic abnormalities of teeth, etc. - systemic: defects in PMN quality or quantity, uncontrolled diabetes, immunosuppressed. d. factors that influence prognosis: - levels of oral hygiene. - interest and ability. - age. -systemic. -tobacco *smokers have higher incidence and more severe periodontitis. *local stain allows more plaque formation. *systemic manifestations: mild PMN dysfunction, peripheral vasoconstriction in periodontium. - Nicotine: *Decreases blood supply to tissue *Decreases function of fibroblast with regard to wound healing *Decreases phagocytosis of PMN e. Smokeless tobacco: - grit in tobacco abrasive. - contains approx 100 irritants and toxins. - mucobuccal fold leukoplakia effect. - discoloration and abrasion of teeth over time. - caries due to high sugar content. f. mobility. Tooth Mobility Classification Miller’s Classification Class I – first detectable sign of movement Class II – movement of > 1mm in any direction Class III – movement of > 1mm in any direction and vertical depression or rotation g. extension of max incisors: - sinus location, may dictate respective or regenerative approach. 2. Treatment plan possibilities: a None, patient does not want treatment. b periodontal therapy. c extraction. 3. Phases of treatment plan:
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a non-surgical: - laboratory test, medical/dental consults. - eliminate pain/infection, address chief complaint. - prepare tissues for surgery. - remove etiological factors by mechanical means. - increase oral hygiene. - caries control, endo, extractions, ortho, occl adj. - antimicrobial therapy. - antibiotics. - peridex. - evaluation of oral hygiene. - evaluation of response to factors listed above. b. reeval appointment, confirm or alter remaining treatment plan. c. surgical phase (corrective phase): - may not be needed at this point. - pt may not want surg. - OH not adequate. - sensitive teeth, high root caries rate. - original sensodyne = strontium chloride. - mint sensodyne = potassium nitrate. d. remaining dental care: - oper, prosth, final occl adj prn. e. maintenance phase: - monitor and reinforce hygiene. - monitor the health of periodontium. - scale and root plane on a regular basis as needed. - reprobe, not necessary every year in non-active disease patient. - up-date radiographs evry 2 yrs or as needed. VII. NON-SURGICAL PHASE Non-surgical therapy includes oral hygiene, oral rinses, antibiotic therapy, scaling and root planing. 1. Treatment Plan: goals of therapy. - make tooth biologically acceptable to surrounding tissues. - pocket elimination is minor goal. - remove etiologic factors. - correct deformities caused by etiologic factors. - make maintenance of established health easier for patient. - respective, make pockets shallower or regenerative. - combination of both. - prevent disease, reinforce OH. - maintain health, function and esthetics. - determine severity of disease. A. ORAL HYGIENE: a. May be most important part b. How far does a toothbrush penetrate below the free gingival margin? 0.9mm c. What is the Bass Method of brushing? Toothbrush bristles applied at a 45 degree angle with the bristles toward the gingival sulcus. Brush moved in a rotary motion. d. What is the Charters Method of brushing? Bristles are applied at a 45 degree angle coronally. Brush moved in a rotary motion. e. What is the size of a toothbrush bristle? .007 inch f. Flossing is 80% effective in removing interdental plaque in the presence of an interdental papilla. Dental floss penetrates how far subgingivally? 1.5 mm g. In the absence of a interdental papilla – Brushing/Flossing 55% effective, Perio-Aid 80%, Interdental Brush – 95% effective. h. Establish co-therapist role of patient. c. Nyman and Linde 1977: - prior to surg did one-time session of OHI. - did different surgical techniques.
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- followed couple years. - at follow-up did perio eval and checked level of OH. - all pts with poor plaque control disease progressed. - documented plaque removal necessary before surgery. d. Linsey 1982: - one time session OHI w/ no reinforcement. - received nonsurgical periodontal therapy. - 3 month maintenance. - disease returned. - conservative therapy with maintenance also requires good oral hygiene for success. e. monitoring techniques, stain plaque at all appointments. - need objective index. - O'Leary plaque index: - (total # teeth) x 4 = total tooth surfaces, FLMD. - count # surfaces with plaque butting up to gingival margin. - (# with plaque)/(total surf) x 100 = % plaque. - lower is better. - < 10% acceptable, > 10% inconsistent with health, do not continue to surgical phase. - Modified O’Leary based on # of surfaces without plaque, therefore more of a positive motivator, with a higher percentage being better B. MOUTHRINSES Listerine, Peridex and PerioGard all acceptable by ADA. Other: Sanguinarine (Viadent), Oxygenating agents (H2O2), Quaternary Ammonium Compounds (Scope, Cepacol) - adjunct not substitute. - rinses penetrate 0.2 – 1.2 mm into the sulcus, surface tension and outflow of gingival crevicular fluid decrease ability to penetrate without force. - used with patient that need extra help: immunocompromised patient. post oral surgery or periodontal surgery. orthodontic bands. post radiation patient. a. Listerine: - phenolic related oils - contains essential oils, including thymol, methyl salicylate, eucalyptol, and benzoic acid. - mouthrinse with the highest alcohol content = Listerine 26.9%; Cool Mint = 21.6% - 25- 35% reduction in gingivitis. b. Peridex or Colgates PerioGard: - active ingredient: .12% chlorahexidine gluconate. - reduces plaque > than Listerine, 50 - 80% reduction in gingivitis. - has substantivity because of (+) charge bonds to hard and soft tissue. - lasts up to 24 hours in mouth. - stains teeth and tongue brown. - cause slight calculus formation. - temp alteration of taste. - should be last thing you do after brushing and flossing. - use separately from fluoride rinses by 30 min - Requires a prescription c. Pre-Brushing rinses -Plax-- the benefit of pre-rinsing with water has been established, however it does not appear to be enhanced with this product. Plax is not ADA approved FORCED IRRIGATION a. Forced irrigation at the gingival margin penetrates 1.8 mm b. Tip placed subgingivally penetrates 70% of the pocket depths in pockets < 6 mm deep. c. Pressures of irrigating devices 60-90 psi C. ANTIBIOTICS USE:
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a.
b.
c.
d.
e.
Mechanisms of actions of antibiotics 1. Reversible inhibition of protein synthesis – TCN, Erthromycin, Clindamycin 2. Inhibition of cell wall synthesis – PCN, Cephalosporins 3. Increase in cell wall permeability – Chlorhexidine, Triclosan 4. Inhibition of DNA synthesis – Metronidazole, Ciprofloxacin Systemic- mainly limited to refectory cases; cases where there is a systemic disease, eg AIDS; or cases where A.a. is thought to be the causative organism, eg.,in juvenile periodontitis. Several regimens exist with TCN, Amoxicillin, Augmentin, Cleocin, and Flagyl being the antibiotics of choice either individually or in combination. Specific indications: 1. Adult Periodontitis - antibiotics not indicated unless A.a is known pathogen, then TCN. 2. Juvenile Periodontitis - since A.a. is causative organism, use TCN. 3. ANUG - usually responds to conventional therapy, however metronidazole may be of use due to the spirochetes and obligate anaerobes 4. Refractory Periodontitis-consider serial drug regimens after culture and sensitivity testing. Doxycycline followed by either Augmentin (250 mg TID of each for 7 days) or metronidazole or combination plus ciprofloxacin (500mg each BID for 8 days) 5. HIV-Related Periodontitis - consider metronidazole to enhance reduction of Gram (-) organisms 6. Additional Uses: Root surface conditioning Use with graft materials Use with GTR/GBR techniques Acute periodontal conditions Antibiotic Regimens TCN 250 mg qid X 21 days Doxycycline 100 mg daily X 21 days Clindamycin 150 mg qid X 7 days Metronidazole 250 mg tid X 7 days Augmentin 250 mg tid X 14 days Local delivery1. Actisite®. A Tetracycline fiber developed by Goodson - a polymer fiber and ethyl acetate 25% saturated with tetracycline. Placed without anesthesia using a blunt instrument like retraction cord packer. -leave in place 1-2 weeks -can use adhesive (in kit) to hold in place -remove with cotton pliers -not to take place of initial prep or anti-infective phase of therapy use only after traditional methods have been employed. -biggest use in refectory cases, ailing implants, or the perio abscess **Six months following the fiber regimen the mean probing depth reduction was 0.73mm.
Attached gingiva, AG: a. How much is enough, what are indications for grafting. b. function is to anchor btw FGM and alveolar mucosa. - dissipates forces from muscle fibers through alveolar mucosa. c. width 0-9 mm, widest areas in max/mand incisors, narrowest in bicuspid area. - ideal width Lange and Low 1972- 2 mm keratinized 1 mm attached. - 1982 Dorfman if keep free of inflamm get by with 0mm. d. Thickness: - mean thickness 1.25 mm. - on palate .1-.6 mm, mean .36 mm. - recommended thickness of graft 1-1.5 mm. - trying to transfer CT not epithelial component. e. Restorative needs: - Maynard and Wilson: - put margin in sulcus need 5 mm, 2 mm free and 3 mm attached. X. PERIDODONTAL PLASTIC SURGICAL PROCEDURES: A. Frenum Procedures B. Apically Positioned Flap C. Pedicle Grafts
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1. Laterally Positioned Flap 2. Obliquely Rotated Flap 3. Double Papilla Flap 4. Coronally Positioned Flap 5. Semilunar Flap D. Free Gingival (Soft Tissue) Grafts E. Connective Tissue Grafts F. Guided Tissue Regeneration in Conjunction with Coronally Positioned Flaps ------------------------------------MORE DETAIL---------------------------------------------A. Frenum procedures - Henry (1976) – Frenum contain no muscl e, just connective tissue - Frenectomy INDICATIONS: few, usually augmentation should be considered Preventive problem with lip or tongue movement Prosthodontic – interferences Orthodontics – midline diastema Purely esthetic problem
B. Apically positoned flap
ADVANTAGES *Control amount of keratinized tissue *Versatile pocket reduction *Maximum bone coverage *Minimal bone loss *Access to root surfaces DISADVANTAGES *Limits the treatment of intrabony defects C. Pedicle grafts – Base of flap retains its own blood supply. Requires adequate donor site. 1. Laterally positioned Lateral sliding graft – Grupe and Warren (1956) Repair of Isolated gingival defects Lateral sliding graft for multiple teeth – Hattler (1967) Split thickness flap moved ½ a tooth laterally; papilla over mid-root INDICATIONS *Inadequate gingiva *Esthetic concern *Root Sensitivity ADVANTAGES * Single Site * Maintain perfusion to graft *Good color match *Predictable root coverage DISADVANTAGES *Inadequate donor tissue *Very prominent teeth *Interproximal bone loss *Active periodontitis Wound Healing – 7 days (new JE); 7-21 days (new CT attachment) 2. Obliquely rotated – Variation on LPF 3. Double papilla – Ross/ Cohen (1968) – Adjacent papilla rotated over root and sutured 4. Coronally positioned – Allen / Miller (1989) need 3 mm keratinized tissue over site. INDICATIONS *Inadequate gingiva *Esthetics *Root Sensitivity ADVANTAGES *Easier to treat multiple adjacent sites compared to other techniques
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*Predictable root coverage DISADVANTAGES *Multiple surgical sites *Multiple surgical procedures 5. Semilunar coronally positioned flap – Tarnow (1968) Semilunar incision over root, tissue moved coronally
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D. Free gingival grafts Used extensively to augment keratinized tissue and extend the vestibule Generally poor results for root coverage Sullivan & Atkins (1968) – pioneers of this technique P.D. Miller (1985) vigorous root planing to flatten root surface citric acid vigorously burnished into root horizontal incisions at level of adjacent CEJs butt joints with tissue adjacent to recipient bed Thick grafts: 2-2.5 mm thick Peripheral sutures to stabilize grafts INDICATIONS *Increase gingival width *Cover denuded roots – “thick graft” technique only *Deepen vestibule *Ridge Augmentation ADVANTAGES *Predictable *Easy to perform *Ample supply of donor tissues *Treat multiple teeth simultaneously DISADVANTAGES *Two surgical sites *Tissue color discrepancies *Graft may be overly thick when mature *Poor esthetics *Quantity of donor material is limited
E. Connective tissue grafts -indications include inadequate donor site for lateral pedicle, isolated wide gingival recession, multiple root exposures and recession adjacent to an edentulous ridge that also requires ridge augmentation. a. -
Langer and Langer (1983): Flap Type Partial thickness flap reflection CT graft from palate placed into recipient site Flap replaced to cover graft.
b. Raetzke (1985): Pouch Type - Partial thickness envelope or “pouch” created - CT graft from palate placed into pouch INDICATIONS *Inadequate donor site for lateral pedicle *Isolated wide gingival recession *Multiple root exposures *Recession adjacent to an edentulous ridge that also requires ridge augmentation ADVANTAGES *Versatile techniques *Esthetic root coverage *Can treat isolated wide areas of recession *Can use in areas with inadequate donor sites for pedicle grafts *Donor tissue not limited by rugae
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*Double blood supply to graft *Easier to stabilize than thick FGG *Less discomfort at palatal donor site DISADVANTAGES *Two surgical sites *More difficult techniques for graft harvest *May have inadequate CT in thin tissue F. Guided Tissue Regeneration ADVANTAGES *Should yield a new CT attachement via a long junctional epithelium DISADVANTAGES *Technique still fairly new *Potential for early membrane exposure and additional recession *Difficult to establish necessary “space” under the membrane Indications for augmenting zone of attached gingiva: - Ericson & Linde 84 - subgingival restoration or ortho treatment may cause recession if little or no attached gingiva is present and oral hygiene is not perfect. - Improves plaque control. - minimal AG that can't be maint free of inflamm. - fixed or removable prosthesis placed in area. - cosmetic or root surf sensitivity. - ortho movement of teeth out of alveolus. Miller's classification of recession based on root coverage predictability: -Class I: Recession does not extend to or beyond the MGJ. No loss of interproximal bone or soft tissue. -Class II: Recession extends to or beyond the MGJ. No loss of interdental bone or soft tissue -Class III: Recession extends to or beyond the MGJ. Loss of interdental bone or soft tissue is apical to the CEJ, but coronal to the apical extent of the marginal tissue recession. -Class IV: Recession extends to or beyond the MGJ. Loss of interdental bone extends to the level of the apical extent of marginal tissue recession. ** Total root coverage can be predicted in a Class I or II, only partial coverage in a Class III, and no coverage is expected in a Class IV lesion - Lateral sliding graft vs free gingival graft: - if goal is root coverage use lat sliding flap. - if goal is increasing zone of AG use FG graft. - Citric acid on root surg: - Hancock reported little difference in FG graft. shrinkage related to thickness of graft: - primary contraction > with thick graft. - Thin - less primary, more secondary. - Thick - more primary less secondary. - once scars down secondary contract > with thin graft. - Biologic width, Ramjford: - dimensional relationship btw crest alveolar bone. - CT attachment 1 mm (1.07) length. - JE 1 mm (0.96) length. - Crown lengthening procedure: - indications: root fx, root caries, root perforation. - like to have 3 mm or more tooth above crest of bone.
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- rationale: - maintain healthy periodontium. - better retention for crown. - easier impression taking. - procedures that lengthen crown: - gingivectomy. - apically positioned flap w or wo osteoplasty. - orthodontics, forced tooth eruption: - incise crestal fibers q2wks. - may need crown lengthening also. - retention 6 to 8 wks before crown prep. XI Surgical Phase: 1. Rationale for perio surgery: - < 3 mm pocket scaled ok. - 3-5 mm pocket scaling effectiveness falls off rapidly. - > 5 mm pocket scaling effectiveness not good. - 1-3 mm closed scaling ok. - 4-6 mm open flap more successful. - > 6 mm open flap 50% successful. 2. New Attachment - reunion of connective tissue or epithelium to a pathologically exposed root surface: may include new cementum 3. Reattachment: - reunion of connective tissue with a root exposed surface by incision or injury, but with viable PDL cells. - not new attach but reattachment procedure. - i.e. super crestal fibrotomy. 4. Peridodontal Regeneration techniques of new attachment: - goal is to put back like it was. - architecture and function of the periodontium is completely restored with new alveolar bone, new PDL and cementum. - i.e. bone grafts- percentage of success directly related to # of remaining osseous walls. 5. Periodontal Repair: - reestablishment of continuity with out full restoration of architecture and function XII. Wound healing: - inflammation 1st 24 hours then over at 4 days. - Epi starts 1st = .5-1.0mm/day of movement. - needs to be near blood supply approx. .25mm away. - migration and mitosis 24-36hours after clot formation 6- 12hrs. - Connective tissue repone follows epi, 3-4 days. - Bone: Osteoclastic (13 hrs to 3 days). Osteoblastic (3-7 days with flap). - Healing is under the function of cellular guides (genetic) you cannot accelerate, but can inhibit. - Cells have to shut down their normal function and start repair. Rates: - Currettage Epit 3-7 days / CT - 7 to 15 days. - Gingivectomy Epit 7-14 days / CT 14 to 35 days. - Flaps Epit 7 days / CT 14 days. - Pedicle flap Epit 10-14 days / CT 21 days. - FGG Epit 8-14 days / CT 17 - 30 days. XIII. Soft tissue new attachment procedures
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1. Indications: - severe periodontitis. - advanced furcation involvement. - may get some regeneration with flap curettage. 2. New attachment is goal. a. closed curettage. b. ENAP: Subgingival curettage with a knife. - not for pockets that apical extent is below MGJ. - incision to base of pocket. 3. Modified ENAP: - incision to crest of bone. - indications, suprabony pockets (5mm or less), max/mand anterior for esthetics. 4. Modified Widman: 3 incisions. - 1st: .5-1 mm from FGM to crest of bone. - 2nd: sulcular incision. - 3rd: horizontal incision. - minimal flap reflection not past MGJ. - scale and root plane above healthy CT tissue. - (original Weidman was full thickness apically positioned flap). Indications: Esthetics Severe Periodontitis Intra Bony Pockets High Caries Rate Root Sensitivity Allows access to defects, access to roots w/ minimal recession. Disadvantages: May heal with soft tissue craters 5. Flap curettage: - usually done secondarily to scaling. - by definition means curettage of pocket with finger pressure on gingival unit. - flap procedure for debridement(FPD) not to used in pockets less than or equal to 4mm. - option in chronic adult periodontitis that do not lend themselves to regeneration or the pts option. - indications, severe perio, advanced furcation. - advantages, may get regeneration, improves interproximal attachment, facilitates root debridement. - disadvantages no osseous recontouring. 6. Scaling: - instrumentation to remove all supragingival uncalcified and calcified accretions and all gross subgingival accretions. 7. Root planing: - instrumentation to remove microbial flora on root surface or lying free in the pocket, all flecks of calculus, and all contaminated cementum. - remove endotoxin: - complex polysaccharide in gram (-) bacterial cell wall. - why? studies have shown that cultured fibroblasts will not grow on root surfaces contaminated with endotoxin. - Gross scaling alone resulted in endotoxin much greater than for those of healthy root surfaces. - Root planning got endotoxin down to within one nanogram of noninvolved healthy tooth. 8. Hand Curette vs Ultrasonics: - hand curette are better but not big difference. - after scaling with hand curette 2 nanograms endotoxin left. - ultrasonics 16.8 nanograms endotoxin left. - control or untreated teeth had 106 nanograms left. - ultrasonics 90% as effective as curette. - do not know what threshold level of endotoxin is. Resective techniques: - apically repositioned flap with osseous recontouring. - indications generalized mild to moderate periodontitis.
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- major restorative plan do not wait long for healing. - most predictable, economics/cheaper because less visits. - results in minimal bone loss ( 0.4 to 0.6mm bone loss from flap reflection). - contraindications: - inadequate plaque control. - compromise sound adjacent areas. - inadequate attachment remaining. - root caries. - root sensitivity. Severe isolated defects: - bone grafts. - ortho to extrude tooth. - root resection. - maintenance. - extraction. Generalized deep defects: - new attachment procedure. - modified Widman. - flap curettage. - resective procedure. FURCATION MANAGEMENT Anatomy of Maxillary Molar Teeth a. Location of Furcation Entrance from CEJ Mesial – 3.6 mm Buccal- 4 mm Distal – 5 mm b. Location of Furcation Entrance 1) Mesial – widest root extending 2/3 width of the crown buccally-lingually, hence the furcation entrance is located more palatally and is more easily detected from the palatal side. 2) Distal – located at midpoint of tooth in buccal –palatal dimension, therefore can be detected from either a buccal or palatal approach. c. Concavities and Ridges interfere with root preparation and hygiene - the width of the furcation is smaller than the curette 58% of the time Anatomy of Mandibular Molar Teeth a. Location of Furcation Entrance from CEJ 1) Buccal – 3 mm 2) Lingual – 4 mm b. Surface Area of Attachment 1) Mesial Root – 37% 2) Distal Root – 32.4% 3) Root Trunk – 30.5% c. Internal Furcation Anatomy a) Concavities – present on the distal of the mesial root and the mesial of the distal root 100% of the time b) Intermediate bifurcation ridge – cementum ridge that extends in a mesial-distal direction, present 73% of the time c) Accessory Canals d) Width of Furcation – smaller than a curette 58% of the time ______ Anatomy of Maxillary Premolars Furcations a. Bifurcated 37-56% of the time, trifurcated 4% of the time; the furcation location varies but tends to be in the apical half of the tooth, resulting in a very long root trunk; invasion of this furcation by periodontitis usually results in loss of the tooth. b. If the tooth is single-rooted, a deep mesial groove is virtually always present; less
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c. ______
Commonly a more shallow groove can be found on the distal surface of the root; these grooves are extremely difficult and unpredictable to treat if they become periodontally involved. As a rule, maxillary premolars with furcation involvement should be considered to Have a poor or hopeless prognosis. Few of these teeth do well long term.
Etiology of Furcation Involvement a. Primary Factor – bacterial plaque b. Contributing Factors – Amount of alveolar bone loss Pulpal Pathology Iatrogenic Factors Factitial Injury c. Predisposing Factors Furcation Location Cervical Enamel Projections (No Attachment) – 17% Max Molars - 29% Mand Molars Thickness of Overlying Gingiva and Bone Root Anatomy Enamel Pearls Incidence and Distribution of Furcation Invasion a. b. c.
d.
Incidence increase with age First molars most common Buccal furcation most common – usually due to toothbrush induced recession Most common resesected root – DB root of 1st maxillary molar
CLASSIFICATION I.
Glickman Classification – horizontal probing 1)Grade 1 – incipient, pocket formation into furcation fluting, interradicular bone is intact. 2)Grade 2 – moderate, loss of interradicular bone but not through and through 3)Grade 3 – through and through, gingival tissue occludes orifices 4)Grade 4 – exposed, high and dry II. Lindhe and Nyman’s Classification – horizontal probing 1) Degree I - 3mm 3) Degree III – through and through III.Tarnow & Fletcher – vertical loss from the roof of the furcation apically 1) Subclass A – vertical loss 0-3 mm 2) Subclass B – vertical loss 4-6 mm 3) Subclaass C – vertical loss > 6mm Rationale for Furcation Treatment a. Regeneration of lost attachment apparatus – tx of choice but not always possible. b. Access for oral hygiene c. Access for root preparation d. Pocket Elimination e. Treatment of non-periodontic conditions i. Root Caries ii. Fractures iii. Root Resorption iv.Endodontic Complications i.e. perforations, broken instruments FURCATION THERAPY - extraction, scale root plane, odontoplasty, raise roof(tunneling), root resection, apical position flaps with osseous surgery. 19
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obliteration with IRM or amalgam.
Definitions 1. Root Resection. The separation of a root that may or may not include the retention of that root or the removal with accomplanying odontoplasty. 2. Root Amputation: The removal of a root from a multirooted tooth. 3. Hemisection: The surgical separation of a multirooted tooth, especially a mandibular molar, through the furcation in such a way that a root and the associated portion of the crown may be removed. 4. Root Separation: Splitting of a mandibular molar with the retention of both fragments. Ie. Bicuspidization Hamp’s treatment based on degree of furcation involvement (Linde and Nyman’s furcation classification system) (1) Degree I furcation involvement – scaling, root planing, furcation operation (to facilitate plaque control, full thickness flap, odontoplasty to open the furcation entrance, osteoplasty to recontour bony defects) (2) Degree II – furcation operation, tunnel preparation, root resection, tooth extraction (3) Degree III – tunnel preparation, root resection, tooth extraction Treatment options 1. Regeneration Best in F or L grade II furcations associated with an intrabony component Less success in M or D Maxillary Furcations Unpredictable results in grade III defects Combination of bone graft + membrane most predictable Less recession, greater horizontal attachment gain with Guidor Vs. Goretex 2. Resection 1) Root Amp – Usually Max Molars 2) Hemisection – Usually Man Molars 3) Root Separation - Tx of grade III furcations with adequate bone support around both roots 4) Tunneling – Create a grade IV furcation; requires horizontal bone loss and divergent roots Indications for resection Severe bone loss affecting one or more root Grade II or III furcation involvements Unfavorable root proximity with adjacent teeth Root fracture, perforation, caries, or resorption of root When required endo treatment of a particular root can’t be performed Contraindications for resection Insufficient bone supporting remaining roots Unfavorable anatomic situations (long root trunk, fused roots) Lack of usefulness of remaining roots Unable to perform endo treatment in remaining roots Lack of usefulness of remaining roots Large discrepancies in adjacent proximal bone heights Expense or time constraints Inadequate oral hygiene Nonrestorability of remaining roots Restorative Considerations (1) Full Coverage is recommended if a root has been removed (2) Root Resected teeth may be used as abutmens for fixed and removable prostheses. The length of the span and the remaining support have to be considered when determining whether a particular tooth is suitable as an abutment. Keep pontics narrow on FPDs. Failures 1) Langer study – 100 patients who had root resection evaluated 10 years after tx.
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50% of the failures occurred between 5-7 years. Most failures due to: a. fractures – most common reason for failure b. caries c. endodontic complications 2) Basten Study – 32 patients with 49 root-resected molars. Survival rate was 92% and time was 12 years. The prognosis for root-resected molars may be Better than previously believed.
mean survival
Failures of root resection. - most failures due to fractures, caries, periodontitis, endo complications. ___________________________________________________ Indications for Osseous Surgery - infrabony pocket not amenable to graft. - open up furcation. - Crown lengthening. - obtain material for graft. - for better flap closure. - ledges, tori or irregularities. Two wall bony defect most common Three wall defect best results when using bone graft. Surgical Therapy Provide simplest therapy that is likely to provide clinical stability. Periodontitis less prevalent than in past. - incidence going down. - because you have gingivitis does not mean will have periodontitis. Regenerative procedures becoming more predictable. - current emphasis on periodontology: - eliminate etiology. - correct defects by adding to periodontium. Areas of regeneration: 1. Bone grafting: - regeneration of bone does not necessarily mean new PDL, cementum, and CT attachment. - can get bone regener and still have long JE attach. 2. Root conditioning: - mechanical. - chemical. 3. Guided tissue regeneration: - gortex membrane. - the purposeful selection of cell types that repopulate a wound with the intention of directing the healing tissue composition. Bone Grafting: Gross, JS, Bone Grafting Materials For Dental Applications: A Practical Guide, Compend. Oct 1997;18(10):1013-1036. 1. Types of grafts: autogenous - same person. allograft - same species. xenograft - different species. alloplasts. - natural or synthetic materials 2. Bone growth potential of grafts. - Osteogenic – graft has viable cells which actually produce bone - Osteoinductive – graft stimulates/induces new bone growth.
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Osteoconductive – template or trellis for new bone growth.
3. Osteogenic: - autogenous graft. - the only osteogenic material is hematopoietic bone marrow. - most adults intraoral marrow is fatty or fibrous. - must go to hip or create hematopoietic marrow in oral cavity. - plan tooth extraction for bone donor site. - create pseudo extraction site. - make "well" in bone, go back later to get hematopoietic bone marrow. - how long after extraction before harvesting marrow? - 1982 study said 8-12 weeks. - 1989 study said 4 weeks. ** take bone sooner, it has little mature bone but lots of osteogenic potential. 4. Osteoinductive: - these grafts induce bone to grow from surrounding area. - does not have potential to grow bone by itself. - autogenous grafts (from same person): - osseous coagulum, bone blend. - conductive but has some inductive potential. - osseous coagulum conductive because it is mineralized. - during healing demineralization occurs and some Bone Morphogenic Protein is released to get inductive effect. - allografts (from same species): - freeze dried decalcified bone. DFDBA - inductive due to bone morphogenic protein, BMP, left after decalcification. - decalcification process gets rid of inorganic component leaves organic component. - organic component releases BMP that has ability to induce bone growth. 5. Osteoconductive: - acts as scaffold for bone formation. - cannot make bone, cannot induce bone to form. - most of bone grafts and all alloplastic grafts are osteoconductive. autogenous: - osseous coagulum, bone blend. - has some inductive effect. - most conductive hip marrow > DFDBA alloplastic: - bone substitutes. - ceramics: - most popular. - hydroxyapatite or tricalcium phosphate. - non-resorbable. - polylactic acid and polyglycolic acid PLA/PGA: - resorbable. - in future may be carrier for genetically engineered proteins and growth factors which will be Osteoinductive. ** Remember growing new bone does not necessarily mean getting new cementum, PDL, and CT attachment. Root Conditioning: 1. Growth factors: - hot area in research. - many cells have growth factors specific to them. - hundreds exist. - if could paint cementoblast growth factor on root surf may get cementoblast to migrate and proliferate.
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- enhance one cell and retard another. 2. Citric acid: - showed promise in animal studies. - controversial in humans. - still considered to be experimental. - purpose is to decalcify root surface: - direct antibacterial properties pH=1 - allows collagen to collagen healing between newly forming PDL and root surface. - after flap replacement 1st thing in healing decalcification of bone occurs even without citric a: - if utilized burnish on roots for 3-5 min 3. Fibronectin: - occurs naturally. - necessary for CT cells to attach to one another and to other objects such as root surface. - no evidence that painting it on root surface in humans does any good. - may be enough occurring naturally on root surf and do not need to add more. - experimental. Guided tissue regeneration: - allows CT to participate in healing while preventing epithelial tissues. - gortex: - expanded porous Teflon membrane. - used in osseous defect, furcation or interproximal. Technique: - flap, scale root plane, osteoplasty. - flap gets no circulation from alveolar vascular bed. - place gortex over defect, Teflon sutures. - cementum, PDL, CT included in healing. - epithelial tissues excluded from healing. - allows more time for bone, CT, PDL to form. - prevents rapid long JE formation. - leave gortex in for 4-6 weeks. - antibiotics for 3 weeks. - peridex for 4 weeks. - good success rate. - Avoid flossing, and don’t probe the area for at least 6 months. Maintenance: Shallhorn and Snider: Compromised maintenance - when factors such as poor systemic health or poor plaque control prevent corrective therapy Preventive maintenance - in periodontally healthy individuals Trial maintenance - to control disease while assessing borderline defects such as minimal gingiva or certain furcation defects Post treatment maintenance - to prevent recurrence of disease - goal to maintain health by preventing recurrence of disease. - monitoring, reinforcing OH, rescaling as required. - necessary. - If absent and OH poor case will be failure or disease will speed up after surgery. - 50-70 articles, both clinical and microbiologic studies: - show 4 month return to disease. - 3 month recall is good maintenance interval. - some need shorter interval if continue break down. - others longer if no active disease. - tailor maintenance to each individual. - recall not successful if home care is poor. - Bugs can repopulate in 2 to 5 months.
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Classification of ridge defects: (Siebert) Class I - Buccolingual loss of tissue with normal ridge height in an apico-coronal dimension Class II - Apico-coronal loss of tissue with normal ridge width in a buccolingual dimension Class III - Combination buccolingual and apico-coronal loss of tissue resulting in loss of normal height and width 1996 World Workshop in Periodontics NON-SURGICAL POCKET THERAPY: MECHANICAL Based on existing data, one could argue that after the age of 20 years, 0.1 mm to 0.2 mm is a justifiable range reflective of the mean annual rate of progression for untreated periodontal disease. Depending upon the study, the most significant risk indicators have been tooth type, initial attachment loss or bone height at baseline, moderate and severe gingival inflammation, presence of subgingival calculus, age and smoking. Some studies indicate no correlation with one factor, but is true for multiple factors. Holds true for even younger age groups. Those patients who have their periodontal disease treated and receive continual supportive therapy will lose significantly fewer teeth than patients that remain untreated. (3.5X) Scaling = instrumentation of the crown and root surfaces of the teeth to remove plaque, calculus, and stains from these surfaces. Root planing = a definitive treatment procedure designed to remove cementum or surface dentin that is rough, impregnated with calculus, or contaminated with toxins or microorganisms. There is considerable evidence supporting scaling and root planing as an essential and effective component of therapy for the inflammatory periodontal diseases. The clinical benefits of scaling and root planing are derived from the removal of subgingival plaque and calculus and disruption of the subgingival microflora and therefore a delay in the repopulation of pathogenic microbes. However, subgingival flora has supragingival origins. Consequently, effective control of supragingival plaque combined with frequent professional subgingival therapy is critical for long-term control of inflammatory periodontal disease. Measurable endpoints used in studies include: loss or gain of attachment levels, probing depth, gingival inflammation, bleeding on probing, and changes in subgingival microbial flora. Clinical attachment levels and scaling and root planing Sites of 1-3 mm pockets lost attachment of -0.34 to -0.42 mm Sites of 4-6 mm pockets had a mean gain of 0.55 mm Sites of > 7 mm pockets had mean gain of 1.29 mm Used to possibly explain attachment loss on facial surfaces of teeth due to trauma (toothbrushing) and when treating adjacent sites. Healing of periodontal tissues following scaling and root planing Regeneration of the root-epithelial interface as a long-junctional epithelial attachment which precluded the formation of a new connective tissue attachment. Occurs within 1 to 2 weeks Get gradual reduction of inflammation with < in inflammatory cell populations, < crevicular fluid flow, repair of connective tissue matrix. Factors affecting measurement of clinical attachment levels
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Differences between duplicate recordings can vary between 1 to 2 mm. Probing depth > by 0.3 to 0.6 mm in inflamed pockets. Other factors: access and visibility, probe diameter, probing force and velocity, probe angulation, local anatomy, presence or absence of easily defined land marks from which to take measurements. Automated or pressure sensitive probes have not improved intra- or inter-examiner reliability. Probing depth and scaling and root planing Attachment level measurements are the major emphasis of researchers, but lack emphasis by clinicians. Two reasons are problems in obtaining accurate measurements and the more important is that clinical attachment levels may be statistically significant, they border on being clinically insignificant. Due to problems of long-term maintenance, the practicing clinician more often relates to changes in probing depth. Depending on the clinical parameters measured, one could argue that studies comparing scaling and root planing with and without surgical access show that more conservative therapy has a long-term effect nearly equal to that accomplished with surgical access. True for single rooted teeth but not multirooted. Get improvement in multirooted teeth with continuous deterioration over time. Some studies initially show a greater reduction in probing depth after surgery vs scaling and root planing, the differences become insignificant over time. Nyman and Linde suggest it is not the modality of treatment that matters but the thoroughness of surface treatment. Gingival bleeding and scaling and root planing Lang et al suggested that the absence of bleeding be used as a criterion for stability rather than using the presence of bleeding on probing as a predictor of disease activity. Subgingival microbial flora and scaling and root planing Reported significant reductions in the percentage of motile microbes and spirochetes, Porphyomonas gingivalis, and other gram -negative anaerobic microbes and a concurrent increase in the percentage of cocci and non-motile microbes. Several studies have demonstrated that microbial repopulation of subgingival pockets can be severely inhibited by continual and effective oral hygiene. In contrast, the presence of a supragingival microbial plaque appears to facilitate repopulation of subgingival pockets within 4 to 8 weeks, including high percentages of spirochetes and motile rods. Furcation and scaling and root planing Molars with furcation involvement generally have a compromised prognosis. 19 to 57% of teeth with furcation involvement were lost in 15 years versus 5 to 10% of teeth without furcation involvement. Furcations, in general are less responsive and more difficult to adequately treat using mechanical root therapy. The less favorable clinical response to mechanical non-surgical therapy, typical of molar furcation lesions, is related to furcal anatomy, lack of access, and therefore, the persistence of a pathogenic microbial flora. Effectiveness of scaling and root planing Percentage of surfaces exhibiting residual calculus after scaling and root planing , by experienced operators, with and without surgical access is as follows: 17 to 69% non-surgical and 14 to 24% with surgery. > probing depth = > residual calculus, tooth position did not matter (ant vs post), no statistical difference between furcations between closed (68%) and surgical access (44%). Spent average 9 to 15 minutes per tooth scaling and root planing. As with microbial plaque, clinical success or failure of scaling and root planing may be dependent on a critical mass of residual calculus rather than total elimination. Associated with the reduction in calculus volume below critical mass is the decrease in surface associated microbial plaque and therefore a decrease in bacterial virulence factors e.g., accumulated organic acids, enzymes, endotoxins, and various cell wall antigens. CEMENTUM removal by scaling and root planing
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Removal of all cementum is not a realistic goal. Recent studies would challenge the validity of extensive cementum removal for the sole purpose of removing endotoxin. New studies argue that endotoxins are superficially bound to the root surface and 99% can be removed by gently washing or brushing for 1 minute. Recontamination will occur over a very short period of time anyway. Amount of cementum removed during scaling and root planing. Ascending order of mean root substance removal after 12 strokes: ultrasonic scaler 11.6 (m < sonic scaler 93.5 (m < manual curet 108.9 (m, < rotating diamond bur 118.7 (m. Root surface roughness and scaling and root planing Instrument induced root surface roughness results in an increased surface free-energy, increased surface area, promotion of microbial adherence and colonization and therefore plaque maturation, and compromised plaque removal. Manual versus power-driven instrumentation of root surfaces Studies vary widely in results. Generally, in spite of contradictions concerning root surface roughness, one area of agreement does exist: complete removal of microbial plaque and calculus is not accomplished by either manual or power driven scalers. 1. Regardless of instrument choice, interproximal areas, furcas, cemento-enamel junction, and multirooted teeth in general are most likely to exhibit residual calculus after treatment. 2. As probing depth increases, the power driven instruments become less effective due to limitations in design. New designs are coming out that appear to be more effective. 3. When comparing the manual curet and ultrasonic instruments, the curet appears slightly more efficient but requires more effort , time, and expertise. Again newer ultrasonic head designs appear to be overcoming this problem. 4. A similar comparison between sonic and ultrasonic instruments indicates that sonic instruments to be more efficient. The differences are probably not clinically significant. 5. The best results are probably obtained by combining sonic/ultrasonic instrumentation with manual scaling. Subgingival microbial flora and sonic/ultrasonic instrumentation All are comparable to hand instrumentation and each other Removal of root bound endotoxins by scaling and root planing (manual and sonic/ultrasonic scalers) All are equally effective. Collectively, new finding suggest clinicians may be over-instrumenting root surfaces under the guise of root surface detoxification when this may not be necessary. New designs in sonic/ultrasonic scalers inserts Fiber-optic probe = significant reductions of calculus in 4 to 6 mm pockets (40% vs 5%) Using antimicrobial instead of water for cooling and irrigation effect = some studies show chlorhexidine (0.02%) has some > effect in pockets of 4 to 6 mm, most other studies did not show a difference between chlorhexidine and water. Sonic scalers fitted with plastic tips = showed that this produced a smoother surface than either manual curets, a rubber cup with polishing paste, or the sonic scaler fitted with a metal tip. Changes in clinical parameters following scaling and root planing with sonic/ultrasonic instruments There is little difference in the clinical response between the various types of instrumentation. NON-SURGICAL POCKET THERAPY: PHARMACOTHERAPEUTICS Irrigation methods and delivery devices
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It appears that both supra- and subgingival home irrigation is effective. It should be kept in mind, however, that with any oral hygiene device, it is only as good as the operator, and beneficial results vary widely from patient to patient. Effect on plaque toxicity May be beneficial due to 1) change in plaque composition, 2) flushing out of inflammatory factors, and 3) physical change in tissue integrity. Irrigation may involve specific host-parasite alterations or mechanical stimulation of gingiva may in some way be beneficial. Penetration Subgingival irrigation may penetrate more deeply than previously thought. Since calculus impedes irrigation in deep sites, patients should be instructed to use irrigation after initial debridement has been completed to obtain the most benefit from irrigation therapy. It would appear that maximum results are obtained if the irrigant reaches the base of the pocket either by cannula on a pulsed irrigator or by inserting a blunt irrigating needle on a hand held syringe at least 3 mm subgingivally. Irrigating solutions Water - Majority of studies concluded that water provided equal, and sometime superior, beneficial result when compared to other test medicaments. The implication is that the physiologic flushing of the pocket itself may comprise the primary therapeutic effect of irrigation, regardless of the irrigant used. Chlorhexidine - Has broad spectrum of topical antimicrobial activity, in addition to safety, effectiveness, substantivity, lack of serious side effects, and lack of toxicity that has allowed it to be used extensively in dentistry. CHX activity in the oral cavity is promoted by binding to plaque, salivary pellicle, oral mucosa, and hard structures and its release for up to 24 hours makes it a highly substantive product. Reversible side effects include staining of hard tissues and some dental products, altered taste sensation, supragingival calculus accumulations, and less commonly, a mild mucositis. The literature seems to support a range from 0.02% to 0.2% CHX as efficacious dosage for use in an oral irrigator as a means of reducing gingival inflammation in specific clinical situations. Ones study showed > effect with 2% CHX to enhance effect of SRP. Daily home irrigation with water or CHX appears to be beneficial to maintenance patients. Conc are not firmly established, but need higher conc to help in periodontitis than gingivitis. Peroxides - May be helpful to < AA Fluorides - 1.64% stannous fluoride may help in multiple treatments. Many studies did not agree. Iodine - Seems to be effective, but combination with peroxide and fluorides seem to have the most beneficial effect. Advantage is low cost and very low probability of bacterial resistance. Disadvantage is staining and allergy. Phenolics - Has been shown to < plaque, bacterial cell counts and gingival bleeding. Irrigation with antibiotics Root substantivity - TCN - HCL The amount of antimicrobial activity retained is proportional to the conc of the TCN used for irrigation. 5% = 12 days, 1% = 4 days. However, found 5% TCN did not > effect of SRP versus SRP alone. 10% TCN over longer periods of time ( 5 minutes) did show continued therapeutic release for 1 week. Also showed > attachment gain compared to SRP alone. 0.5% metronidazole showed no benefit over water alone. Topical irrigation with non-steroidal anti-inflammatories ASA - No better than water itself Flurbiprofen, meclofenamic acid, ibuprofen - are being investigated for periodontal inflammatory use. Zinc sulfate, Chloramine-T, - - showed less effect than even water. Paradontax, Tetrapotassium peroxydiphosphate and oxygen - all showed to have an improved effect. Ultrasonics and antimicrobials CHX had mixed results, CHX plus doxycycline and povidone iodine alone or with doxycycline showed good results. Penetration was 100% in 86% of the pockets 3 to 9 mm deep. Safety Seems to be safe without deleterious effects
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Irrigation may cause bacteremia; therefore the evidence does not support recommendations of irrigation for patients at risk for infective endocarditis. Summary Water irrigation at the gingival margin reduces gingivitis, and the addition of antimicrobial agents has some additional clinical efficacy over water irrigation alone. Subgingival irrigation as an adjunct to conventional therapy in periodontitis sites has had mixed results. With the exception of high conc of CHX (2%) or TCN (10%), the addition of the other antimicrobials have resulted in rather unremarkable additional benefits beyond water or saline alone. Prostaglandins: Implication in periodontal disease Bacteria are essential causative agents of periodontal disease. However, in the past 20 years, research has shown the pathogenesis of periodontal disease to involve the host’s inflammatory response. Bacteria and bacterial by products can cause tissue damage and evoke inflammatory response producing metabolites from the breakdown of arachidonic acid by the cyclooxygenase pathway. This gives rise to prostacyclin, thromboxane, and prostaglandins. These metabolites have been implicated in a number of diseases, but in periodontics they have been associated with gingivitis and bone loss. (prostaglandin E 2 is the major player) They find higher levels of prostaglandin in crevicular fluids and gingival tissue samples of subject with periodontal disease versus healthy individuals. (also in areas of radiographic bone loss) Therefore, if NSAIDs inhibit prostaglandin production they might < effect of periodontal disease. Non-prostaglandin pathways in the breakdown of arachidonic acid may also be important. One, lipoxygenase pathway may be important = hydrooxyeicosatetraenoic acid (HETE), especially 12-HETE and 15-HETE, seem important mediators of inflammation in the tissues of patients with diseased gingiva and advanced periodontal disease, respectively. One study showed leukotrienes and HETEs were potent stimulators of bone resorption. The role of NSAIDS in the control of periodontal disease progression Three groups have been investigated 1. Pyrazolone compounds (indomethicin, phenylbutazone, and tolmetin) 2. The phenylproprionic acid derivatives - (Ibuprofin, fenoprofen, ketoprofen, naproxen) 3. Flurbiprofen and the oxicams - specifically piroxicam. All have shown to < bone loss compared to control groups either by topical or systemic application. No real studies yet on effective doses. May not be practical if high doses are necessary. Also seem to be effective in bone loss around implants. Triclosan inhibits the cyclooxygenase and lipoxygenase pathways with similar efficacy. Research concerns: 1) Which pathway is primarily responsible for the metabolites associated with periodontal progression, the cyclooxygenase, the lipoxygenase, or a combination of the two pathways causing the most destruction 2) Which specific NSAID or combination is the most efficacious in halting periodontal disease. Topical and sustained release antimicrobials A variety of new supragingival antimicrobials aimed at controlling plaque and gingivitis include: a broad spectrum adhesive antibiotic; sustained-release CHX and arginin varnishes; CHX polymeric coating; and cetypyridinium chloride methacrylic acid copolymer. Recently developed subgingival topical and sustained release agents for treating or maintaining periodontitis sites include: gels containing CHX, metronidazole, clindamycin, TCN, and flurbiprofen; acrylic strips with CHX. metronidazole, or TCN; antimicrobial ointments with minocycline; controlled release devices and bioresorbable materials containing ofloxacin, doxycycline, TCN, CHX, and methylene blue; non-resorbable TCN-loaded ethylene vinyl acetate fibers; and locally delivered antimicrobial microencapsulated minocycline polymer. Some resistance has been seen to antimicrobials used. CHX caused no detectable changes. MET had variable effects. TCN and doxycycline did show resistant organisms.
28
Locally administered antibiotics as a monotherapy has been shown in some studies to have a similar effect as SRP. Monotherapy approach is questionable since use should be in recurrent or refractory cases which are preceded by mechanical therapy or are applied in conjunction with SRP. Monotherapy may extend maintenance visits. The evidence supports the fact that when traditional therapies fail to arrest the disease, topical or locally delivered sustained-released antimicrobial therapy generally has some effect, at least over a short period of time. Locally applied antimicrobials should be regarded as an adjuncts to mechanical periodontal therapy in the treatment of recurrent and refractory patients. Systemic antibiotic Refractory periodontitis is now that definition as described by van Winkelhoff = attachment loss despite optimal subgingival debridement and performance of excellent hygiene by the patient. TCN - Most commonly prescribed antibiotic used in periodontics - Include TCN-HCl, minocycline, doxycycline, all of which inhibit most microorganisms that are believed to be a factor in periodontics. Bacteriostatic in nature. - TCN conc in the gingival crevice is 2 to 10 times that in serum which allows a high drug conc to be delivered into the periodontal pocket. - Good against AA - Like most in this group, has important function in reducing collagenase activity. Based on evidence available, it appears that the use of TCN in adult periodontitis is generally not warranted. Has been used successfully with juvenile periodontitis. Various regimens have been used. Shows long term stability and resolution of defects. Seems directly related to the control of AA. Seems important that family members, including the family dog be treated, to avoid reinfection with AA. Seems to work well with refractory periodontitis. Can show dramatic repair and regeneration of lost periodontal tissues following systemic administration either alone or in combination with other forms of periodontal therapy in severe adult periodontitis. Suppression of AA with a 2-week dose of TCN prior to the standard prophylaxis for infective endocarditis has been recommended for LJP patients at risk for infections. Indications - Early onset periodontitis - LJP, GJP, RPP, and refractory cases. - Debridement and surgery have failed to eliminate AA, systemic treatment needed. - Not justified in adult periodontitis Contraindications - Children under 8, patients on low dose BCPs, renal or hepatic disease. Long-term low-dose TCN - Big area of research now. Doxycycline - Unlike TCN, can be given with food or dairy products since the decrease in absorption is only about 20% versus 50% with TCN Both doxycycline and minocycline can be given to patients with renal dysfunction, unlike TCN, which is eliminated essentially unchanged by glomerular filtration. No indications for adult periodontitis Seems to be useful in refractory periodontitis and if a patient still seems resistant adding metronidazole seems to work in most cases. Does not seem to help out in Juvenile perio Chemically modified TCN Hot area of research - Discovered that certain host-derived enzymes called matrix metalloproteinases (MMPs) can be inhibited by TCNs. The work is to enhance this activity of new TCN and < antibacterial effect, because these
29
new drugs seem to work just as well in inhibiting bone loss and gingival collagenolytic activity even though they do not suppress the bacteria. Minocycline Seems effective against LJP but not GJP Does not < AA like others. Questionable choice for infections caused by AA. Metronidazole Serum and crevicular levels of MET have been shown to reach minimum inhibitory conc (MIC) levels for most periodontal pathogens. Is effective against 10 pure strains of oral spirochetes and were found to eliminate spirochetes from NUG lesions. It is a direct-acting amebicide/trichomonacide that binds and degrades DNA in the organism. Is the drug of choice for subgingival plaque consisting primarily of anerobic gram-neg rods and spirochetes. It is bactericidal rather than bacteriostatic, which allows it to function effectively independently of the host defense system. May be of some help in severe adult periodontitis, especially administered 1 week post SRP. Most effective in eliminated AA in Juvenile periodontitis, superior to rest of the TCNs. Refractory periodontitis with or without other antibiotic combinations including ciprofloxacin, amoxicillin or doxycycline, has been successfully treated for up to two years following periodontal debridement plus MET. Ciprofloxacin Broad spectrum bacteriocidal agent that inhibits DNA needed for replication. Good against periodontal pathogens, but has minimal effect against streptococcal microbes. May facilitate the repopulation of the pocket with a microbial flora more associated with periodontal health. May interfere with growth patterns so do not use in young children and teenagers. Amoxicillin/Clavulanate May be effective with refractory periodontitis Clindamycin May be effective with refractory periodontitis Combination therapy MET/AMX, MET/TCN, MET/Spiramycin, MET/ciprofloxacin, Amx + Clavulante/DOX all proved to be effective. Antibiotic therapy should be reserved for the situations that cannot be managed solely with mechanical therapy, such as severe or acute infections, early onset periodontal diseases, and refractory cases. NON-SURGICAL POCKET THERAPY: DENTAL OCCLUSION While occlusal forces do not initiate periodontitis, results are inconclusive on the interactions between occlusion and the progression of attachment loss due to inflammatory periodontal disease. Periodontitis can be treated and periodontal health maintained without occlusal adjustment and despite the obvious presence of traumatic occlusal forces. A clinician’s decision whether or not to use occlusal adjustment as a component of periodontal therapy should be related to an evaluation of clinical factors involving patient comfort and function and not based on the assumption that occlusal adjustment is necessary to stop the progression of periodontitis. PERIODONTAL DISEASE: PATHOGENESIS Introduction: This is a new section in the World Workshop, and is based on data not only obtained from dental research specifically, but also extrapolated from medical research and applied to the discussion on periodontal disease.
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1,400 articles reviewed, 375 selected for inclusion in this section. The authors stated that they not only critically evaluated the articles, their reviews were biased by their own beliefs regarding the pathogenisis of periodontal disease, and the last section of this three part review is a “self indulgent desire to accomodate all significant findings into a unifying theory of pathogenesis,” which they entitled the critical path model. The first section is an overview of the pathogenesis of periodontal disease, and the second section focuses on the molecular and cellular pathogenesis of periodontal disease. Perspective and Overview: began with the non-specific plaque hypothesis of the 50’s, 60’s, and 70-’s gone beyond the specific plaque hypothesis current viewpoint that states the periodontopathic bacterial flora is necessary but not sufficient for disease, or that periodontal diseases are specific mixed infections which cause periodontal destruction in the appropriately susceptible host only 9% to 16% of the variability of in disease expression can be explained by the levels of specific microbes smoking can explain the same amount of disease expression, possibly raising the question as to whether antismoking programs might prevent as much periodontal disease as anti-plaque programs (very controversial) what this indicates is that there are many host and environmental factors which dramatically modify the expression of disease disease expression is a combination of host, microbial agent, and environmental factors epidemiological studies have renewed the emphasis on host response in pathogenesis for three reasons: 1) fundamental studies of inflammation have demonstrated wide variation in the magnitude of the inflammatory response from one subject to another; 2) microbial parameters can only explain a relatively small amount of disease incidence and prevalence; 3) studies of twins have suggested that overall about half the variation in periodontal disease expression is controlled by genetic, not microbial, factors periodontal disease has been shown as a risk factor for the developement of atherosclerosis, myocardial infarction, and stroke, with the odds raised from 1.6 to 2.1 times that of individuals without periodontal disease. It was postulated that the chronic systemic exposure to periodontal bacteria, endotoxin, and cytokines may contribute to atheroma development and thromboembolic phenomena periodontitis is also a risk factor for low birthweight pre-term delivery in pregnant mothers. Pregnant mothers with severe periodontitis showed a 7.5 to 7.9 fold increased risk for pre-term LBW. Indications are that low level challenges with P. gingivalis endotoxin, or non-disseminating subcutaneous P. gingivalis infections are capable of dramatically suppressing fetal growth. Molecular Signals and Cellular Processes: possible explanation for the low magnitude of association of microbial flora with disease expression is that not all strains of pathogenic organisms which belong to a specific genus and species posses the same virulence traits microbial virulence is determined by two specific traits: 1) virulence properties which enable the organism to successfully colonize and compete in an ecological niche; and 2) traits which confer the ability to evade the host subgingival microorganisms have been shown to be assacharolytic and anaerobic or facultative, and are capable of metabolizing the protiens within the gingival crevicular fluid, not requiring saliva and dietary carbohydrates as a nutrient source therefore, bacteria evade the antimicrobial activity of compliment and antibody by several mechanisms: 1) P. gingivalis sectetes polysaccharide capsules which prevent complement protiens and antibody from binding to it’s outer surface; 2) some strains release surface blebs containing bacterial antigens providing a binding site for compliment away from the bacterial surface antibody response is generally protective in nature, and it is theorized that, given the episodic nature of the disease, a systemic or local challenge of organisms may boost the immune response, an event that would bring the flora back under control. This may be brought on by scaling and root planing, essentially reimmunizing the patient and enhancing the serum antibody response. It is not known how much of the positive effects seen following scaling and root planing are a result of this reimmunization inflammation of the periodontium is a protective host response to the microbial burden of plaque. The junctional and sulcular epithelium are in constant contact with a high density microbial mass of approximately 10 to the 11th power becteria, which approximates the same bacterial density of the lower bowel. The inflammation provides protection and mediates the destruction of the periodontal tissues
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the supression of PGE2 synthesis with the use of NSAID’s greatly diminishes attachment and bone loss and thereby attenuates periodontal disease progression. The therapeutic efficacy of these agents can be impressive, comparing favorably with the efficacy of fluoride for the prevention of caries. They should be available soon possibly as topical agents in the form of rinses, gels, or toothpaste
Critical Path Model of Pathogenesis and the Role of Risk Factors: in the critical path model of pathogenesis, a virulent flora and the evasion of neutrophil clearance is a requisite for disease aquisition and the individual host response plays a primary role in driving the severity of disease expression the patient which responds to the indigenous flora with an inflammatory process would provide the ideal ecological advantage for the emergence for the black-pigmented organisms. This permits further proliferation of these pathogens due to the changes in the environment and may explain the episodic nature of the disease stress from physical, environmental, and social factors can cause a 2 log increase in bacterial density, leading to impaired neutrophil clearance, an enhanced inflammatory response, and further promoting bacterial overgrowth PERIODONTAL DISEASE: MICROBIAL FACTORS Introduction: This section was researched in 2 ways; first a computer search was done using key words appropriate for the microbial focus of this review. An example would be that the bacteria AA. was entered and the articles from the last five years relating to this pathogen were reviewed. Second, a search was made of the key periodontal journals for articles related to microbial topics. From this search, principal questions were addressed and the answers to these questions are the topic areas for this section. Conceptual Considerations: Most periodontal disease is caused by bacteria in dental plaque. While the infectious etiology of periodontal disease is generally accepted, there is still discussion as to the relative importance of individual bacterial species within dental plaque. The non-specific plaque hypothesis was based on the assumption that a homogenous mass of bacteria accumulates that exceeds the host defense capabilities, thereby causing periodontal disease. The specific plaque hypothesis by contrast states that dental plaque isolated from periodontitis lesions are qualitatively distinct from those isolated from healthy sites. This is the more accepted hypothesis. In order to implicate a particular organism, it must meet certain specific requirements, including: 1) the presence of high numbers of the organism in the periodontal lesion compared to either its absence or presence in low numbers in healthy sites. Also of interest here is the critical threshold of the organism needed to see clinical signs of disease; 2) elimination of these microorganisms from the site should result in clinical improvement; 3) there is a host immune response to the microorganism including antibody formation or cell mediated immune resonses; 4) there is a production of virulence factors that can be correlated with clinical disease; and 5) appropriate animal models demonstrate tissue destruction in the presence of these microorganisms. Approximately a dozen bacteria have been implicated in the formation of periodontal disease. prominent among these mainly gram-negative bacteria are Aa., Bacteriodes forsythus, Campylobacter rectus, Fusobacterium nucleatum, Prevotella intermedia/nigrescens, Porphyromonas gingivalis, Peptostreptococcus micros, and Streptococcus intermedius. These have been determined through numerous longitudinal studies that, despite their usefulness, have the distinct drawback of being unable to reliably culture the diseased site at the specific time connective tissue attachment is lost. Therefore, the question remains if the species that is cultured are the actual cause of the attachment loss or just a secondary invading factor. Some of these microorganisms are definitely linked to the cause of the disease, and there is a move to change the nomenclature of periodontal disease to reflect the causitive factor, such as “Actinobacillary periodontitis”. Others are not so closely linked to the disease but are seen often enough to raise the level of suspicion. The three species most implicated are Aa., B. forsythus, and P. gingivalis. Another area of interest has been whether or not the bacteria involved are exogenous or endogenous. This might alter treatment modalities depending on the orgin of the organism. Bacterial culturing continues to be the gold standard of microbiological assays, although it is hampered by the inability to culture non-viable or non-cultivable bacteria, providing false negative results. The use of synthetic oligonucleotide primers in the polymerase chain reaction assay is capable of detecting a single organism, resuting 32
in the highest sensitivity of any of the assays currently available. 25 or more subgingival samples must be taken to achieve a 95% confidence level that a subject is not infected with Aa. 6 or more random sites or 3 or more sites with probing depths of greater than 5 mm are needed for the same accuracy with P. gingivalis and B. forsythus, and 4 or more sites with probing depths greater than 5 mm are needed for P. intermedia. Since smoking has been implicated in periodontal disease, several studies were done to determine the changes, if any, in the bacterial flora found in smokers versus non-smokers. One study could not demonstrate a difference, although another did show among smokers a significantly higher level of P. forsythus (2.3 times higher), as well as an increased risk of infection. It is becoming increasingly clear that there is a significant difference within species of periodontal pathogens with sime strains being much more virulent than others. Some stains of Aa. are capable of producing 10 to 20 times more leukotoxins than other strains, and certain assays are now capable of reading the gene sequences of the bacteria in order to determine which strain is present. The Effects of Periodontal Therapy: Scaling and root planing shows not a generalized reduction in the proportion of all plaque as might be expected. Instead, there is an inverse relationship between the periodontal pathogens and those seen in healthy tissue, with an increase in streptococci and other oral cocci. Aa. has been shown to be very difficult to eradicate, with sc/rp actually increasing the relative population of Aa. in subgingival areas. Antibiotic therapy in conjunction with sc/rp is indicated when treating Aa. With the increased use of membranes in periodontal therapy, studies have been done to determine the effect of the flora on the results. All membranes become completely penetrated within 4 weeks of placement, and those with low levels of gram negative periodontal pathogens showed significantly improved surgical outcomes over those with high levels. Use of metronidazole gels on the surgical sites has shown significant improvement compared to untreated control sites. Healthy dental implants have been shown to be surrounded mainly by gram positive cocci, whereas failing implants are normally surrounded by gram negative anaerobes. Transmission of Periodontal Pathogens Between Families: The methods developed to fingerprint isolates of periodontal pathogens have been used to examine the transmission of these pathogens within families. There is good evidence that periodontal disease is transmitted between families. Despite these findings, re-emergence of periodontal pathogens after treatment was more likely associated with an individual’s own flora rather than that of their spouse. There is, though, little evidence that periodontal disease is contageous. Periodontal pathogens appear to be transmissable only after long-term exposure, and the exact mechanism of transmission remains to be established, although there is evidence that these pathogens remain viable on toothbrushes. MUCOGINGIVAL THERAPY Note: Section 8 is well organized, and the Question and Answer section actually summarizes well the information in the text using the same order as the outline below. Therefore, I did not prepare an exhaustive handout to avoid repetition. I.
Introduction- Definition of terms: 1. Mucogingival Defect – a defect which probes apical to the mucogingival junction. 2. Mucogingival Surgery – plastic surgical procedures disigned to correct defects in morphology, position and/or amount of gingiva surrounding the teeth. 3. Periodontal Plastic Surgery – surgical procedures performed to correct or eliminate anatomic, developmental, or traumatic deformities of the gingiva or alveolar mucosa.
II.
Therapeutic Endpoints of Success Increased gingival dimensions - i.e. increased gingival width, regardless of the number of mm is considered a successful outcome.. Root coverage - gain of clinical attachment . Another variable is decreased root sensitivity. Improved esthetics - subjective...based on the patient. Improved ridge contour, elimination of aberrant frenulum, improved papilla form, etc.
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III.
Indications/Contraindications for Mucogingival therapy Augmentation of the Dimensions of Gingival Tissue Root Coverage - Full coverage can be attained with Class I and II, Only partial coverage with Class III; Class IV not amenable to Tx. Recession classifications: Class I - marginal recession coronal to the mucogingival (MG) line. Class II - extends to or beyond MG line, but no loss of interdental bone or soft tissue. Class III- “ “ “ “ “ “ , with loss of interdental bone or soft tissue, but coronal to the marginal recession. Class IV - extends beyond MG line, with interdental bone or soft tissue loss apical to the marginal recession. Augmentation of the Edentulous ridge Elimination of aberrent frenulum Prevention of ridge collapse associated with tooth extraction Crown lengthening Exposure of teeth that are not likely to erupt Loss of interdental papilla which presents an esthetic and/or phonetic defect General Considerations Plaque control - poor OH have less favorable outcome. Smoking - light smokers (( 5 per day) same healing as non-smokers, but excessive smokers < root coverage. Age: no evidence that it affects outcome of surgery. F. Contraindications: same as for any other periodontal surgery
IV.
Procedures that are Justified in Mucogingival Therapy Augmentation of the Dimensions of Gingival Tissue- there is evidence that the most predictable procedures for gingival augmentation are pedicle and free autogenous grafts of gingiva or masticatory mucosa from the palate. Under ordinary circumstances, “denudation” procedures are not justified as a means for widening the gingival zone. Root Coverage Procedures- pedicle soft tissue grafts , free soft tissue grafts, or combination can be considered justified in the tx of recession type defects. Augmentation of the Edentulous Ridge
V.
Predictability of Root Coverage Rotational Flaps Coronally Advanced Flaps Guided Tissue Regeneration Full Thickness Free Soft Tissue Graft Free Connective Tissue Graft
VI.
Role of Root Surface Modification in Mucogingival Procedures aimed at Root Coverage Root Planing - evidence that it does effect the nature of the attachment. Root Surface Conditioning- no evidence that citric acid or tetracycline helps.
VII.
Dento-Gingival Anatomy That is established Following Root Coverage Procedures
VIII.
Long Term Stability of the Healing Result Following Mucogingival Procedures Augmentation of the Dimensions of Gingival Tissue Root Coverage Procedures Augmentation of the Edentulous Ridge SUPPORTIVE PERIODONTAL THERAPY
I.
Introduction: A.
Various Authors Have Described Recall/Maintenance Therapy As: -Periodontal Maintenance (Ferrari)
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-The Maintenance Phase Of Periodontal Therapy (Ramfjord, Schick, Also Gottsegen) -Maintenance Care (Ramfjord) -Preventive Periodontal Maintenance (Allen) -Periodontal Maintenance Therapy (Schallhorn) -Post-Operative Maintenance Care (Schmid) B.
Supportive Periodontal Therapy: -The Preferred Term To Describe Recall/Maintenance Therapy.
-Avoids The Negative Psychological/Financial Connotations That Are Often Associated With Recall/Maintenance Therapy As Perceived By Patients. C. Definition: The Preventive, Diagnostic, And Therapeutic Measures Accomplished In An Ongoing Program For Sustaining Periodontal Health. -This Ongoing Preventive Program Operates At 3
Ii.
Levels.
1.
Prevent Inception Of Disease
2.
Prevent Progression Of Existing Disease
3.
Prevent Recurrence Of Disease After Corrective Therapy.
Categories Of Maintenance (Schallhorn & Snider) - Offer A Broad View Of Supportive Periodontal Therapy A.
Preventive Maintenance Therapy In Periodontally
Healthy Individuals.
B. Trial Maintenance Therapy To Control Disease While Assessing Borderline Defects Such As Minimal Gingiva Or Furcation Defects. C. Compromise Maintenance When Factors Such As Poor Systemic Health Or Poor Plaque Control Prevent Corrective Therapy. D. III.
Post Treatment Maintenance Therapy To Prevent Recurrence Of Disease.
JUSTIFICATION FOR MAINTENANCE **Horning, G.M., et al.: The prevalence of periodontitis in a military population. JADA 121:616,1990. -What is the prevalence of periodontal disease?
-Patients diagnosed and treated justify the need for PERIODONTAL THERAPY. A.
SUPPORTIVE
MAINTENANCE AFTER NON-SURGICAL THERAPY
-Maintenance(professional mechanical debridement) along with optimal patient hygiene practices secure over time the results obtained with active non-surgical therapy. B.
MAINTENANCE AFTER SURGICAL THERAPY
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-It has been demonstrated that lack of maintenance care or infrequent plaque control will result in recurrence of periodontal disease. *Axelsson,P., and Lindhe,J.: The significance of maintenance care in the treatment of periodontal disease. J Clin Periodontol 8:281,1981. - This article demonstrated the significance of not obtaining regular supervised maintenance following surgical therapy. C.
MUCOGINGIVAL CONSIDERATIONS
-Minimizing inflammation through maintenance is effective in sustaining attachment levels despite the width of the keratinized gingiva (Dorfman et al. 1980). **Ramfjord,S.P.: Maintenance care for treated periodontitis patients. J Clin Periodontol 14:433437,1987. - This article addresses the maintenance care of treated periodontitis patients. IV.
TOOTH LOSS STUDIES A.
UNTREATED DISEASE
-Studies by Loe,Becker,Buckley,and Crowley demonstrated that adults with untreated periodontitis had an extremely high rate of tooth loss. B.
TREATED PATIENTS
-Conversely, studies have shown that patients with periodontitis, even in the advanced stages, who receive treatment accompanied with periodic maintenance care can maintain most of their teeth. *Hirschfeld,L., Wasserman,B.: A long term survey of tooth loss in 600 treated periodontal patients. J of Clin Periodontol 1978:5:225-237. -Classic study of tooth mortality due to periodontal disease. -Periodontal disease is bilaterally symmetrical. -Patterns of tooth loss, Maxillary molars most susceptible,followed by mandibular molars. Most resistant were the mandibular cuspids. -With periodontal tx, get prolonged tooth retention *Goldman,M.J.,Ross,I.F.,and Goteiner,D.: Effect of periodontal therapy on patients maintained for 15 years or longer, a retrospective study. J. Periodontol 57:347353,1986. -This study looked at tooth loss subsequent to periodontal therapy. -Study also made light to the fact that tooth loss could be minimized with periodontal treatment and routine maintenance. C.
FURCATION INVASION
-It has been demonstrated that of all the teeth in the oral cavity, the molars are the most susceptible to periodontal destruction and subsequent loss. *Ross,I.,and Thompson,R.A.: Long term study on tooth retention in the treatment of maxillary molars with furcation involvement. J Periodontol 49:238-244,1978.
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-Disadvantages associated with surgical tx of furcations. occurs. V.
-Even with furcation involvement, teeth can be successfully treated and kept for years if maintenance OBJECTIVES OF SUPPORTIVE PERIODONTAL THERAPY THE PRIME OBJECTIVE OF SUPPORTIVE PERIODONTAL THERAPY IS: -PRESERVATION OF THE HEALTH OF THE DENTAL AND ORAL SOFT TISSUES.
VI.
MAINTENANCE PROCEDURES A.
PATIENT NEEDS AT MAINT. APPT. VARY DEPENDING ON: -Previous treatment -Existing periodontal health status -number of teeth present -level of plaque control -caries activity -amount of calculus -systemic considerations
B.
PROCEDURES INCLUDE: -MEDICAL/DENTAL HISTORY REVIEW *Pt. health not static, *SBE Prophylaxis -RADIOGRAPHIC REVIEW *BWX at q maint. appt, not justifiable. *BWX at maint. appts., only if clinical findings warrant. *No clinical caries or high risk factors, BWX q 18 to 36 months. -OCSE -DENTAL EXAM -PERIO EXAM *Probing of all teeth, compare with previous charts and measurements. *Measure attachment loss *Bleeding assessment
-PLAQUE EVALUATION *Evaluate patient participation in oral hygiene. -PCI -SCALING AND ROOT PLANING *When periodontal health is satisfactory at maint. appt.,scal/prophy indicated, root planing contraindicated-shallow pockets lose attachment. -POLISHING C.
MAINTENANCE INTERVAL: -Depends on the state of the patient's periodontal health at the maintenance appt. -Responsibility for maintenance, Dentist/Periodontist. -Time interval- variable, depends on patient's needs.
*Listgarten,M. Schifter, C. Differential dark field microscopy of subgingival bacteria as an aid in selecting recall intervals: Results after 18 months. J Clin Periodontol 1982:305-316.
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VII.
COMPLIANCE WITH MAINTENANCE *Wilson,T.,et al.: The results of efforts to improve compliance with supportive periodontal treatment in a private practice. J Periodontol 1993,64:311-314. -Review of compliance with periodontal patients. -1000 pts. over 8 yrs., 16% had complete compliance.
VIII.
REEVALUATION AND RETREATMENT A.
REEVALUATION: 1.
Every maintenance appt. should include a reevaluation phase.
2. Compare probing depths, attachment levels, look for bleeding upon probing, suppuration, mobility, radiographic changes. *BOP indicates inflammation/disease activity. *If probing depth increases 2-3mm, destruction is active. 3.
Progressive destruction: localized/generalized
*Localized breakdown may be due to local factors such as caries, overhangs, food impaction, cracked tooth, or isolated poor oral hygiene. alcohol abuse, and stress. B.
*Generalized breakdown may be due to systemic factors such as diabetes, drug and
RETREATMENT: 1. Chace's criteria for failure: -increase in probing depths -BOP -Increasing bone loss -Increasing mobility 2.
Reasons for failure -Inadequate oral hygiene -Inadequate root preparation -Improper surgical technique -Systemic factors
3.
Retreatment options: -Scaling and root planing -surgery -antibiotics Periodontal Implications: Medically Compromised and Older Adults
- age does not have an influence on healing of the periodontal tissues or on the incidence of recurrent disease. - the well-controlled diabetic patient is similar to non-diabetic individuals relative to treatment planning and expected response to therapy. - medications associated with gingival overgrowth include anticonvulsants, cyclosporins, and calcium channel blockers. PREVENTION Preventive periodontics - includes health promotion, treatment, and rehabilitation. Preventive measures are subdivided into 3 categories as related to disease progression: Primary prevention: promotion of optimum health or specific disease prevention.
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Secondary prevention: usually accomplished by prompt and adequate treatment, based on early and accurate diagnostic methods as well as effective therapeutic measures. Tertiary prevention: preventive efforts applied during corrective therapy, with dual goals of disability limitation as well as rehabilitation. For effective preventive measures, it is necessary to recognize, identify, and eliminate or minimize both the etiologic factors and the risk factors associated with the disease process. Diagnosis: bleeding on probing is not sufficient to indicate a high probability of progression to periodontal disease, although its absence is related to effective prevention. Risk factors: it has emerged that the destructive periodontal diseases result from the interaction of environmental, host, and microbial factors. Risk factors associated with the inflammatory periodontal diseases include: bacterial plaque, calculus, age, smoking, and certain systemic diseases. Evidence for the use of chemotherapeutic aids in prevention Reports concerning the efficacy of chlorhexidine, prebrushing rinses, cetylpyridium chloride, and phenolic compounds have appeared in the literature. chlorhexidine, when applied as an oral rinse, continues to prove effective in both reducing and preventing supragingival bacterial deposits and gingival inflammation. It was noted that chlorhexidine was least effective in the interproximal areas where exposure to the agent was lowest sodium benzoate prebrushing rinses have yet to demonstrate any long-term effectiveness. Short term results using rinses containing cetylpyridium chloride as the active agent also failed to demonstrate any long term effectiveness in plaque and gingivitis reductions; when cetylpyridium chloride was combined wih a degradable controlled-release system, it was noted that significant plaque reductions occurred stannous fluoride preparations may have some beneficial effect on plaque and gingivitis reduction, but further long term evaluations will be required sodium fluoride is only anticariogenic; stannous fluoride is both antibacterial and acts against root sensitivity reports continue to indicate the effectiveness of rinsing with a commercially available phenolic compound that consists of a combination of essential oils, as an adjunctive measure to toothbrushing for the reduction of both bacterial plaque and gingival inflammation Triclosan has received substantial interest as a preventive agent to be incorporated in a toothpaste vehicle. While triclosan alone has some modest effect, its effectiveness is enhanced when combined with other agents such as zinc citrate, or with copolymer of methoxyethylene and maleic acid. Both of these preparations have demonstrated significant reductions in bacterial plaque deposits and gingival inflammation. The copolymer formulation has also shown promise as a prebrushing rinse. Evidence for supportive periodontal treatment (SPT) The need for and efficacy of SPT appears to be adequately documented. Determination of the ideal interval for each patient should be based on: 1) their inital presentation, 2) factors determined during therapy, and 3) response to initial therapy. Finally, parameters to predict which individuals will be compliant with SPT are yet to be determined.
Introduction: Improved Clinical Decision Making Using the Evidence-Based Approach: Periodontal Diseases: Epidemiology I. A fundamental prerequisite for any epidemiology study is an accurate description of the disease under investigation. Unfortunately, there is no uniform criteria for the diagnosis of periodontal disease. Inconsistently, studies have used gingivitis, probing depths, clinical attachment levels, and radiographically assessed alveolar bone loss. There are no set threshold values for what makes a pocket "deep" or "pathologic", or how many areas of the mouth need to be affected to be classified as perio disease. 2. Early-Onset Studies: Studies tend to show less than 1% of adolescents with localized juvenile periodontitis, and less than 0.2% with generalized JPD. White females>white males for localized JPD, opposite for blacks. Blacks more frequently affected with GJPD.
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3. Adult Periodontal Diseases: Again, lack of uniform criteria makes comparisons difficult. Disease very prevalent, but it would appear that JE>OE. LJE vs. CT attachment Junctional Epithelium Resistance To Periodontal Breakdown Magnusson, Runstad (JCP 83 32-11): LJE has similar characteristics as regular JE. Monkeys, ligature induced perio, OFD, tissues biopsied and compared to controls. Similar histologic values, no difference in attachment levels Beaumont, O'Leary (JP 84 32-12): LJE/CT attachment equal in disease resistance. Beagles, ligature induced perio, 14 days OFD with 60 day healing, controls brushed daily w/ 2 wk prophy, both groups 4-20 ligature perio phase, animals sacrificed, probing similar, no difference in attachment levels. Barrington anti-LJE BOWERS DOESN’T LIKE LJE, PREFERS TO REGENERATE ATTACHMENT CONNECTIVE TISSUE Components: Cells: (5%)- Fibroblasts make up 65% of all CT cells, also mast cells, PMN's, macrophages, lymphocytes, plasma cells Fibers: (60%)- Mainly Collagen fibers, but reticular and elastic fibers also Ground substance (35%)- protein-polysaccharide macro-molecules made up of proteoglycans and glycoproteins, function in cell to cell and cell- matrix interactions. Fibronectin is a good example. Prominent Proteoglycans Dermatan sulfate in gingiva/PDL, (BOARD QUESTION) Chondroitan sulfate in bone/cementum (BOARD QUESTION) Factoids: Nobuto (JPR,89): SEM, Morphological features of tissue are determined by the vascular architecture within the tissue. Polson et al (JP, 81 2-14): Inflamed CT increases at the expense of the overlying epithelium which decreases a proportionate amount. COLLAGEN In healthy gingiva, collagen accounts for 60% of total protein. Tensile strength is a function of the amount of crosslinking by lysine residues. (BOARD QUESTION) TYPE 1: TYPE 2: TYPE 3: TYPE 4:
Skin, dentin, tendon, ligaments, bone fascia, uterus Hyaline cartilage, cornea. Skin, arteries, muscle, lung, liver. Basement membrane
Prockop et al (NEJM,79 2-3): 3 polypeptide chains, alpha chains,1000 amino acid, single left, triple helix right handed. biosynthesis: Fibroblast is main cell responsible but other cells include osteoblasts, odontoblasts, epithelial cells and chondrocytes. Formation: production alpha chains on surface of RER, intracellular peptides (procollagen) extra -globular peptides, becomes tropocollagen 1) Hydroxylation (intracellular) (gly-x-y) x=proline, y=hydroxproline requires O 2, Fe+ +, Alpha ketoglutarate, Ascorbate (Vit C) 2) Glycosylation (carbohydrate addition) in golgi, triple helix formation. procollagen
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3) Secreted extracellularly where endopitidases cleave the propeptides forming tropocollagen 4) Collagen fibril, spontaneous aggregation of tropocollagen, fibrils coalesce to become fibers which result in bundles. Fibroblasts: Mariotti and Cochran (JP, 90): PDL fibroblasts differ from gingival fibroblasts in proliferation rates and macromolecule synthesis with human PDLF confluent in 6 days vs. 4 days for GF when looking at #'s and cell cycle analysis. Ogata (JP 95 2-32) PDL fibroblasts have different characteristics than gingival fibroblasts Disease:
Narayanan and Page (JBC,76 2-13): Fibroblasts from normal tissue synthesized type I collagen (7090%), and type III collagen (5-30%). Fibroblasts from diseased tissue synthesized type I collagen and unusual collagen type I dimer. unable to produce type III. Page and Ammons (AOB,74 2-9): with inflammation there is an interference with the high level of collagen production and turnover, rather than from destruction of previously existent collagenous substances. Barnabell ( 76): Chronic Pdtis = decreased synthesis and normal degradation = net loss collagen.
Collagen Synthesis/Degradation in health and disease: Mammalian collagenase: 75% from N terminal ¼ and 3/4 pieces of double helix Bacterial collagenase: Acts along entire Gly-x-y triplet to form small peptides. Christner Collagenase Host origin Derived from diseased PDL’s not healthy PDL’s Cleaves ¼, 3/4 Produced by fibroblasts and epithelial cells Selvig (JPR, 68 2-1): Nonbanded fibrils appear to be related to the decomposition of collagen (collagenolysis) both in health and disease. Chavrier et al (JPR,84 2-5,6): 2 patterns, #1 dense bundles of thick collagen fiber mostly type I which is stable, Pattern # 2 is Type I and III collagen which III dominates and is more loosely arranged and found near the BM, blood vessels, and easily remodeled the ratio of Type I:Type III is 7:1 Defects of Collagen Synthesis Ehlers-Danlos Syndrome: Decreased rate of Type 3 synthesis. Osteogenesis imperfecta Marfans Syndrome. PERIODONTAL LIGAMENT (PDL) Functions of PDL:
Formative (eruption nutrition) Supportive (main purpose) Sensitive
Factoids: Coolidge (JADA,37 2-17): Hourglass shaped Dimensions of the PDL 11-16 yrs: 0.21 mm Hvy fxn: 0.18 mm 32-50 yrs: 0.18 mm No fxn: 0.13 mm 51-67 yrs: 0.15 mm embedded: 0.08 mm Rippen (JPR 76, 2-21): Collagen turnover in PDL is very high occurring the whole width, the variation in rate is determined upon tooth movement. normal function the apex is more, heavy function the cervical portion is more. Pitaru and Melcher (JPR 87, 2-16) PDL fibers orient perpendicular to demin root surface and parallel to nondemin dentin surface. Dentin surface may influence morphology of PDL Fullmer (JOP 74, 2-2): Oxytalin fibers, increase in size to functional stress. Johnson (JPR,92): Elauvin fibers, provide elasticity, oxytalin fibers resist mechanical stress
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PDL Fibers: Smukler, Dreyer (JPR 69, 2-20): Alveolar crest, horizontal, oblique, and apical fibers. Oblique fibers more numerous. Pitaru and Melcher (JPR 87, 2-16) character of dentin surface may influence morphology of PDL. In non-demineralized surfaces fibers orient parallel to the surface but if the surface is demineralized the fibers orient perpendicular to the dentin surface. Pneumonic for remembering fiber anatomy: Bone has big bundles Sementum has small strands Radiographically " widened PDL space" Van der Linden (JP 70, 2-18): Increased width of PDL by x-ray may not always be inflammation, it may be due to anatomy or radiograph exposure increased root radius wider PDL increased exposure time wider PDL increased kVp narrower PDL jaw thickness No influence on PDL horizontal angulation narrowing of PDL in crestal area Nerve Endings: Lambrichts et al (JPR ,92): Free nerve endings- mostly stem from unmyelinated fibers (pain and heat ) Ruffini-like fibers- mostly found in the apical part of the PDL (slowly adapting mechano-receptors) Lamellated corpuscles- extremely edocytic and are in close contact with each other (rapidly adapting mechano-receptors.
INTERMEDIATE PLEXUS: Yes: No:
Sicher (OS, 59 2-22): functional reorientation of the principle fibers, allows changes to occur without total loss of old fibers, and tears during traction occurs here as unsplicing of the bundles. Zwarych & Quigley (JDR, 65 2-23): mice, histologic sections molars, intermediate plexus did not exist and that the principal fibers were continuous from the alveolar bone to the cementum. Fiber bundles which attached to the alveolar bone were large in diameter but less numerous than those inserting into cementum. Melcher & Correia (JPR,71 2-25): Rats erupting molars, fibers go whole distance, some remodeling of fibers of the PDL and are most active in the half of the ligament adjacent to alveolar bone. No evidence of Intermediate plexus. Sevdja (JP 73 2-25) Scanning SEM’s of the PDL. Two fiber groups, supporting and buttressing
EPITHELIAL RESTS: Valderhaug and Zander (67 Periodontics, 2-27): Range from 27-41µm in distance to root, most numerous in cervical areas of the root, closest to root at apex. Spouge (JP 84, 2-29): ER's may act as a thin edge of a wedge to facilitate apical migration of JE during pathology, horizontal cords of cells, may be activated forming lateral periodontal cysts, pocket formation? Thesleff (JPR 87, 2-30): Epithelial rests have many receptors that bind Epidermal Growth Factor (EGF). Filipowicz (JP 82, 16-20) Proliferation of epithelial elements other than crevicular could be implicated in isolated periodontal defects (lateral periodontal cysts)
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BONE Types of Bone Woven bone: developing or fetal bone, seen in wound healing, less oriented matrix, not weight bearing, highly cellular, highly labile. Also called spongy bone, forms in grafts at 2 months (gelatinous) Lamellar bone: Organized, replaces woven bone. (4 months in a graft). Bundle bone: Contain Sharpey's fibers insertions of tendons and ligaments (BOARD QUESTION), lacks lamellation of mature bone Composite: woven bone lattice filled with lamellar bone - primary osteon. Endochondral has cartilaginous precursor this is the way most bones are formed Intramembranous no cartilaginous precursor. Most facial /skull bones and clavicle Urist (67): The bone induction principle: Induction is cellular differentiation due to physiochemical effect of one tissue on another, for bone this is usually an undifferentiated perivascular mesenchymal cell differentiating into osteoblasts, chondroblasts. Reddi et al (Ortho Clin N Am 87, 35.3): 3 phases of bone induction: 1. Chemotaxis by fibronectin, BMPs 2. Mitosis (proliferation of mesenchymal cells) 3. Differentiation (cartilage formation, vascular invasion, bone differentiation). Sequence in rats: 1 min: release of PDGFs, binding of plasma fibronectin to implant matrix 1 hr: chemotaxis of PMNs, release of proteolytic E’s (collagenase, elastase 3-18 hr: release of chemotactic factors for fibroblasts 1 day: chemotaxis and attachment of fibroblasts 2 day: protein & nucleic acid synthesis, release of non-PDGFs 3 day: mesenchymal cell proliferation, Type III collagen 5 day: diff of chondroblasts 7 day: syn cartilage & Type II collagen 9 day: calcification of cartilage, vascular invasion, Type IV collagen around capillaries 10-12 days: formation osteoblasts, bone mineralization, Type I collagen 12-18 days: osteoclasts, release of collagenase 21days: bone differentiation ALVEOLAR CREST RESORPTION: Ritchey and Orban (JP 53, 3-1): In the absence of disease alveolar bone levels follow a line parallel to the CEJs. Bone 1-2 mm apical to CEJ. (BOARD QUESTION) Boyle (JP 73 3-2): Reduction in alveolar crest height with age is 0.017 mm/yr., statistically significant, clinically insignificant. Pietrokovski and Massler (JPD 67, 3-19): After extraction, greater resorption took place on the buccal vs. lingual Roberts: 30% loss in first 4-5 yrs, dependent not only on disuse atrophy but bone metabolism for patient. Sennerby (AOS 88, 25-12): Implant therapy greatly reduces bone resorption distal to fixtures compared to complete dentures DETECTION OF CRESTAL RESORPTION Hausmann (JP 90 3-3): Traditional radiographs inaccurate for diagnosing crestal resorption, advocates subtraction radiography, single and dual photon absorptiometry and radiopharmaceuticals Jeffcoat (JP 92 3-4): Use of subtraction radiography and automated probe results in most accurate detection of attachment loss. Direct digital radiography uses 90% less radiation (BOARD QUESTION) Fixott-Everett grid incorporated into film or taped on film pack Schei Ruler measures percentage of bone lost as a proportion of root length Problems with conventional radiography 1. bone loss undetected until 30-50% of mineral lost 2. foreshortening, elongation 3. poor film processing 4. variations in exposure 5. two dimensional picture of three dimensional teeth
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FENESTRATIONS AND DEHISCENCES: Elliot and Bowers: (Periodontics, 63 3-6): Incidence 20%. Fenestrations 3X more common in max, Dehisc 2x more common in Mand, Bilaterally, Max 1st molar, Mand canines Don’t root plane fenestrations and try to keep incisions away from fenestrations. Edel (JCP, 81 3-7): Mand Max Fenestrations 5.4 17.7 Dehiscence 5.5 2.1 LAMINA DURA Manson (JP 63, 3-8): Lamina dura is radiographic artifact, white line in which X-rays pass tangentially, wooden models. Greenstein et al (JP 81, 3-9): Presence or absence of crestal lamina dura not related to clinical evidence of BOP, PD or AL. Lang & Hill (77): Lamina dura clarity affected by: convex, concave root surface, root curvature, CEJ level and alveolar bone thickness. PDL thickness affected by horizontal and vertical angulation. Rams et al (JCP 95, 3-10): Lamina dura correlated with the absence of disease. Presence in health or periodontal stability. Absence of LD does not necessarily mean disease Diseases which cause a loss of lamina dura: Hyperparathyroidism, Paget's, Scleroderma, Gaucher's. Diseases which cause thickened lamina dura: EXOSTOSES Larato (JP 72, 3-11): Mexican skulls, 30% exhibited palatal exostoses, greatest in tuberosity region. Nery (JP 77, 3-12): Varied racial skulls, 40.5% had palatal exostoses, some racial variation, highest incidence in 40-55 year olds Differential for mandibular Tori (Benign Tumors) Torus mandibularis, multiple exostoses, osteoma, buttressing bone (Glickman) OSSEOUS DEFECTS Manson (JCP 76, 3-13): Most common defect was the interdental crater, 1/3 of all defects, 2/3 of all mandibular Great diversity of defects due to type of bone, vascularity cortical plates etc. Tal (JP 84, 3-14): Studied African mandibles. Craters most common defect (84%) lingual wall higher. 2 wall most common. Bowers disagrees that two wall craters are the most common defect Tal (JP 84, 3-16): Frequency of intrabony defects increases with increasing interproximal distance. Significance when between 2.1-4.1 mm, no longer significant when 4.6 mm. 2 defects if 3.1 mm. Horizontal loss if bone crest narrow. Richardson, Chadroff, Bowers (JP 90, 9-8): Apical extent of calculus is found 1/2 the total depth of defect. The mean distance between the base of the calculus and base of the defect was found to increase with the depth of the defect. Karn (JP 84, 3-15) Proposed classification system for osseous defects, crater, trench, moat, ramp plane. Heins & Wieder (JDR 76, 3-17): Minimum distance (0.1 to 0.5 mm: 90% cancellous bone + lamina dura + PDL 60% blacks, adv. perio cases. SICKLE CELL ANEMIA-Stepladder appearance of bone. Crawford (JP 88 14-9): Sickle cell disease does not influence periodontitis. Large marrow spaces are the predominant dental manifestation of sickle cell anemia. (BOARD QUESTION) LAMINA DURA Manson (JP 63 3-8): Lamina dura is radiographic artifact, white line in which X-rays pass tangentially, wooden models. Greenstein et al (JP 81 3-9): Presence or absence of crestal lamina dura not related to clinical evidence of BOP, PD or AL. Lang & Hill (77): Lamina dura clarity affected by: convex, concave root surface, root curvature, CEJ level and alveolar bone thickness. PDL thickness affected by horizontal and vertical angulation. Rams et al (JCP 95 3-10): Lamina dura correlated with the absence of disease. presence in health or periodontal stability. Absence of LD does not necessarily mean disease Diseases which cause a loss of lamina dura: Hyperparathyroidism, Paget's, Scleroderma, Gaucher's. Diseases which cause thickened lamina dura: PDL Van der Linden & Van Aken (JP 70, 2-18): Radiographic PDL affected by root shape, exposure time, kV, bone morphology and horizontal angulation, phantom models made of wax, aluminum, plaster of Paris. LESIONS THAT ALTER PDL Widened PDL: Osteosarcoma, chondrosarcoma and scleroderma Loss of PDL: Hyperparathyroidism, Central Giant Cell Granuloma, Paget's disease, Scleroderma and Gardner’s Syndrome.. PDL THICKNESS Coolidge (JADA 37, 2-17): Hourglass shaped. Average: 0.18 mm, decreases with age, increases in heavy function. 0.21 young, 0.18 mid, 0.15 old Pihlstrom & Ramfjord (JP 71, 17-4): In non-function, thinning of PDL, (BOARD QUESTION) Atrophy of PDL fibers, osteoporosis of bone increased cementum thickness Van der Linden Radiographic PDL affected by root radius, length of exposure, KVP, root concavities, horizontal beam angle. CEMENTUM THICKNESS Zander (JDR 58, 5-1): AVE 0.076 mm 19 y.o.), split-mouth study, Sx (MWF) and non-Sx Tx. Both treatments equal and effective. Improvement over 2 yrs, then LOA . Swedish prophies done, (borderline surgery) (BOARD QUESTION) What kind of surgery was done? Waerhaug (JP 77): 21 pts (12-24yrs) treated with gingivectomy, pocket elimination, S/RP, Hemisection, 10% loss of teeth from 1-27 yrs. The plaque front migrates apically 2-5 µm/day in JP vs. 0.2- 1µm/day in AP. Antibiotics: Slots and Rosling (JP 83): 3 wks of S/RP does not reduce subG levels of Aa in LJP lesions. 3 weeks of TCN necessary to eliminate Aa, 6 LJP pts Mandell, Tripodi, Savitt, Goodson, Socransky (JP 88, 10-16): 4 LJP pts, regimens of therapy: (1) local TCN delivery via monolithic fibers, (2) systemic doxycycline (100mg/day X 14 days), (3) full thickness flap surgery and doxycycline. Doxycycline + Sx, effective in controlling disease and eliminating Aa. Actisite alone ineffective in eliminating Aa, due to tissue invasion of Aa. Novak, Polson, Adair (JP 88): Tetracycline only (no surgery or S/RP) in early LJP was effective, 250 mg 4x day for 3-6 weeks. Few patients, short study, no culturing. Kornman and Robertson (JP 85, 10-10): 8 JP pts, S/RP alone no effect S/RP w/ TCN effective in mafority of Aa (+) and BPB (+) sites Sx w/ TCN effective for all Aa (+) and BPB (+) sites. All sites initially had Aa averaging 33.8% of the total cultivable flora. Decrease in Aa was an excellent predictor of clinical success. Suggests microbiological diagnosis helps select treatment and monitor its effectiveness. Inability of SRP alone to resolve JP may be due to tissue invasion by Aa. Mandell, Socransky (JP 88, 10-18): Initial preparation in LJP is unnecessary and disease and Aa levels can be controlled with surgery + doxycycline. (initial prep can be useful to decrease the microbial load and monitor patients oral hygiene before surgery). Mandell ,Socransky (JP,88): Initial preparation in LJP is unnecessary and disease can be controled with surgery + doxycycline. Evans, Yukna (JP,89): Use of TCP, HA, FDBA with TCN was effective at re-entry. Everette and Baer (64): Treatment with selective occlusal adjustment and orthodontic extrusion. Christersson, Zambon (JCP,93): With TCN treatment only, Aa was reduced by not eliminated in all cases, Aa has high negative predictive value thus a good endpoint to therapy. Maintenance: Gunsolley, Zambon (JP 94, 10-33): Sites infected with A.a. and P.g. had PD increase of 0.65mm. P.g. and not A.a. may be predictive of attachment loss. Keep pts on short maintenance. GJP
Hormand, Frandsen (JCP 79, 10-3): Female to male ratio decreased with age, suggesting that females were affected earlier and were exposed to the disease process longer. The number of involved teeth increased w/ age, following a pattern that was almost exclusively localized in younger patients becoming more generalized with age. The authors suggested that the generalized form is not a "contamination" of JP sites by overlying AP, due to the amount of destruction and symmetrical involvement. Firalti, Gurel, Cebeci (JCP 96, 10-41): Slight elevation in the CD4/CD8 ratio for GPP patients compared to controls.
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RAPIDLY PROGRESSIVE PERIODONTITIS: Page (JP 83 8-34 10-31):7 Case Reports of Rapidly Progressive Periodontitis. 1. Age of onset between puberty and 35 2. Lesions generalized, no consistent pattern of lesions 3. some patients may have had LJP previously 4. Severe and rapid bone destruction, may stop spontaneously 5. During acute phase, tissues acutely inflammed. 6. Microbial deposits variable. 7. 83% have neutrophil or monocyte defects 8. May have systemic manifestations including weight loss depression and malaise 9. Some are remarkably responsive to treatment Suzuki (88): Type A: 14-26yo, generalized lesions, depressed chemotaxis, minimal etiology, decreased AMLR, (autologous mixed lymphocyte reaction) genetic implications. Type B: 26-35 yo, generalized lesions, plaque and calculus, AMLR, WNL, normal/depressed chemotaxis DiMurro (JP 87, 10-32): P ging may inhibit PMN’s, blame the bug! Kamma (94): 73 RPP lesions. Pg, Fn. seen in greater than 90% of lesions. Pi seen in 88% and Bf in 53%. ? Differential Between GJP and RPP Type A: GJP= Age 12-26, increased AMLR, no chemotaxis defects, low caries RPP= Age 14-26, decreased AMLR, chemotactic defects, variable caries rate Crawford (1975): First to describe RPP Katz: (JCP 88, 13-23) Hypothesis that RPP and rheumatoid arthritis are similar diseases. HLA-DR 4 is increased in RPP. Altered T cell ratios in RPP. TREATMENT of RPP: Kornman: Metronidazole + Augmentin or Amoxicillin is beneficial to treat RPP. Van Winklehoff: Perform initial therapy quickly i.e. in 2 days to 1 week and place pts on antibiotic regimen for 1 week. Regimen consists of 500mg metronidazole b.i.d. + 375mg amoxicillin t.i.d. If amoxicillin allergy, give cephalosporins. PERIODONTITIS ASSOCIATED WITH SYSTEMIC DISEASE Predisposing to periodontitis in children and adolescents Down's Syndrome, Type 1 Diabetes, Papillon-Lefevre Syndrome, Chediak-Higashi syndrome (AutoRessesive, lysosomes clump, PMN have poor chemotaxis.), Nutritional disorders, hypophosphatasia (mineralization), Granulocyte disorders- Agranulocytosis (decrease in #), chronic neutropenia, cyclic neutropenia, Lazy leukocyte syndrome, Leukocyte adhesion deficiency (LAD) seen in PPD, described by Waldrop (87): Deficiency or complete absence of cell surface glycoproteins (MAC-1, LFA-1, p150,95) on neutrophils and monocytes. TX: extraction soon, bone transplant, Implants ACUTE NECROTIZING ULCERATIVE GINGIVITIS Not a communicable disease ANUG Criteria: Barnes (JP 73, 16-3): 1) BOP (95%), 2) blunted interdental papilla (94%), 3) pain (86%), 4) pseudomembrane (73%), 5) fetor oris (84%) 6) young (90%. RIA difficult to do chairside. Tsuchida: Periotron: GCF flow rates Eley & Cox (92): GCF proteases, Cathepsin B, elastase, trypsin, dipeptidyl peptidase all may be correlated to Att. Loss pre/post Tx. Goodson: GCF replaces itself in 1:25 sec Indicators of Periodontal Disease Activity in GCF
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Bacteria and their products: Darkfield/phase contrast analysis, GCF and plaque for endotoxin, hydrogen sulfide, butyrate, polyamines, enzymes, bacterial collagenase, leukotoxin (Aa). Host cells and their products: PMN counts, acid hydrolases, neutral proteases, lactoferrin, acid and alkaline phosphatase, lysozyme, ß-galactosidase / glucuronidase, proteolytic enzymes (Cathepsin D, elastase, collagenase) Host factors: Antibodies, complement cascade, prostaglandins, cytokines. Products of tissue Injury: GCF levels of lactate dehydrogenase, aspartate aminotransferrase (marker for tissue destruction released by activated macrophages BOARD QUESTION), polyamines, glycosaminoglycans, B-Glucuronidase (marker for CT ground substance breakdown). Offenbacher: GCF PGE2 used to predict attach loss with high sensitivity, spec, predictive values >90%. RIA difficult to do chairside. Lamster et al (JPR 91): PMN response is associated with active periodontal disease in pts with Adult periodontitis, as evidenced by the high levels of -Glucoronidase and a-2-macroglobin. (BOARD QUESTION) Lamster (JCP 94): 140 txd patients on maintenance and 10 untxd patients with AP. An increase in glucuronidase was seen with increasing PD and also with increasing BOP. -glucuronidase levels may correlate with periodontal status. (BOARD QUESTION) Gustafsson (JCP 92 19-6) Elevated granulocyte elastase activity in the GCF could be an indicator of patients at risk for periodontitis. Page (JP 92 19-8) GCF tests - no one test the “magic marker” Collagenase responsible for much tissue destruction Cathepsin intracellular cysteine proteases which degrade extracellular matrix. Neutral Proteases Alkaline phosphatase associated with bone metabolism and neutrophilic granulocytes -Glucuronidase level of enzyme correlated with inflammation, pocket depth and alveolar bone loss Arylsulfatase, same as Glucuronidase Aspartate Aminotransferase released by dead or dying cells Cytokines IL-1, TNF implicated in severe destruction. Prostaglandins PGE2 strongly associated with attachment loss. Antibodies to periodontopathic bacteria PREDICTING ATTACHMENT LOSS: CLINICAL PARAMETERS NO: Badersten (90): Non-molars, 39 pts, used PI, BOP, Supp, PD. PI +BOP not very predictable 30%, PD most predictable. Goodson, Tanner, et al (82): Existence of periodontal pockets alone cannot substantiate the existence of active disease Jenkins (88): Plaque, gingival inflammation, and pocket depth are poor predictors for attachment loss. Lindhe, Haffajee, Socransky (JCP,83): data did not support that sites with more advanced attachment loss are more prone to additional destruction. Results showed that 11.6% had LOA > 3 mm over 6 years (untreated), but looking further into the results one finds that 37% had LOA > 2 mm, and 78% LOA > 1 mm. Also showed 33% sites having LOA in 1st 3yrs had further LOA in nest 3 yrs. Pontoriero, Nyman, Lindhe (JCP,88): Angular bone defects do not appear susceptible to recurrent breakdown. Haffajee, Socransky, Goodson (JCP 83 7-22) Examined many different clinical parameters for sensitivity and specificity for disease activity. No parameter had high sensitivity and specificity. YES:
Haffajee (88): 33 active sites several years, most sites having significant LOA had greater PD and LOA initially Claffey (91): Diagnostic predictability (sensitivity) was greatest in sites with residual PD and bleeding frequency > 75%. Lindhe (JCP,89): Sites in older patients were more likely to exhibit progression of disease. Sites with previous attachment loss were at a higher risk for further disease progression. Most breakdown interproximal, progression in small number of subjects. Albander (90): Sites previously exposed to loss of periodontal support are more likely to undergo further loss of support.
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Machtei et al (93 JP): 51 subjects, 581 sites, 1 yr. measured quarterly with Florida probe. Deep sites (>7mm) had significantly > mean loss (1.03mm) compared to moderate (4-7 mm) loss ( .34mm ) and shallow (0-4mm) loss (.1mm) Grossi (JP,95): Smoking, Age, Diabetes, Pg, B.f. are associated with attachment loss, inverse with allergies, kidney problems. Beck et al (JP 94 6-23): Piedmont study, elderly population , 3 yr. longitudinal , findings: during two 18 month periods AL and pocket depth are related to probability of future breakdown in individual sites. AL during one period related to AL in subsequent periods. Supports episodic theory of AL. Why Treat a 7mm Pocket? YES: Lindhe (89): Sites with previous attachment loss and interproximal were at a higher risk for further disease progression. Grbic (92): 75 pts, 6 month monitoring, sites with 4-7mm attachment loss had greatest incidence of attachment loss. sites with > 8mm attachment loss regardless of age had increased risk of AL. Deas (91): 21 pts, CADIA vs. PAL over 9 months: Initially deeper sites had more probing attachment loss. No changes radiographically. Non-disease related density changes were related to technical variations. Bannerstein (90): 5 yr. >7mm 53% LOA, Increase attachment loss 1 mm 76% LOA Claffey (90): 3½ yr. > 7mm 50% LOA, Increase attachment loss 1 mm 66%, + BOP 87% LOA Vanooteghem (JCP 87, 30-20): monitored sites > 7mm 2 yrs, 1.5 mm + of LOA 42% non-molar sites and 44% furcations. Lindhe, Socransky, Nyman et al (JCP,82): "Critical probing depths" as a result of regression analysis when using the following treatment groups: Do nothing < 2.9 mm > S/RP < 4.2 mm > MWF. Treatment of shallow sites results in loss of attachment. Wolff (JCP 93): Odds ratio for the following bacteria in >5mm. P.g. (3.9) A.a. (3.0) E.c. (2.7) NO: Jenkins (88): Plaque, gingival inflammation, and pocket depth are poor predictors for attachment loss. . RADIOGRAPHIC Deas (91): 21 pts, CADIA vs. PAL over 9 months: Initially deeper sites had more probing attachment loss. No changes radiographically. Non-disease related density changes were related to technical variations. AGE Highest risk factor for attachment loss: Grossi (JP 94): odds ratio 1.72 for (35-44), 9.01 for (65-74). If >45 y.o., diabetic, mod-heavy smoker, and Pg, Bf + Þ 30xs higher risk of LOA Grbic (91): increases with age with 60-69yr Þ 89% LOA, previous loss < 4.0 Þ 19%, 4-5 Þ 50%, >5 Þ 85% Machtei (94): studied AL changes over 1 yr. period in 3 different age groups (28-40, 41-50, 51-64). 3 mo measurements via Florida probe revealed no greater rate of LOA as age increases. More LOA is seen in older individuals which suggests that LOA is due to the result of accumulated LOA over a lifetime and not due to increased rate of destruction. MICROBIOLOGY Bragd et al (87): Recovery of Aa, Pg, and Pi together from a site had a 85% sensitivity and specificity for predicting future disease activity. Also Slots (88). Wennstrom (OIOB 87): Sites after tx lacking P.g., P.i., and A.a. showed no further breakdown. These results indicate a good negative predictive value---when these bacteria are absent, the areas tend to remain stable. Preus (JCP 95): Looked at Sri Lankans. P.i. 76%, P.g. 40%, A.a. 15% presence. 11% of the pts had no disease, 14% with gingivitis, 59% moderate AP, 16% severe AP. P.g. and P.i. were significant in moderate and advanced cases but not in gingivitis or healthy cases. A.a. was not seen in non-diseased sites. BL: Lack of the big 3 may indicate a good NPV (stable sites). Vertical Defects: Papapanou, Wennstrom (JCP 91): 10 yr. retrospective study. Angular vs. horizontal patterns of bone loss as predictors for future bone loss. 201 pts. Radiographs taken 10 yrs apart. Angular defects classified according to depth. Tooth loss was 13% in horizontal defects, 22% in 2mm deep defects, 46%
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in 2-4mm defects, and 68% in >4mm defects. As predictors of >2mm bone loss: 8% sensitivity, 94% spec, 28% PPV, 77% NPV. PROBING Dependent on: Force, Angulation, Tip Diameter, Health of Periodontium Probing Force: Freed (JP 83 7-10): Evaluated different people’s probing forces, found a wide variation. Interexaminer range 5 - 135 grams, mean 44 grams, greatest in posterior, distal, and when searching van der Velden (JCP,78): 0.75N most reproducible Chamberlain (85): same 0.75 N Proye: variation in force 15g-50g resulted in mean PD change from 0.7-0.9mm, 32% increase in BOP with increased force Chamberlain: change in force .25N-.50N changed PD 0.8-1.3 mm & .25-.75N changed 1.2-2.0 mm Lang increased BOP can be elicited from healthy tissues if > 0.25 N used (BOARD QUESTION) Angulation: Persson (JPR 91): Line angle probing underestimates disease. REPRODUCIBILITY OF PROBING MEASUREMENTS Van der Velden (JCP 80 7-03): Repeated probings with light forces do not increase BOP, heavy forces do increase BOP. In inflamed tissues probe was .18 mm occlusal to coronal part of CT. (Differs from Armitage) Van der Velden (JCP 80 7-05) Standardized probing of .75 N does not lead to a more reproducible pocket measurement. Tactile sense is lost with automated probe. Abbas (JPR 7-9) Intensive standardization training was less important than bleeding on probing in increasing reproducibility. Badersten (JCP 84, 7-11): Certain teeth/areas more reproducible than others, incisors better than posterior teeth, buccals better, shallow better, and after therapy probing, stents improve reproducibility. 90% reproducibility with 1 mm. Stent > CEJ after training Wang et al (JP 95 7-12): conventional (UNC) vs. automated force controlled probe (Interprobe). The reproducibility differences were smaller for the manual probes vs. the electronic probe. (BOARD QUESTION) Van der Zee (JCP 91 7-14) Variations in probe tip diameter and markings are source for probing error. Pihlstrom (JP 92 7-15): Calibration between examiners needed, automated probes don't really improve intra and inter- examiner reproducibility as much as once thought, The UNC probe is manual probe of choice, use the same probe for all exams. Kalkwarf (JP,86): Manual vs. pressure controlled probing force, controlled force more objective, intraexaminer reliability 100% both, pressure controlled have tendency to read deeper in > 6 mm PD. STENTS PRO Badersten (JCP 84, 7-11): Stents improve reproducibility compared to CEJ, certain teeth/areas more reproducible than others. Clark (JCP 87 6-18): Measurements using stent more reliable than subG CEJ readings. CON Watts (JCP 87 6-22): Stent and no stent not that different especially in the buccal area, lingual harder to measure. AUTOMATED PROBES Gibbs et al (JCP 88 18-10): The Florida Probe, standard deviation of 0.28mm with stent, 0.58 mm without stent, 0.82mm conventional probe Jeffcoat et al: The Alabama probe, controlled force probe which record location of CEJ (BOARD QUESTION) Wang (JCP 95, 7-12): No sig advantage of automated force controlled probe then conventional manual probe. Probe penetration in Health and Disease Armitage (JCP 77 7-1): 25g, beagles, Health 0.39 short apical JE, Gingivitis: 0.10 short JE, Periodontitis: 0.24 past JE into CT
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Polson (JCP 80 7-06): In health, 25g, 0.25 coronal to CT, 0.70 apical to base of sulcus Glavin and Loe (67): greater variation in PD in inflamed tissues vs. healthy tissues Robinson & Vitek (71): strong correlation between GI and probe penetration. Spray (78): healthy CT fibers act as a "hammock" to prevent probe penetration Caton, Greenstein, Polson (JP,81): Inflamed tissues less resistance to probe penetration. > probing depths with visible signs of inflammation, Probe tip remained in JE whether inflamed or BOP. Aguero et al (JP 95 7-07): Gingival inflammation didn’t influence probe position relative to the base of the pocket, but is located below the most coronal aspect of the CT attachment. (.15mm) Probe penetration Before/After Therapy Fowler (JCP,82): humans. .50N, disease: Probe extended into CT and was apical to bone crest in 7 of 12 specimens. Treated: 0.73mm coronal to base of JE, Untreated 0.45 mm apical to JE. Magnusson (JCP 80 7-2): Humans, used metal strips to determine penetration into tissue. non-treated: 0.29mm into CT (past JE), Treated: 0.31mm coronal to CT (within JE) Listgarten Decreased probings after therapy due in part to decreased penetration of tissues Bacteria Transfer with Probe Barnett (JP 82 7-08) : Bacteria is transferred with probe as seen with SEM. Cultivable?? BOWERSprobably pertains more to pts who are immunosuppressed. Christersson (85): Probing techniques can transfer Aa with immediate colonization, however, 3 weeks later Aa cannot be sampled. Critical Probing Depths Lindhe (JCP 82 18-23) Overall patients OH more important than probing depths. If PDCPD gain attachment after therapy CPD Root planing 3 mm Surgery 4 mm Ramfjord and the Michigan studies came to the same conclusions PROBING FURCATIONS Moriarty (JCP 88 6-24): Reproducibility of probing measurements decreased with increasing pocket depth and degree of root separation. Probe penetration in the furcation results in tissue damage i.e. penetration into the connective tissue. Penetrating 2.1 mm, thus need more probing sites (4). Moriarty (JCP 89 7-13) Histo of probes in furcations revealed penetration of probe into CT and often on to bone. Zappa (JP,93) : Overestimates using the Ramfjord and Hamp classification system. Mealey (JP,94): Post anesthesia probing improves horizontal and vertical diagnostic accuracy compared to standard probing. Tendency to underestimate 1-1.5 mm before anesthesia. (BOARD QUESTION) BONE SOUNDING TRANSGINGIVAL PROBING Renvert (81): difference between bone levels by transgingival probing and surgical measurement 0.3 mm Ursell (JCP 89 18-11): difference between transgingival probing & surgical measurements mean 0.12 mm. very few vertical defects measured MISCELLANEOUS Newton = A unit of force which produces an acceleration of 1 meter/ second on a mass of 1 kilogram. Pond = (500 ponds = 5 Newtons) Conclusions: Post-treatment reductions in PD and gains in AL may be related primarily to improvement in tissue quality rather than quantitative alterations in CT and JE levels. BLEEDING ON PROBING Gingival Index: Loe & Silness (JP 63 6-1): 0,1,2,3: 0 = health, 1= visual inflammation but no bleeding upon stimulation, 2 = bleeding when sulcus rubbed with blunt instrument, 3 = spontaneous bleeding.
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Diagnose Gingivitis: Visual, Tissue manipulation, Eastman, GI, BOP BOP and Inflammation: Greenstein, Caton, Polson (JP 81 7-16): Histo, sites with BOP had greater inflammation than sites without BOP Davenport (JP 82 7-18): Bleeding sites have greater % infiltrated CT & plasma cells, less mononuclear cells, had thinned or ulcerated areas, tortuous strands of rete pegs in CT. Caton (JP 88 7-31): When sites changed from bleeding to non-bleeding there was a reduction in the amount of inflammatory cells. Increased collagen, fibroblast and endothelial cells. (BOARD QUESTION) Baab (JCP 86, 8-7) (DDFM) Cultured bacteria in bleeding and non-bleeding sites. Bacteria not significantly different. Spirochetes more related to PD, AL, and GI than BOP. Used means of GI PI and Bleeding Index. CORRELATION WITH GINGIVITIS: Polson (81): Histological study, correlates periodontal inflammation with bleeding after stimulation of gingival sulcus. Meitner (79): BOP is an earlier indicator of gingivitis than visual signs Chaves et al (JCP 93): Probing depth > 4mm correlated high with GI, but GI and BOP in shallow PD low. CORRELATION WITH BACTERIA: Armitage (JP 82, 7-19): BOP correlated with increased spirochetes & and other motile species. Listgarten (JCP 81, 7-17): DDFM may be helpful in identifying patients at risk for attachment loss, later they reversed themselves and said it wasn’t helpful. DISEASE ACTIVITY: Claffey: Deep pockets with BOP are best predictor of AL, long term monitoring necessary. Kaldahl and Kalkwarf (JCP,89): 15-80 % of sites changed BOP status during the study, not reliable as a predictor of attachment loss. Lang (JCP 86 7-27): Measured AL, BOP at successive appts. 4/4 times BOP: 30 % chance of AL. 1/4 times 3% chance of AL, Sensitivity 56%. Prevalence of AL 0.85 BOP is a limited but useful indicator for diagnosis. Chaves (91): 5 year longitudinal study: high specificity and predictability (93 %) for absence of BOP as indicator of no AL. Lang et al (JCP 90 19-2): If bleeding is not present, predicts future health. If bleeding is present, it doesn’t necessarily indicate disease. BOP had 98% neg. predictive. value and 6% pos. predict. value (pts 2-5 yrs in maintenance).Adult perio pts Joss, Adler, Lang (94): 4.5 yr. supportive therapy study of sites with > 2mm LOA. 2/3rds of sites losing >2mm had BOP 30% of the time. Only in 1/5th of those sites losing attachment did the sites bleed less than 20% of the time. Therefore, most sites that lose attachment will usually bleed at one time or another, but BOP is not a good predictor of LOA. Conclusion:
1) BOP has very low positive predictive value (+) 2) BOP has very high PV(-) 3) Must determine prevalence of disease parameter 4) High Specificity: Absence predicts health: Chaves (91), Lang (90) 5) Low Sensitivity: Poor predictor of periodontal disease Kaldahl, Lang. 6) More of a measure of inflammation, rather than disease activity. 7) Absence of BOP is a good indicator for maintenance of periodontal stability.
RELATED TO PROBING FORCE: Proye: Increased probing force = increased BOP. 25g to 50g change .7 to .9 increase & increase in BOP Lang (JCP,91): Probing force greater than 25N causes false + due to tissue injury. Korayiannis (92): Confirms findings.
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Mombelli ( ): Probing forces of 25g (.25N) necessary for detecting tissue changes before and after therapy. Chamberlain (85): 0.25 N probing force does not reach base of deeper pockets. .25N to .50N (.8 1.3mm) & when .25N to .75N (1.25-2.0) Van der Velden (80): 0.75 N gives more reproducible BOP. Do Deeper Pockets Bleed More? YES Chaves (JCP,93): Positive correlation with increasing pocket depth and BOP with Florida Probe and 20g probing force. GI scores correlated with plaque index. Sherman (90): Deeper pockets have an increased incidence of BOP. Suppuration: Passo (88): variety of histologic presentations, associated with severe inflammation but see little information, nonsupporating sites often have as much in not more inflammation, usually a greater area of inflammation & more PMN's Kaldahl (JP,90): low sensitivity (0-7%), High specificity (97-100%) With Pv(+) as frequency of suppuration increased so did chance of loss of attachment if 8/8 times 50% had loss of attachment, Pv(-) (85-86%) thus stability without suppuration. Haffajee
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ENDO-PERIO Simon & Glick (JP 72 20-6): 1° ENDO: Blownout furcation with no adjacent bone loss. Responds to ENDO tx only. 1° ENDO 2° PERIO: Prognosis depends on periodontal therapy. 1° PERIO: Perio without endo symptoms 1° PERIO 2° ENDO: Perio to apex and possible accessory canal. True combined: Endo and Perio meet along root. RARE Bender and Seltzer (OS 63 72 20-1/5): Pulpodontic - periodontic syndrome (periodontal lesions produce degenerative pulpal changes) Langland (JP 74 20-9): Inflammation from lateral canal will damage pulp, but necrosis won’t occur until the apical foramen is involved Simring & Goldberg (JP 64 20-2): Retrograde periodontitis. Abou-Ross (JPD 82 20-15) Stressed pulp theory. Dental procedures stress pulp so may require endo. A fibers destroyed before c fibers. Bergenholtz, Nyman (JP, 84 20-26): Pulp necrosis developed more frequently in teeth which following periodontal treatment, were used as abutments (15% v. 3%). Rubach (OS, 65 20-3): EPT value with 2 dentin, but not diffuse calcifications, denticles or age. Tal (GD 84): Clinical Features
Vitality Usual Area of Swelling Pain Probing Sinus Tract Location Radiograph Local Factors Etiology
Pulpal Lesions
Periodontal Lesions
Non-Vital Vestibule Intermittent Throbbing Narrow, Isolated Defect Mucosa Localized bone loss Variable Deep Caries or Restoration
Vital Attached Gingiva Dull, Continuous Generalized Defect Attached Gingiva, Sulcus Generalized Bone loss of area Calculus Possibly Non-restored
TREATMENT: Harrington (DCNA 79 20-13): The true combined lesion occurs when independent periodontal and periapical lesions are present but not communicating. Overall prognosis depends on periodontal therapy which should be performed following endodontic therapy. ACCESSORY CANALS IN MOLARS: Prevalence of accessory canals depends on how the tooth was prepared (etched) and how the dye was put in (under pressure or vacuum) Burch 76%, Vertucci (OS, 78): 46%, 80% D canal, 20% M canal, greater dist from pulp floor-furca incidence lateral and furcation canals Gutman (JP, 78): 28%, 25.5% furca only, 10.2% lateral root surface. Lowman & Burke (OS, 73 20-8): 59% incidence after S/RP. 55%max, 63% Mand 1. Endo lesion treated first, 2. Wait 10-12 weeks before initiating perio treatment. Seltzer, Bender (OS, 63 20-1): lateral and accessory canals were located primarily in the bi - and trifurcated regions in molars. Periodontal tissues may have degenerative effect on pulp. Rubach (JP, 65 20-4): 45% of teeth exhibited lateral canals with majority located at the apex, stated that pulpitis can be caused by periodontal origin 8% of pulpitis or necrotic canals associated with periodontal lesions. MICROBIOLOGY OF CANALS/PERIODONTITIS Kipioti (OS 84 20-14): Bacteria in caries free necrotic teeth with advanced periodontal disease resembled the bacteria in the perio pocket. Suggests that endo is caused by perio.
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Jansson (JCP 95): Monkeys. Infected teeth had 20% more pocket epithelium and healthy teeth had 10% more CT coverage. Roots were devoid of cementum but surrounded by healthy periodontium. BL: Endodontic infections in periodontally prone pts may augment periodontitis propagation. Kerekes (90): Cross infection with perio bacteria can cause pulpal pathology ENDO LEADS TO PERIO (Generally a well accepted hypothesis - experimentally demonstrated, intuitively acceptable, clinically evident): Seltzer, Bender (JP,67): dogs &monkeys, mechanical pulp exposures to demonstrate that periodontal lesions were initiated and perpetuated by inflamed or necrotic pulps. Periodontal lesions can be initiated and perpetuated by inflamed or necrotic pulps. Jansson (JP, 93 20-11): PA lesion vertical bone loss, increased PD. Jansson (JCP, 93 20-12): PA lesion increased radiographic bone loss, increased PD, weak study, slightly widened PDL = endo infection no vitality testing. PERIO LEADS TO ENDO (Generally a less well accepted hypothesis - difficult to demonstrate experimentally, may be related to the inability to define “endodontic health” at any one moment): Kipioti (OS, 84 20-14): See above Kobayashi (IEJ, 90): 15 teeth (Dx as non-vital via EPT) associated with advanced perio lesions, access, bacterial culturing and microscopic analysis: The occurrence of micro-orgs common to both sites in study suggests that the periodontal pocket may be a possible source of root canal infection. Rubach (JP, 65 20-4): Pulpitis/necrosis can occur as result of periodontal disease involving accessary canals. 45% teeth access. canals. Jansson (JCP 95): See above CRACKED TOOTH SYNDROME Cracked tooth associated with cold sensitivity and localized vertical bone loss. Cameron(JADA 76 20-24): Pain on pressure or thermal sensitivity. Mandibular 2nd molar most frequently involved (40%). Look for wear facets, steep cusps and deep fossae. Cameron (JADA,76): 75% cracked teeth on vital teeth. Gher et al (JADA, 1987 20-28): 90% fractures were posterior teeth. 79% of fractures were vertical, 69% had endo comleted (71% had endo started). Hiatt (JP 73 20-22) Mandibular 2nd molars most frequently fractured (BOARD QUESTION) VITAL ROOT RESECTION Endo prior to amputation is the treatment of choice. Pro: Smukler (JP 76 20-16): Endo 2 weeks post amputation without adverse clinical/ histo effects Pro: Haskel (JP 80 20-18): “Wedge procedure”, 10 pts, 26 vital root amps, 3 cases 1-5 month tested vital, 8 cases tested vital for 3 years. Vital root resection can be a final procedure. 66% vital @ 3 years. Con: Gerstein (JP 77 20-17) Vital root resection is only an interim measure. High risk procedure. Langer (81): 100 pts, 10 yr. follow-up, 38 failed (84% after 5 years), 47% of failures due to fracture. 66% success with vital root resections MN molars highest failure rate due to fractures. (BOARD QUESTION) Most failures 5-7 years post surgery. HEALING WITH RCT TREATED TEETH Morris (JP 57 20-19): Healing of CT occurs equally with cementum vital/non-vital, Dentin: No regeneration to dentin of non-vital teeth. Diem and Bowers (JP 74 20-20): Monkeys, Non-diseased teeth, 4 treatment modes: Vital, Pulpectomy, RCT with CPCP paperpoints, and RCT with gutta percha. Notch at base of defects. Saw regeneration of cementum regardless of pulpal status. Surgically created defects. Dunlap et al (JP,81): Growth of fibroblasts occurred on root planed teeth of vital and non-vital teeth. Method similar to Aleo studies. Breault (JP 95 20-21): in vitro. Fibroblast attachment was reduced when exposed to formocresol or warm gutta percha without sealer. (BOARD QUESTION) Prichard (JP 83): Recommended that prior to perio surgery, endo tx should consist of instrumentation only. Then following healing after perio surgery, complete obturation of the canal could be performed. Sanders (JP 83): Only 33% of endo txd teeth demonstrated complete or greater than 50% bone fill with autographs and FDBA. 65% of vital teeth revealed complete or greater than 50% defect fill.
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ORTHODONTICS HISTO of Tooth Movement: Reitan (AJO 67 22-1): Orthodontic Movement: Increases vascularization and bone resorption, PDL compression, disruption of the blood supply, hyalinization, and bone necrosis. Hyalinization is a bad thing, caused by excessive orthodontic force. Slows down tooth movement. During initial period of tooth movement hyalinization of fibrous tissue and undermining resorption of bone occurs on the pressure side thus widening PDL space. During the secondary period the fiber bundles on the tension side will be stretched and resist further tooth movement. Relapse is caused by muscle function and rearrangement of alveolar fiber system. MALALIGNMENT YES: Buckley: (JP 72 22-3) 954 Irish factory workers, Periodontal disease increased with age but not with increasing malalignment Artun (JCP 87 22-27) Small increase in attachment loss in malaligned MN ant teeth. Malocclusion is a modifying factor in periodontal disease. Griffiths, Addy (JCP 81, 9-29): Plaque accumulation greater in malpositioned teeth, dental students had cleaner teeth. Plaque depends more on position of segment than presence of malaligned teeth. Max ant had < plaque that Mand ant. More difficult to clean, but not more disease. NO:
Ingerval (77): Dental students in study: plaque, not malalignment, cause of perio.
Tissue response: GINGIVA: Zachrisson (AO 72 22-4): Inflammation occurs 1-2 months after start of orthodontics despite good OH, but resolves 1 month after therapy. No permanent damage. Patients aged 11-15. Histologically inflammatory infiltrate increased during active therapy and resolved after debanding. Ericsson (JCP 72 22-15): Ortho can move plaque subGly and allow formation of pockets Prichard (JP 75 22-10): 4 bicuspid extractions, sequelae: tissue clefting, open contacts, 66% incidence of periodontal disease in these pts. Trosello (JP 79 22-16) Most gingival conditions for ortho treated patients are the same as for non-ortho treated patients i.e. plaque, inflammation, sulcus depth, tissue bunching, gingival clefting recession. Ortho treated patients did have more MG defects and root resorption than non-ortho treated patients. Batenhorst (JP 74 22-8): Moved teeth facially, teeth accidentally extruded, width of attached tissues increased, MGJ did not change. Epithelial attachment stayed at CEJ except on the facial. Epithelial attachment on the facial was longer and more apical. Bone apposition around the tooth except on the facial. Alveolar dehiscences developed when teeth moved facially. Ten Cate (AJO 76 22-14) Fibroblast involved in CT remodeling. Synthesizes and degrades collagen BONE: Polson: (JP 84 22-22) Examined patients 10 years after ortho, ortho had no effect on alveolar crest levels except on the distal surfaces of molars where there was more bone in orth treated patients, get LJE when teeth moved into defects. Karring (82): Incisors moved out of bone then returned to socket allowed bone to reform Fenestrations/Dehiscences: Wingard/Bowers (JP 76 22-13): Facial tipping does not routinely result in bony dehiscences RESORPTION:
Trosello (JP 79 22-16): Prichard:
16-17% incidence in ortho patients 2.3% in non-ortho patients 55% incidence.
TREATMENT MODALITIES: FORCED ERUPTION Ingber (JP 74 22-9): Forced eruption for treatment of intrabony defects or teeth fractured subGly improves crown root ratio. Can be used for fractured teeth, teeth treatment planed for extraction to regenerate bone EXTRUSION OF IMPACTED TEETH 81
Kokich (DCNA 93 22-20) Technique article. Most commonly impacted MX tooth is the canine, comprises 2% of ortho patients. Usually palatally positioned. Central incisor second most commonly impacted tooth. Techniques - Gingivectomy, APF, closed flap technique. MOLAR UPRIGHTING Newman (79): Molar uprighting, Brown also. Simon (JPD 84 22-21) Uprighting technique article Brown (JP 74 22-6) Molar uprighting will decrease pocket on mesial surface of molars. FIBEROTOMY Edwards (AJO 70 22-2) Supracrestal fiberotomy indicated after de-rotations. Improves retention CORTICOTOMY Gantes (JP 90 22-29) Corticotomy facilitated orthodontics caused minimal perio changes, reduced ortho treatment time. Not a common procedure in orthodontics MUCOGINGIVAL CONCERNS PRIOR TO ORTHO (?Graft Prior to Ortho) YES: Coatam (JP 81 22-19): FGG is indicated if there is no attached gingiva prior to starting ortho treatment. If its not done it could lead to gingival clefting. Orthodontic therapy can cause changes in the width of keratinized gingiva, and those patients with 0mm of keratinized gingiva had 28% incidence of cleft formation. Study examined only incisors and canines. Artun (JCP 86 22-27): Orthodontic correction of labially erupted canines resulted in teeth with less attached gingiva and more recession than untreated canines. Trossello (JP 79 22-16): Incidence of MG defects was twice as high in ortho treated patients compared to controls. Foushee (JP 85 22-24) Patients receiving orthognathic surgery had decreased width of attached tissue due to contraction of scar tissue. Graft before surgery. NO:
Wennstrom (JCP 87 22-26): Monkeys, gingival recession is not affected with orthodontic tooth movement. Buc-Ling thickness more important
SPONTANEOUS REPOSTIONING Manor (JCP 84 22-23): 2 pts case reports perio surgery may result in spontaneous repositioning of migrated teeth, ortho post surgery. PATHOLOGICAL TOOTH MOVEMENT? TenCate (76): Orthodontic tooth movement is a pathologic process from which the tooth recovers. Physiologic tooth movement: Tooth eruption, or movement with orderly remodeling and therefore no damage to the PDL. INTRUSION Steffensson and Storey (IJPR,93): Case study, small forces of 5-10 grams, attachment didn't follow tooth, specific sites and periodontal health of the area required. Ericsson: (JCP 77 22-15) Intrusion with poor oral hygiene can move bacteria subGly which can lead to attachment loss. IMPLANTS AND ORTHODONTICS Kokich - Implants used as anchorage for complex orthodontic movement. Fixtures restored with crowns after orthodontic treatment completed. MICROBIOLOGY AND ORTHODONTICS Diamanti-Kipioti (JCP 87 22-28) There is an increase in periodontopathic bacteria with sub-G banding. Pocket depth also increases. (BOARD QUESTION) RESTORATIVE PHASE Changing Concepts in Periodontics Ramfjord (JPD 84 21-1) Refutes perio myths 1. Crevices >3 mm are progressive periodontal lesions
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2. Surgical sculpting to resemble horizontal atrophy is necessary to prevent further loss of attachment 3. Complete plaque control is required 4. Furcation involvement signifies a poor prognosis treat furcas with hemisection or root amputation 5. The deeper the pocket the poorer the prognosis 6. Advanced periodontitis cannot be stopped 7. Healing after scaling and root planing is enhanced by soft tissue curettage. 8. Less than 1 mm of attached keratinized tissue will continue to lose attachment 9. Blanching as a result of lip pull indicates a need for MG surgery 10. Teeth with increased mobility need splinting and occlusal adjustment. Biological width Gargiulo (JP,61): 30 human jaws, histo, Sulcus Ave. 0.69 mm range 0 - 5.36 Ave. range 0.61 -1.76 EA avg. 0.97 mm range 0.08-3.72 Ave. range 0.71 - 1.35 CT Ave. 1.07 mm range 0-6.52 Ave. range 1.06 - 1.08 Ingber (Alpha Omegan 77, 21-2): Review. Ave. distance crown margin:alveolar crest 3 mm for preservation of alveolar health. Vacek, Gher (IJPRD,94): Histomorphometrics on 171 tooth surfaces of cadavers Sulcus Ave. 1.32 ± 0.80 mm range 0.26 - 6.03 mm EA Ave. 1.14 ± 0.49mm range 0.32-3.27 mm CT Ave. 0.77 ± 0.29 mm range 0.29-1.84 mm LOA Ave. 2.95 ± 1.70 mm range 0.60-8.73 mm Notables:1) No correlation between LOA and CT or biologic 2) Although there was variability in CT it was the least variable 3) Epithelium attachment was greater on tooth surfaces adjacent to restorations 4) CT and EA were greater in the posterior segments. Tal (JCP 89 21-23) Effect of violation of biologic width, width restored with recession and bone loss. Dog study, Class V amalgams placed at alveolar crest Cohen: Coined the term biological width, 2.04 to bone Ramfjord: Refutes biological width, says tissues will adapt. Maynard, Wilson (JP,79): Margins should be kept in the crevicular physiologic dimension. Wagonberg, Langer (IJPRD, 89): 5-5.25 mm of tooth structure above the osseous crest is required. Ante's law: The abutment teeth should be of the same or greater root area as edentulous teeth being replaced. Nyman (81 21-14): Refutes Ante's law. Of 60 bridges, only 5 met this requirement yet all remained functional (5-8yrs) Lundgren (JCP,91): Reduced periodontium can be restored with good plaque control. OK to tie implants to natural teeth Shortened Dental Arch: Kayser (IJPRD 89): Premolar occlusion OK; < 4 occlusal units per arch questionable, Premolar or equivalent make 1unit, molar 2 units. Overhanging Margins: Jeffcoat (JP 80 21-6): 100 pts, correlation between Med and Lg overhangs and bone loss. Small overhangs did not result in increased alveolar bone loss. Lang (JCP 83 21-8): Crossover design, inlays with overhangs, more BOP and increased Bacteroides sp. Rodriguez-Ferrer (JCP 80 21-7): Effect gingival health b/c of plaque retention. Remove as part of initial therapy. Pack (JCP 90 21-9) 56% prevalence of overhangs very high. 64.3% PDv> 3 mm, 32% BOP. Brunsvold and Lane (90): 33% of Pts have 25% of restorations with overhangs Spinks (86): Diamond tips and curettes the best for removal Wang et al (JP,93): Molars with crowns or proximal restorations had higher % of furcation invasion and more attachment loss, but only greater mobility if great among of attachment loss. Supra vs. SubG Margins:
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Silness (JPR 70, 21-11): Margins below the gingival crest showed greater amounts of plaque, gingivitis, and probing depth, supraG is more appropriate. Choice between full and ¾ crown not as important as the supra-sub gingival margin choice Silness (71): Full coverage crowns had larger amounts of plaque, more severe gingivitis, and increased PD Valderhaug (JDR 76 21-13): shows the same in 5 year study. Increased pocketing: 1.2 mm Ave ALOSS subG 0.8 mm Ave ALOSS at gingiva 0.06 mm Ave ALOSS supraG Dragoo and Williams (IJPRD 81 21-21,22): Addresses tissue reaction to restorative procedures, place retraction cord prior to preparation, placement of subG margins with existing periodontitis may exacerbate the disease, electrosurgery causes extensive damage to epithelium and connective tissue, Loe and Silness " injuries are reversible as long as the lesions can heal against a clean tooth surface. Tarnow (JCP 86, 21-22): SubG margins recession and limited gingival inflammatin. Tal (JCP 89 21-23) Effect of violation of biologic width with amalgam, width restored with recession and bone loss. Dog study, Class V amalgams placed at alveolar crest Flores de-Jacoby (89): Support for supraG margins, subG crowns margins had increased motile rods and spirochetes, Silness and Roystrand (JCP 84, 9-24): Healthier if space b/w ant teeth. Also had less fillings. Proximal gingival health related to plaque retention. Pts with restorations had more disease than those without. Maynard (79): SupraG crown margins have less clinical signs of inflammation, X-sectional study Crown Contour: Sackett (JP 76 21-12): overcontouring the buccal, axial third of the tooth may be a factor which predisposes the gingival tissues to inflammatory disease. Crowl (JPD,90): Emergence Profiles of restoration affects the effectiveness of oral hygiene. Acid etched resin bonded bridge: Thayer et al (IJP, 93): 5 to 15 year study, Caries rate 6%, success was 81% without trauma. 61% with trauma. Priest (IJPRD,95): 77 resin bonded bridges 1-11yr duration. 39% became dislodged. Major factors concerning dislodgment were the luting agent and the prep design. Mucogingival Concerns: Stetler and Bissada (87): SubG margins need 2 mm of attached gingiva Maynard and Wilson (79): Minimum of 3 mm of attached gingival, 5 mm Keratinized tissue before restorative. Wait 6 weeks before impressions and prosthetic surgery. Amalgam restorations and caries: Albander et al (JP,95): In adolescents, 227 pts, defective restorations and caries had significant effect on gingival inflammation at that site and the proximal adjacent area. lower bone height was associated with these areas. Composite Restorations and Porcelain Veneers: Blank (JPD 78 21-20): Well finished composites do not adversely affect the health of the gingiva Dragoo (IJPRD 97 75-87) Possible attachment to glass ionomer composite hybrid (Gerestore Dyract) Kourkouta (JCP 94): Gingival health with porcelain veneers. No sig. reduction in GI. Decrease in PI. Larato (72): Composites have more inflammation Overdentures: C. Becker, Kaldahl (IJRPD 84, 21-32): Overdenture concept to protect periodontium Lauceillo & Ciancio (85 21-33): Longitudinal study, good results, stressed maintenance Renner et al (JPD 84 21-31): 4 yr., 36% developed root caries, mobility mixed, tissues usually bleed, tissues edematous. Jorgensen (JCP 94 21-30): 40 pts. Pts who wear their overdentures day and night had more periodontitis and caries than those who did not wear their overdentures continuously. Johnson (OS 74 21-34) Vital root submergence in monkeys. Vitality remained unchanged.
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Combination Syndrome: Loss of maxillary teeth with remaining mandibular teeth, leads to resorption of maxillary arch, and supereruption of the mandibular anterior teeth. Removable Partial Dentures: Bissada (JP 74 21-17): 68 pts with 3 types of RPD’s, Metallic bases were more favorable with less inflammatory responses. Keep margin of RPD 5-6 mm away from gingival margin. Bergman et al (JPD 85 21-19): Compared well maintained patients with RPD’s to controls, found that subjects had similar plaque, gingivitis and mobility. (BOARD QUESTION) Orr (92): Partials margins should be at least 3 mm from the gingival margin for oral hygiene. Gerstein, King (JP 84): Use of removable partials for splinting in tx of mobility, helps with oral hygiene & preserves tooth structure. Chandler (JPD 84, 20-17): Increased inflammation in gingiva apical to clasp arms at 8 & (years recall compared to 1 & 2 year recalls, no significant increase periodontal breakdown or caries. Root Submergence: Bowers (IJPRD 88, 21-35): Technique described, healing usually completed by 3 months. Johnson (JOS 74, 21-34): Vital root submergence is possible and maintains bone. SUBPONTIC OSSEOUS HYPERPLASIA Ruffin, Waldrop, Aufdemorte (OOO, 93): Cause is multifactorial, like Tori and exostoses are considered to result in part from genetic predisposition, functional stimulation (occlusal stress), mild chronic irritation. Surgical removal may be indicated for prosthetics , esthetics, and phonetics, biopsy, interference with oral hygiene. reoccurrence has been known to occur. Wasson (JPD 93 3-18) SAA Implants to Natural Teeth: Biana, Ericsson, Lindhe (JCP 95): 10 beagles. 6 month loading of bridge of natural tooth to implant, Histo revealed no alteration of gingiva or periodontal tissue. CANTILEVERS Lundgren, Laurell (87): excellent long-term prognosis. May be due to perfect occlusal contact, no working or non-working side contacts, and optimal retention.
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Etiology / Risk Factors Epidemiology Prevalence - the total number of cases of a disease in existence at a certain time in a designated area There is a point in the v of prevalence just as prev is a point in time. Incidence - The rate at which a certain event occurs. The number of new cases of a specific disease occurs during a certain period. INCIDENCE OF PERIODONTAL DISEASE Marshall-Day (55): 1st epidemiology study, Gingivitis Male > Female (88% vs. 80%) declines in late teens then increases through adulthood, Periodontitis: Males>Females, bone loss and mobility increased with age, after 35 tooth loss rapid. Van der Velden (91): Incidence at 15 yrs = 5%, at 60 yrs = 80% (2 mm attachment loss). Cross sectional: Brown (JP 89 6-30): Measured only 6 teeth at mesial line angle, large n= 2600, US pop. 15% healthy, 36% of adult population had periodontitis (> 4mm pocket depth)., 8% advanced periodontitis (at least one pocket > 6mm ) (BOARD QUESTION) NIH Study of Oral Health (1987 6-14) Bad study, underestimated prevalence of periodontal disease in America. Problems include: populations excluded, multiple examiners, no radiographs, randomly selected quadrants to probe, sites chosen that normally don’t break down, could not angle probe, estimates admittedly conservative, very low BOP estimates, very low pocketing rates only 1% had a 6 mm probing. Poorly written. Horning (JADA 90 6-16) Military population, 37% gingivitis only, 33% early periodontitis, 14% moderate periodontitis, 15% advanced periodontitis, .5% LJP, .5% necrotizing gingivitis. Predominantly young male, all had radiographs, no healthy category, full mouth circumferential probings. PD more common in Filipinos. (BOARD QUESTION) Johnson (JCP 88 6-26) Perio is a disease which affects only a minority of the population worldwide. Prevalence of severe perio 7-15%. GINGIVITIS INCIDENCE AAP Position statement (92): 18-64 y.o., 47% male and 39% females with at least 1 site with BOP. Brown, Loe (JP 89 6-30): 50% have gingivitis. UNTREATED PERIODONTAL DISEASE PROGRESSION Loe (JP 78 6-7): The natural history of periodontal disease: Pts before 40yrs of age, longitudinal study of development and progression of perio in Sri Lankans and Norwegians, supports continuous progression. Attach loss Norwegians: 0.07-.13 mm/yr., Sri Lank 0.3mm/yr Loe (JCP 86 6-12): Wide variety of rates of progression, RP 8%, MP 81%, NP 11% in Sri Lankans Becker (JP 79 6-8): 30 diagnosed but untreated periodontitis pts, recalled 10 yrs, perio is progressive and rapid if untreated. mean tooth loss 0.36 per year. Molars most frequently lost. Lindhe and Haffajee (JCP 83 6-9) Two populations, American and Swedish, no treatment 3.9% of sites lost 2 mm of attachment, showed sites with advanced AL are not more prone to further loss. Implied disease is not continuous. (BOARD QUESTION) 2-3% of sites lose >2.5 mm of clinical attachment FAMILIAL PERIODONTAL DISEASE Proband is the 1st individual of a familial pattern with the disease. Michalowicz 91: 100+ Identical twins, found correlation between siblings. Monozygotic twins of different environments. Page: LJP X-Linked dominant transfer Hart (92): Due to limited incidence of male to male transfer, the genetic transfer of LJP may be autosomal. Suzuki: Genetic link to RPP Boughman (92): LJP and GJP, + antibody status not related to siblings with disease (phenotypic transfer pattern not expected mechanism. AGE AND PERIODONTAL DISEASE INCIDENCE: Gilbert (92): 65 yr. or more pts, not a deep pocket disease, but attachment loss is extremely common, 62% of seniors have some evidence of attachment loss.
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EFFECTS ON TISSUES Boyle (JP 73 3-2) Statistically significant loss of bone with increasing age, clinically insignificant Matheny Older patients have increased vessels and BP, decreased vessels with active flow and oxygen saturation Van der Velden (JCP 84 14-16) gradual breakdown of periodontium with age but the cause of this might be either age or cumulative effect of longer exposure to periodontitis, The epithelium becomes thinner, less keratinized and shows increased cell density. CT becomes denser, coarsely textured and exhibits fewer cellular elements, decreased osteoblasts at bone/PDL interface. Continual cemental apposition. Gradual recession. Ten Cate (69): With increasing age, there is decreased ground substance of collagen, decreased collagen turnover. Tonna (76): Age effects on regenerative capacities of bone and cementum are minimal (BNL mouse model) RESPONSE TO THERAPY: Lindhe (JCP 85 14-17): Studied age on healing after periodontal surgery and found no significant difference between three age groups ( 49 ). Similar changes in Attachment levels, PD, and degree of gingivitis seen in all pts. Abbas (84): Compared healing of older vs. younger pts, Wound healing was longer in patients more susceptible to disease (it was the younger population). Healing time was also increased with extent of disease. Greenwell (89): Regenerative therapy should be used on all geriatric pts who are not medically compromised. World Workshop (89) " The elderly patient with moderate alveolar bone loss has a better prognosis than the younger patient with the same amount of gingival and osseous destruction." Aging Female/ Osteoporosis: Norderyd et al (JP,93): Estrogen supplement in the 50-64 yr. old presented with less gingival bleeding than controls von Wowern (JP 94): 12 osteoporotic females and 14 normal females with the same PI, GI, and BOP were examined. The osteoporotic women had greater LOA as well as decreased bone mineral content of the mandible and forearm. Suggests that osteoporotic women may be more at risk for LOA. Klemetti (JCP,94): Individuals with high mineral content in skeletal bone seem to retain their teeth with deep periodontal pockets. Summary: no clear cut link between osteoporosis and periodontal disease. PLAQUE AS AN ETIOLOGY HOW DOES PLAQUE FORM AND WHAT BACTERIA ARE ASSOCIATED WITH ITS FORMATION? Studies basically indicate the following basic sequence in plaque formation: pellicle formation G+ colonization Filament colonization G- and spirochetal colonization CHRONOLOGICAL PLAQUE DEVELOPMENT SupraG: Gram + (actinomyces and streptococci) attach very quickly to salivary proteins of the pellicle, thus if you clean often you repeat the attachment process. Actinomyces viscosis big player in supraG plaque - Intrinsic growth rate/death influenced by a) oral hygiene b) Gram (-) produce inhibitory factors c) PMN's, specific antibodies d) food - Gram (-) Anaerobes, microaerophillic are fed by gram (+) bact. extracellular products and tissue breakdown products, -when you starve they will elicit more tissue breakdown for food, - influenced by PMN's, Ab, and O2 levels Listgarten (JP 75 8-14): Epoxy resin crowns, light and EM study: 1. 1 mm pellicle with G+ cocci attached. 2. filamentous bacteria attached to tooth. 3. Inner cocci were replaced with filaments. 4. Spirochetes associated with outer surface and sulcular epithelium. Theilade (66): Plaque matures in 14 days.
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Loe, Jensen, Theilade (JP 65 8-01): Experimental gingivitis. Developed in 15-21 days without oral hygiene resolved in 7 days (BOARD QUESTION) Phase I: (2 days), gram + cocci and rods w/ 30% gram (-) cocci and rods Phase II: (1-4 days), Increase in # fusobacteria and filaments Phase III: (4-9 days), Spirilla and Spirochetes (Gingivitis) Vrahopoulos (92): SubG plaque layers: 1) Nearest Cementum- densely packed Gram (+) cocci perpendicular to the root 2) Superficial layer- Mainly gram (-) rods and cocci 3) Middle layer- Gram (+) filaments and spirochetes 4) Loose pattern- Corn cob formation, Rosettes, "test tube brushes" mainly spirochetes Offenbacher et al. (JCP 88 8-10): Colonization sequence needed for successful colonization. Small spirochetes needed for colonization of medium spirochetes and mediums needed for large. Conrads, et al (JP 96, 8-5): Pg and Aa not present in health, P nigrescens is found in health and Pi is found in disease. PLAQUE FORMATION (INFLUENCE OF TOOTH TYPE/GINGIVITIS) Quirynen (91): Plaque formation was faster in patients with higher gingival indexes. Plaque forms faster on upper premolars/molars, and lower front teeth. Also increases during the night. Ramberg (JCP,95): plaque forms faster adjacent to gingivitis. 1st Bacteria to form on Pellicle: Strep sanguis ATTACHED PLAQUE: SupraG: Strep mutans, S. sanguis, S. mitis, S. salivarius, lactobacillus, actinomyces SubG: S mitis, S. sanguis, Eubacterium, Bifidobacterium, A viscosus, A naeslundii, Propionibacterium, Bacterionema matruchotii. UNATTACHED PLAQUE: SubG: Pg, Pi, Bacteroides, Fusobacterium, Capnocytophaga, Selenomonas, Campylobacter, Actinobacillus. IS IT THE AMOUNT OF PLAQUE OR THE SPECIFIC "BUGS" WHICH ARE IMPORTANT? Today's philosophy incorporates components of both the specific and non-specific plaque hypotheses, as well as the idea that plaque alone is not the only variable associated with periodontal disease. Theilade (JCP 86 8-07): Combined theories, because you cannot eliminate one organism and cure periodontal disease (specific). Also not all plaque causes the same amount of disease. Socransky and Haffajee (JP,92): Disease is caused by " Specific bacteria of the right clonal type with the essential genetic elements in sufficient numbers for that host with appropriate additional species in the right environment" Is plaque amount important? Not necessarily. Sri Lankans had gobs of it and 11% had no progression of disease. SPECIFIC vs. NON-SPECIFIC Plaque Hypothesis Loesch (Oral Sci Rev 75): described the non-specific plaque hypothesis (NSPH) and the specific plaque hypothesis (SPH). NSPH: caries and periodontal disease result from the elaboration of noxious substance by the entire plaque flora, while SPH: suggests that only certain plaque cause infection because of the presence of a pathogen(s) and/or a relative increase in the levels of certain indigenous plaque organisms. Support for Specific Plaque: (Loesche) Dzink (Forsythe) (88): Clusters, Combinations of Cr, Bi, Pg, Bf, Fn. were more numerous in active sites. Slots (88): Pg, Pi, Aa: when all 3 isolated from site it was active with 86%+ sensitivity, spec, predictive values. Listgarten (JP 65 8-12): Spirochetes largely responsible for ANUG lesion. Four zones superficial to deep Bacterial zone, neutrophil rich zone, Necrotic zone, spirochetal infiltration (BOARD QUESTION) Zambon (JCP 85, 8-32): Aa associated with LJP.
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Virulence Factors: LPS, outer membrane proteins, vesicles, toxins, proteolytic enzymes, adherence factors (pilli) hemolysins, fibrinolysins, effects on host cells i.e. fibroblasts, lymphocytes, PMNs, epithelial cells, etc. All factors are expressed to a different degree by bacteria making some more pathogenic than others. Support for Non-Specific Plaque: “ small groups of bacteria produce the pathogenic potential necessary to induce periodontitis of the #’s or proportions are increased in the pocket to certain critical level to overcome the host resistance.” Moore (91): No difference in the bacterial flora of active and inactive sites. Theilade (JCP 86, 8-8): Non-specific plaque theory. Destructive periodontitis as the result of subG colonization, which is favored by such ecological changes as plaque accumulation, gvtis, and gingival exudate. This increases the numbers of microorganisms and alter their proportions, but no single species appears in active sites which is not also commonly present in inactive sites. DOES PLAQUE CAUSE GINGIVITIS AND/OR PERIODONTITIS? PLAQUE CAUSES GINGIVITIS: Loe, Theilade, Jensen (JP 65 8-01): Experimental gingivitis Produce gingivitis in patients with health gingiva by withdrawing oral hygiene. - 9 1st year dental students, teacher, 2 lab techs, reviewed GI and PI at intervals, reviewed bacterial status. - 3 of subjects developed gingivitis in 10 days, 9 subjects between 15 and 21 days. when oral hygiene reinstituted gingiva returned to a healthy state. Loe and Schiott (70): Experimental gingivitis study in which it was found that daily rinsing with a 0.2% CHX solution virtually prevented plaque accumulation and gingivitis development over a 21 day period of no oral hygiene. Holt Wilson Musa (JP 95 8-15) Mycoplasma may cause gingivitis in children. PROVE PLAQUE CAUSES PERIODONTITIS: Loe, Theilade, Jensen (JP 65, 8-1): Experimental gingivitis Maintenance Studies: H&W McFall Wood Goldman Christersson, Zambon, Genco (JCP,91): Opportunistic Infection idea, Indigenous and many exogenous micro-organisms are normally non-pathogenic bacteria but can, under circumstances such as reduced host resistance or overgrowth, cause disease in which case they may be considered opportunistic pathogens. Lindhe (75): Ten beagle dogs brushed twice daily did not develop periodontal disease, while 8/10 beagles that accumulated plaque developed periodontitis with loss of attachment. Gingivitis can proceed to periodontitis, but 2/10 untreated dogs and some sites did not progress suggesting variability in host susceptibility. Sri Lankan Studies: Sri Lankans had significantly more plaque and calculus than their Norwegian counterparts, as well as significantly greater attachment loss and rate of attachment loss. This seems to suggest that plaque is a significant contributing factor in periodontal disease. Keep in mind though that 11% of the Sri Lankans had no disease progression even with all of the local factors present, which goes to show that plaque is not the only variable in periodontitis. PLAQUE AS ETIOLOGY OF DISEASE PROGRESSION: Long term studies of Gothenburg Group i.e.. 14 yr. Lindhe study, Nyman, Rossling studies prove or show that plaque control (every 2 wks) although unrealistic may be the essential component to success to therapy. Ranney (JPR 87 8-19) No bacterial differences between active and inactive sites Tanner (JPR 87 8-20) W. rectus, B. gracilis, E corrodens found more frequently in active sites
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PLAQUE FREE ZONE Corresponds to epithelial attachment, area that doesn’t stain, could be free floating bacteria. Bass (J Den Res 45): First to describe PFZ Saglie (JCP 75, 8-02): Plaque free zone present. Narrowest in anterior. No man’s land between host defenses and advancing plaque front. PFZ decreases as PD increases. Suggests non-surgical treatment. Vrahopoulos (JP 95, 8-03) PFZ is not plaque free, colonies in severe periodontitis resemble colonies in adult periodontitis. No adult periodontitis pts like Saglie (JP, post-JP, RPP), could have been bacterial products or parts and not whole bacteria--“small particles resembling bacteria.”Area that doesn’t stain, could be free floating plaque. Friedman (92): SEM of extracted diseased teeth, showed clear evidence of plaque free zone(not entirely plaque free).Had plaque front + "Zone" + epithelium, spirochetes predominant, always bacteria present usually weird morphology Koch’s Postulates- claim bacterial specificity 1) Bacteria should be able to be isolated from the diseased tissues 2) Pure cultures can be obtained 3) Bacteria when inoculated in experimental animals should cause the disease 4) Bacteria should be isolated from the diseased tissues in the experimental animal. Socransky’s modifications (JP 77) 1) Presence of the putative pathogen in proximity to periodontal lesion and in high numbers compared to either the absence of the bacteria or presence in much smaller numbers in healthy subjects. 2) Patients infected with these periodontal pathogens often develop high levels of antibody in serum, saliva and gingival crevicular fluid and may also develop a cell-mediated immune response to the putative pathogen. 3) Bacteria can often demonstrate in vivo production of virulence factors that can be correlated with clinical histopathology. 4) Clinical treatment that eliminates these bacteria from periodontal lesions should result in clinical improvement. MICROBIOLOGY NON-MOTILE Aa: G(-) , non-motile, facultative anaerobic rod B. forsythus: G(-), non-motile F. nucleatum: G(-), non-motile, anaerobic rod found most frequently in disease and remission (BOARD QUESTION) P. gingivalis: G(-), non-motile, anaerobic, bacillus has proteases which degrade compliment, IgG P. intermedia: G(-), non-motile, anaerobic, bacillus Bacterionema matruchetii: internal calcification E. corrodens: G(-), non-motile, microaerophylic facultative anaerobe, rod, surface translocating. MOTILE Capnocytophaga sp: G(-), motile, capnophyllic, fusiform rods, surface transloc. Treponema denticola: G(-), motile, strict anaerobes Treponema socranskii most commonly sampled spirochete (BOARD QUESTION) Camphylobacter (Wollinella)(sp): G(-), motile, anaerobe, helical curved, straight cells, flagellated. C. rectus: G(-), facultative, motile, can be helical, curved, or straight. Note: It is of importance to remember that facultative organisms (i.e. A.a. and E.c.) are not susceptible to metronidazole because metronidazole is only effective against obligate anaerobes. If using metronidazole and still concerned about A.a., prescribe another antibiotic in addition (i.e. amoxicillin) Extended List: Actinomyces israelii, A. naeslundii, B. capillus, Selenomonas sputigena, Eubacterium timidum, E. brachy, E. nodatum, Lactobacillus minitus, Peptostreptococcus micros, enteric rods + pseudomonads VIRUSES Contreras Slots (OMI 96) CMV EBV have possible role in periodontal diseases
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Sabiston (JCP 86, 16-9) ANUG possible viral origin CMV. CMV and ANUG have many similar characteristics age, higher prevalence in HIV positive patients. FUNGI
Dewit, Cobb, Killoy (IJPRD 85, 16-15):100% of specimens had fungi invading tissues in an acute abscess. Sparse number of bacteria. Should you prescribe anti-fungal instead of antibiotic?
ATTACHED PLAQUE: SupraG: Strep mutans, S. sanguis, S. mitis, S. salivarius, lactobacillus, actinomyces SubG: S mitis, S. sanguis, Eubacterium, Bifidobacterium, A viscosus, A naeslundii, Propionibacterium, Bacterionema matruchotii. UNATTACHED PLAQUE SubG: Pg, Pi, Bacteroides, Fusobacterium, Capnocytophaga, Selenomonas, Camphylobacter, Actinobacillus. So, bacteria normally associated with AP are part of the unattached plaque. MICRO BY DISEASE TYPE: Taken from Periodontal 2000, Socransky and Haffajee, 1994 Gingivitis HIV S.s., S.m. V.p., Actinomyces Sp same as AP A.n,A.v. LJP Strepto RPP Fn.., Adult Perio PPP P.m., C.r. Refractory Aa, Pi, Pg, Ec, Aa, Capno, Pg, Pi, Capno, Pi, Pg, Aa, Aa, Pg, Pi, Fn., C.r. Yeasts Bf, Ec, C.r., Capno, Ec Cr,B.f. Fn.., Treponema, Fn.. E.c.,Candida, B.f., P.m., Enteric rods, Selenomonas P.m. Sp, Eubacterium Sp (Slots 88) (Dzink 85)
(Slots 82)
(Tanner) (Di Murro)
(Delaney)
(Haffajee 88)
ANUG Pi, treponema denticola, fusiforms
(Loesche 82)
Loesche, Syed, Schmidt Morrison (JP 85, 8-17): AP caused by Pg and spirochetes. And we can treat with Flagyl. (We don’t know if spirochetes are the etiologic agent). MICRO OF OTHER CONDITIONS: Peri-implantitis same as AP IDDM NIDDM Smokers
same as AP same as AP, Pg, possibly different serotype Aa, Pg, Pi, #s same in smoking and non-smoking perio pts
Pregnancy
increased numbers of P.i.
Mombelli 87 Apse 89 Zambon Zambon 88 Preber & Bergstrom 92 Kornmon 80
WHY ARE CERTAIN BACTERIA SO VIRULENT? What bacteria can do: 1) May produce toxic products such as lactic acid, hydrogen sulfide, and ammonia 2) Endotoxins which indirectly destroy tissue by setting up destructive inflammatory response. 3) Produce enzymes such as collagenase, hyaluronidase, glycosides 4) Kill PMN’s or alter their function- Capnocytophaga and Pg interfere with chemotaxis, Aa produces leukotoxin which interferes with PMN function. 5) Ag/Ab Response thus tissue destruction. Virulence Factors of P.ging. (1) pilli for adherence
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(2) fimbriae induce T-cell response and antibody production (BOARD QUESTION) (3) capsule which adds resistance to phagocytosis (4) LPS which has indirect effects due to cytokines IL-1, PGE, TNF (5) enzymes: collagenase, trypsin-like activity, degrades complement, (BOARD QUESTION) degrades Ig (6) toxins: ammonia, butyric acid (7) vesicles to evade chlorhexidine (8) Three serotypes (BOARD QUESTION) (9) Can invade into epithelial cells (BOARD QUESTION) Virulence Factors of P.i. (1) pilli (2) capsule (3) LPS Considered less virulent than P.g. because P.i. lacks trypsin-like activity, only partially degrades complement and Ig, and produces low to no toxic products. Gharbia (JP 94, 19-16) P. intermedia and P. nigrescens may be confused with each other Virulence Factors of Aa: (Zambon JCP 85, 8-32) (1) leukotoxin which lyses PMN’s (2) can alter PMN activation (3) lymphocyte suppression factor (4) produces catalase which degrades peroxide. (5) Four Serotypes (Type B - bad!) (6) Tissue destruction factors- LPS (7) Bone resorption inducing toxin (8) Activates t-suppresser cells (9) Can invade epithelial cells (BOARD QUESTION) (10) Facilitate adherence to mucosal surfaces (11) Can invade tissue (12) Collagenase (13) Acid Phosphatase (14) Alkaline Phosphatase (15) fibroblast inhibiting factor (16) epithelial cell inhibiting factor (Fives-Taylor JP 96, 32-33): Bacteriocin, Chemotactic Factor, inhibit DNA & RNA synthesis, decreased fibroblast proliferation, Fc binding-inhibit complement, LPS, adherent, invasivevessicles containing leukotoxin and endotoxin. Differential Darkfield Microscopy (DDFM) technique popular in the early 1980’s thought to be able to diagnose active disease on the basis of percent of spirochetes and motile rods. (MOTILE Capnocytophaga. Treponema denticola: Camphylobacter C. rectus) Listgarten was big advocate. Became part of the Keyes’ technique. Later popularity and relevance faded. Evian (JP 82 8-03) When mean rather than individual values used, with increase in GI and PI, spirochetes and motile rods increased and cocci decreased. Proportions vary considerably. Article quoted to support evidence of spiros causing disease, but this may not be the cause. Taichman (JP 82) Spirochetes important in perpetuation of periodontal disease. Can activate host cells. Baab (JCP 86, 8-7): Cultured bacteria in bleeding and non-bleeding sites. Bacteria not significantly different. Spirochetes more related to PD, ALOSS, and GI than BOP. Sig correlations related to increase ALOSS, PI and GI found with cocci and motile rodsUsed means of GI, PI and Bleeding Index. Race and Gender Differences in Microbiology
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Schenkein (JP 93, 8-11) No microbial differences between sexes. Pathogenic bacteria more prevalent in blacks than whites. (BOARD QUESTION) Racial differences also noted in prevalence of early onset perio. Drake (JP 93 8-27) Blacks have higher prevalence of pathogenic bacteria than whites. Perio also more severe in blacks in the Piedmont study (more Pging). Von Troil-Linden (JCP 95 8-32) Spouses of patients with advanced periodontal disease have a worse perio status than spouses of periodontally healthy individuals. Beck (92) Studied pathogens in Blacks and White. Differences most pronounced for P. ging (BOARD QUESTION) BACTERIAL INVASION Bacterial invasion was not thought to occur for many years. Bacteria in the CT were thought to be an error of biopsy technique. Now bacterial invasion of the periodontal tissues is an accepted concept. YES:
Saglie(JPR 82): SEM of 5 biopsies, 4 had bacterial penetration into epithelium, 1 penetrated into CT. Another study showed Aa, spirochete invasion into epithelium and CT in 1 LJP patient. Saglie (JP 88 8-22) Aa and P ging detected in epithelium and CT of active lesions by immunoperoxidase. 1) High numbers in active sites 2) Decreased with successful treatment 3) Remain high after unsuccessful treatment Nisengard, Bascones (JP 87): Saw bacteria 400µm beyond epithelium to crest of bone in some cases, invading organisms were primarily G(-) Listgarten (JP 65 16-1): ANUG Spirochetes: Superficial to deep 1) Bacterial Zone. 2)Neutrophil rich zone. 3) Necrosis 4) Spirochete infiltration into CT. Frank & Vogel - TEM bacteria seen on the bone Moskow (JCP 92 12-3): Human block sections, periodontitis in maxillary molars can cause thickening of the maxillary sinus mucosa. Lane & O'Neil (JP 84 18-8): Periodontitis can cause chronic sinusitis in rare cases. Engstrom and Egelberg (JP 88 18-5) Perio patients with thick sinus membrane were treated, one year later perio health was better and sinus membrane was thinner
NO:
Silverstein (90): Beagles, controlled biopsy with perfusion, saw a limited # of bacteria in tissues regardless of health. Sussman (JP,69): Human gingival col biopsies, deep tissues no bacteria, limited to superficial plaque & ulcerated areas.
TRANSMISSION BETWEEN FAMILY MEMBERS: van Steenbergen et al (JCP,93): P.g. can be transmitted between spouses and children , A.a more difficult Offenbacher (JP 85 11-7) risk of transmitting bacteria from one spouse to the other. Similar morphotypes in married couples, could be due to similar oral hygiene practices Von Troil-Linden (JCP 95 8-32) Spouses of patients with advanced periodontal disease have a worse perio status than spouses of periodontally healthy individuals. Preus (JP 94 12-01) Transmission of Aa in families 50% of pts with advanced perio had Aa 50% of spouses and 30% of children also had Aa Husband and wife did not have the same serotype of Aa Children with Aa had a serotype identical to that of one parent Christersson (JP 85 8-32) Evaluated possibility of Aa being transmitted from site to site in an individual by the perio probe. Found that Aa was inoculated into healthy sites, but that it didn’t live for long CULTURING Baker (JP 91 19-12): Paper points may not accurately culture bacteria from the base of the pocket. Layered different bacteria and cultured. Make sure all supraG plaque is removed Gunsolley (JP 92, 6-34) Must sample a lot of sites to be sure that Aa is not present (31-35). For other pathogens can use smaller sample number. Van Steenbergen (OMI 93 19-15) Bacterial survival in transport media was ok up to 48 hours. Magnusson: Curette vs. washing, neither more effective.
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Renvert (JP 92): Paper points will sample more bacteria than curettes, even immediately after a curette sample. Sampling in LJP: Savitt: 37 % sites with Aa Zambon: 57 0f 60 pts + for Aa PROTECTIVE BACTERIA?? Dzink et al (85): S sanguis, S. uberis, Viellonella parvula, R. dentocariosa, Capno ochracea, Proprionibacterium acnes associated with sites with gain of attachment/ no loss of attachment. CDR PAUL FAVORITE. Use when he says bacteria cause periodontitis. PATHOGENESIS THEORIES OF PATHOGENESIS Waerhaug (79): Pts without evidence of TFO had vertical defects. Waerhaug: Sphere of influence: 2.5 mm from advancing plaque front. Weinmann (41): 1) Gingival inflammation spreads through blood vessels into the marrow spaces of alveolar bone 2) Spread of inflammation into PDL is secondary, and usually not inflamed 3) Defect morphology depends on location of blood vessels and thickness of bone Glickman (63): Codestruction Theory , necropsy study of 3 patients. Zone of irritation + zone of codestruction, separated by transseptal fibers. Described Buttressing Bone (JP 65 17-1) (both central and peripheral). Akiyoshi & Mori (JP 67 17-3): Inflammation occurs along blood vessels, within alveolar bone causing resorption to start internally. MECHANISM OF POCKET FORMATION Takata (JP 88 11-11): Autopsy study 218 human teeth, pocket formation was initiated by degenerative changes in the 2nd and 3rd cell layers of the innermost cells of the coronal part of the JE. Intraepithelial cleft formation was followed by degeneration and desquamation of cells lining the cleft. ENZYMES Christner (JP 80 11-11) In health, collagenase inhibitor may prevent activation. In disease, bacteria, host PMN’s may produce protease to destroy host collagenase inhibitor. Friedman (JP 83 11-12) The ratio of lysozyme to lactoferrin could be of value as a diagnostic test for LJP patients. Nakamura (JPR 83 11-13) Periodontitis patients have higher salivary levels of enzymes than healthy patients. Sandholm (JCP 86 11-14) Most collagenase is derived from the host not bacteria. Gustafsson (JCP 92 19-6) Increased granulocyte elastase in GCF in perio patients MECHANISM OF RECESSION FORMATION Novaes (JP 75 11-4): Pathogenesis of gingival clefts, Hypertrophy of rete ridges leads to anastomoses of sulcular and oral epithelium, subsequent loss of connective tissue and vasculature, recession. GINGIVITIS DISEASE PROGRESSION Page and Schroeder (Lab Invest 76 11-1): Initial: (2-4 days) Vasculitis, increased GCF, exudate, Increase PMNs, coronal JE alteration, perivascular collagen loss. Early: (4-7 days) Accentuation of initial, lymphoid cell (T-cell Seymour) infiltrate, more collagen loss, proliferation of basal JE. Established: (2-3 weeks) Persistence of acute inflammation, plasma cells predominate, presence of IgG, continued CT loss, apical migration of JE, early pocket formation. Still gingivitis Advanced: Persistence of above, plasma cells predominate Bone loss/ periodontal pockets, quiescence exacerbations. Periodontitis. Modifications:
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Brecx (87): Initial lesion health rather than pathology Wilde: T-cell mediated early lesion Listgarten (JCP 6-11): Most gingivitis lesions do not progress to periodontitis, conclusion from recall based on DDFM study. Schroeder/Lindhe: Change in progression associated with acute inflammation/exudate rather than change in proportion of lymphoid cells i.e. T cell to B cell. TRANSSEPTAL FIBERS: Goldman (JDR,57): Transeptal fibers is a defense mechanism against inflammation and provides stabilization Weinman Inflammation follows the course of blood vessels. Gaps in the transseptal fibers allow passage of inflammation RAPID ATTACHMENT LOSS MAY BE DUE TO CEMENTAL TEARS
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IMMUNOLOGY HEMOPOIETIC STEM CELLS: T-Cells (Lymphoid Progenitor) Differentiate into subpopulations of sensitized T-Lymphocytes, derived of precursor cells processed in the thymus T-Killer cells react with cell surfaces of target cells and kill them. T-D (Delayed hypersensitivity) cells release mediators (lymphokines) which attract macrophages B-Cells (Lymphoid Progenitor) Derived from the same precursor cells but processed in a "bursal equivalent". They differentiate into plasma cells that produce IMMUNOGLOBULINS: IgG: 80%(150K), IgM 13%(900K), IgA 6%(300K), IgD 1%(185K), IgE .02%(280K) Immune Complexes: Glomerulonephritis (Ab to basement membranes), Goodpasture's disease, rheumatoid diseases Arthus Reaction: Injection of antigens with circulating IgG Ab leads to an acute inflammatory reaction peak 6 hrs, causing perivascular necrosis. Reinhardt (JP 88 13-22) Active lesions associated with B cells. Stable lesions T-cells POLYMORPHONUCLEAR LYMPHOCYTES: PMN’s (Myeloid Progenitor) Primary line of defense against infection (91% of cells in GCF), Major protective cell against periodontopathic organisms, Neutrophil deficiencies predispose to rapid, severe destruction of periodontium. 1° Azurophilic granules: myeloperoxidase, lysozyme, neutral proteases, hydrolytic enzymes, H2O 2 required, elastase 2° Specific granules: lysozyme, attacks bacterial cell walls collagenase, lactoferrin deprives Fe, Chelator unique enzyme to PMN’s Lysosomal enzymes = collagenase, hyaluronidase, acid phosphatase 6-8 hrs is the ½ life of a PMN. Goes from stem cell to PMN in 14 days. Kills by oxidative/non-oxidative methods Respiratory burst, phagocytosis, secretion, cytolysis Chediak-Higashi syndrome deficiency in Neutral Serine Proteases Chronic Granulomatous Disease, no respiratory burst Chemotactic defects in LJP, EOP, RPP, diabetics PMN Chemotactic: FMLP: n-forml-Methionyl-Leucine-Phenylalanine: A powerful synthetic chemoattractant for PMNs Boyden Chamber Under Agarose Method Chemotactic Receptors: GP120-90, LFA-1, a-x, CDW-2 are abnormal in PPP (Page:87) Van Dyke: LAD Leukocyte adhesion deficiency: 40% of the population exhibit this to some degree. Kalkwarf (84): PMN defects migration and chemotaxis: LAD (lazy leukocyte syndrome, JOBs syndrome Diabetes, Downs Syndrome, Chediak Higashi Syndrome. Neutrophil considered the first line of defense, an inverse relationship can be demonstrated between severity of periodontal destruction and degree of neutrophil function. Oshrain et al (JCP 86 13-17): Refractory cases appear to have different pattern of leukocyte response with two peaks, total cell counts also less. Phagocytosis: Measured by seeing how many Latex spheres can be ingested COMPLEMENT CASCADE Board Questions C5a profoundly stimulates mast cells, is chemoattractant for neutrophils C5,7,8 members of membrane attack complex Classic and Alternate pathways converge on C3 to activate lytic pathway Complement activates macrophages and lyses cells, increases vascular permeability, involved in mast cell degranulation
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Direct Pathway C1: First component of complement, binds to antibodies that have reacted with antigen C1 acts as an enzyme which cleaves C4 and C2 into C4a, C4b, C2a, C2b. C4b and C2a form C3 convertase which cleaves C3 into C3a and C3b. C3b is responsible for opsonization, forming a complex with C4a and C2b which cleaves C5 into C5a and C5b. C5b reacts with the remaining complement components (C6-C9) to form the attack unit producing a transmembrane channel causing cell lysis. C3a and C5a can act on mast cells to degranulate, and as a chemoattractant for PMNs. Alternate Pathway Endotoxins activate a protein (properidin) system which behaves as C1, C2, and C4 to activate C3 and set off the interactions of the remaining complement components. Plaque can locally stimulate complement production. HYPERSENSITIVITY REACTIONS Type 1: Anaphylaxis: IgE mediated, mast cells (releases heparin, SRS-A bradykinin, prostaglandins and eosinophil chemotactic factors), PCN allergy, bee sting, asthma, allergy to dust, mites hayfever Type 2: Cytotoxic: Tissue bound Ag/Ab complexes IgG, IgM, autoimmune hemolytic anemias, blood transfusion Type 3: Immune complex: IgG,M,A SLE, rheumatoid arthritis, glomerulonephritis (BOARD QUESTION) Type 4: Cell mediated: T-lymphocytes: lymphokine production, TB , sarcoidosis, poison ivy AUTOIMMUNITY Affar (93): Possible autoimmune component to periodontal disease (unequivalent sites affected, weak study) Anusaksatheim (92): Autoimmunity possible due to levels of IgG localized to gingiva. IMMUNE RESPONSE AND PERIODONTAL DISEASE Wilton (91): Pitfalls in immunology trials: Definition of disease, antibiotic use, organisms not causing disease, orgs not removed by treatment, cross reactive antigens, fluctuation of antibody levels. Seymour et al (JCP 79 13-5): Stable site is a T-cell lesion, Progressive site is a B-cell lesion. Thus progression occurs when a lesion shifts to a B-cell. ANTIBODIES: Board QuestionsMolecular weight of IgM is 12 times that of IgG IgG1 (subclass of IgG) has the highest concentration in blood IgG4 doesn’t fix complement Ebersole (JPR 82 13-10): AP, Active AP, LJP pts: 90% of LJP patients had high Ab levels to Aa. 3748% of Advanced Destructive Periodontitis and AP pts had normal responses to all organisms except Bg. 85% of normal had no elevated response to pathogens. Increased Ab and increased organism levels = 84% chance of disease activity Gunsolley et al (87): Failure to mount a substantial Ab response to organisms leads to greater and more widespread periodontal destruction. Gunsolley (JP, 90 13-24): Attempted to classify disease status by serum Ab and compare to clinical disease in periodontitis subjects. No periodontitis group was 100% correct, support heterogenicity, (Severe periodontitis 60%, LJP 78%). McArthur and Clark (JP, 93): Antibodies protect by inhibition of microbial attachment, aggregation, opsonization, and fixation and activation of the complement system. Thus preventing colonization, lysis, and actually killing of microbes and neutralizing of toxic products EFFECT OF THERAPY ON ANTIBODY RESPONSE Vincent (JCP 87 13-18): Successful therapy resulted in significant decrease in levels of Ab reactive with B.g and A.a. Wilton et al (91): Reasons given for failure of antibody levels to fall after treatment: 1) organism chosen for study are not causing the disease 2) organism are not eliminated by treatment and persistence of continuing disease/ colonization
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3) numbers of organisms remain at a level sufficient to maintain antigenic stimulation but not cause disease 4) cross-reactive antigens which maintain antigenic stimulation but not cause disease 5) post-treatment sampling may be too early 6) organisms may be present at other sites of the mouth 7) Ab levels fluctuate during treatment and no treatment Endotoxin Reitschel (SciAm 92 12-4) Endotoxin heat stable, located on the surface of gram negative bacteria. Endotoxin stimulates host cells (usually macrophages) to release inflammatory mediators Endotoxin is composed of Lipid A which is embedded in the membrane and responsible for most of the harm done by endotoxin Functional part of endotoxin (BOARD QUESTION) Polysaccharide Inner core Outer core O-specific chain: most variable and provokes an immune response Mast Cells numerous in health, rare in disease (already used up) contains Histamine, SRS-A, eosinophil chemotactic factor, heparin, bradykinin Prostaglandins inflammatory mediator associated with bone resorption Marks and Miller (JPR 94 12-9) local delivery of PGE1 results in bone formation surprising result Miyagi Prostaglandin production by monocytes decreased by testosterone increased by progesterone increased and decreased by estrogen GROWTH FACTORS Primary action is to differentiate mesenchymal precursor cells into cartilage and bone forming cells. Wozney (90): BMP clones BMPs: Glycoproteins, acid resistant BMP1: Unrelated to other growth factors BMP2: Most potent BMP2-7: Members of the TGF-ß family of molecules, located on chromosome 20 BMP3: Osteogenin BMP6: Membrane protein Vgr-1 BMP7: OP1 Effective in nanogram concentrations. Sigurdsson (JP 95, 34-30): Placement of rh-BMP-2 can regenerate original alveolar bone height and additional apparatus Sato and Urist (84): Minimal effective dose of BMP is approx. 2 ug.40mg (wet weight): optimal dose 10 g. Bowers (JP,91): Combination of DFDBA and Osteogenin enhanced regeneration (new attachment) 1.92 mm compared to DFDBA alone 1.31mm in submerged and 2.33 mm compared to 1.72 mm in nonsubmerged respectively. Boyne (IJPRD 97 11-25) rhBMP-2 with collagen sponge used successfully for sinus floor augmentation. Gained 8 mm of bone. Cochran, Nummikoski, Jones, Makins Turek Buser (IJOMI 97): rhBMP-2 can sig stimulate bone formation in critical-sized defects around dental implants. rhBMP-2/mem (4.1 mm) > rhBMP-2/ mem (3.7 mm) > rhBMP-2/mem (2.4 mm) > rhBMP-2/ mem (2.2 mm).
TGF-ß Transforming Growth Factor-ß A polypeptide hormone, found in bone and platelets, activated by low pH (wound healing/resorption), inhibits growth of epithelial cells and stimulates mesenchymal cells, increases the production of Type 1 collagen.
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Wahl (93): A cytokine in acute and chronic inflammatory sites, chemoattractant for blood neutrophils, monocytes, lymphocytes. Stimulates secretion of cytokines induced by bacterial products. Combines with other cytokines to stimulate osteoclasts to resorb bone. FIBRONECTIN Glycoprotein, widely distributed, important cell binding properties, stimulates wound repair and scar formation, influences the movement of fibroblasts into the developing clot, in general stimulates mesenchymal cells, and inhibits epithelial cells. LAMININ Glycoprotein, influences the adhesion, growth, migration of cells, most important is adhesion of epithelial cells to basement membranes, a potent chemoattractant for epithelial cells. INSULIN-LIKE GROWTH FACTORS Somatomedin C, IGF-I+II serum proteins produced in liver, fibroblasts upon stimulation by growth hormone, IGF stimulates cartilage, bone formation, increases alkaline phosphatase activity. Lynch (JP,91) PLATELET DERIVED GROWTH FACTORS Has potent effects on osteoblast migration and mitogenesis. (BOARD QUESTION) PDGF-AA made by bone cells. Polypeptide growth factors, synthesized by osteoblasts, macrophages, platelets, stimulates bone DNA and protein synthesis, bone resorption, released at wounds to stimulate cell division, nanogram amounts will stimulate mesenchymal cell proliferation. Lynch 91 Giannoble (JP 94 6-37) Compared responses to PDGF/IGF-1 in monkeys and dogs. Lynch et al (JP,91):Dog study. PDGF and IDGF-1 had more regeneration, 2-fold above controls, no barriers, than controls. Dill (93): Possible link to phenytoin overgrowth. Rutherford et al (JPR 92, 34-25): Monkeys, ligature created lesions (P.g) treated with PDGF/IGF-1 revealed new cementum with attached fibers coronal to cemental notch with new bone formation even a horizontal area of resorption. 1st demonstration that recombinant human growth factors induce regeneration in primates. Oates, Rouse, Cochran (JP 93): in vitro, PDGF-AA and PDGF-BB are major mitogens for human PDL cells, TGF-B1 is a weak mitogen but modulates the response of the two isoforms of PDGF. IL-1B is not mitogenic and is inhibitory to PDL cell mitogenesis in hinge concentration. TNFa/b: TUMOR NECROSIS FACTOR a & b Cytokines which can directly stimulate osteoclast formation from precursors. Can also bind to osteoblasts and stimulate mature osteoclast formation. Stashenko (JP 91 12-2) IL-1 important mediator in pathology of periodontal disease. TNF next, IL-1 less important lowest tissue concentration Rutherford (92): Monkeys, OFD + human PDGF+IDGF got more regeneration (new cementum and functionally oriented PDL) vs. placebo or debridement only. METALLOPROTEINASES Proteolytic enzymes (collagenase), possible role in bone resorption via cytokine activation. CYTOKINES Biologic Activity Activation of Bone Resorption Inhibition of Bone Resorption Inhibition of Bone Formation Mitogenic Activation of Fibroblasts Fibroblast Proliferation Neutrophil Stimulation T-Cell Proliferation
IL-1a/ß
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B-Cell Proliferation IC-1ß: ¯ alkaline phosphatase levels, stimulates PDL cell formation into fibroblasts rather than differentiation to osteogenic progenitor cell lines. CALCULUS COMPOSITION: Organic: 15-20% with Protein 50-60%, Carbohydrates 12-20%, Lipids 10-15% Inorganic: Calcium 20-29% (higher in subG), Phosphorus 16-18% Crystalline forms: Brushite, Octacalcium Phosphate, Magnesium Whitlockite, Hydroxyapatite FORMATION: Oshrain, Salkind, Mandel (JP 71): SupraG calcification begins before subG calcification. SubG cuticle derived from GCF, while supraG appears to be salivary in origin. No relationship b/t age of plaque and onset of calcification or onset and degree of calcification. Mineralization appeared to proceed by coalescence of foci. Friskopp, Hammarstrom (JP 80, 9-5): Calcification begins between the microorganisms. SupraG calculus: covered by filamentous organisms arranged perpendicular to surface. SubG calculus: bandlike clusters covered by cocci, rods and filaments, no distinct orientation. Both had heterogeneous core, covered by soft, loose layer of microorganisms. Sidaway (80): G+ rods have intracellular calcification, but G- rods produce extracellular calcification, which may be significant in early plaque calcification. -Calculus formation is always preceded by plaque formation, forms the organic matrix -Calcification can begin within 4-8 hours (Tibbits70). -50% mineralized by 2 days -Up to 90% mineralized by 12 days, rate variable Turesky (JP 92 15-7) Calculus formation reduced if pt is taking blockers, diuretics anticholinergics, synthroid and allopurinol despite large amounts of plaque. THEORIES of MINERALIZATION: 1. Booster mechanism: In plaque there is Ca+PO4- ionic forms which cannot alone ppt crystalline forms, but environmental conditions alter i.e. pH drop, loss of CO 2, NH4+, pH increase. allows crystals to form. Lindhe 2. Epitaxic: Nucleation points are critical, not Ca+, PO4-, nucleators include: collagen, tissue breakdown components in GCF. This is what occurs with Peridex. 3. Inhibition Theory: Pyrophosphates can stop it, but something deactivates them and calcification begins 4. Transformation Immature crystalline forms (brushite) change to larger more mature forms (Hydroxyapatite) SUPRAG AND SUBG CALCULUS (Friskopp, JP 83) SupraG SubG Coronal to gingival margin Apical to gingival margin White, Yellow , darkens with age Brown, Black Softer and more easily removed Hard and tenacious Site preference distribution Generalized distribution Minerals primarily from saliva Minerals primarily from GCF, Varied morphology, highly mineralized associated with disease Heterogeneous Homogenous Horizontal sm. & large crystals Vertical sm. crystals only Filamentous organisms Rods, Filaments CALCULUS ATTACHMENT Zander (JP 53): LM 1) Secondary cuticle interface.
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2) Locking in cementum irregularities (surface irregularities) where Sharpey's fibers attached. 3) Locking into resorptive cementum bays/mechanical undercuts (resorptive defects). 4) Direct penetration of bacteria into cementum. Moskow (JP 69, 9-2): Cemental tears in region of CEJ. Often site of plaque and calculus attachment. Canis (JP 79, 9-4): SEM, rejects bacterial penetration, (BOARD QUESTION) saw cuticular attachment, mechanical locking, direct attachment of calculus matrix to root. Selvig (JPR 70): Direct contact of calcified matrix to tooth structure. Richardson, Chadroff, Bowers (JP 90, 9-8): Part of HENA study. Apical extent of calculus is found 1/2 the total depth of defect. The mean distance between the base of the calculus and base of the defect was found to increase with the depth of the defect. Pyrophosphate: Believed to inhibit calcification by preventing the initial calcification nucleus from growing, possibly by “poisoning” growth centers of the crystals. Zacherl (JADA 87): Dentifrice containing 0.24% NaF, 3.3% pyrophosphate showed 37% reduction in supraG calculus in 6 months. Lobene (J Prev D 86): Dentifrice containing 0.24% NaF, 3.3% pyrophosphate showed 44% reduction in supraG calculus in 3 months. Rosling & Linkhe (Comp 87): Crest 3.3% soluble pyrophosphate (tetrasodium & disodium PP) & 0.23% NaF Colgate pyrophosphate (tetrasodium and tetrapotasium PP). After 3 months of BID brushing, sig diff in calculus formation after 6 months, calculus in Crest & Colgate reduce 9% & 42.2% compared to placebo. TISSUE RESPONSE TO CALCULUS Pathogenic Potential: Tissue proximity, Impediment of oral hygiene, niche for bacteria (porosity) Hatfield Cells died if soaked with diseased roots Allen & Kerr (JP 65, 9-1): Sterile and non-sterile calculus placed in peritoneum of guinea pigs. SC caused mild irritation, (foreign body reaction) NSC caused severe infection/ abscesses. Fujikawa (JP 88, 9-7): Dog. Retained calculus after surgery, resulted in increased inflammation, remove calculus during surgery!!! Healing took 120 days in non-scaled areas and 30 days in instrumented areas. At all evaluation periods and in both instrumented and non-instrumented sites, inflammation was more intense when calculus was present. Listgarten & Ellegaard (JPR 73, 1-33): Monkeys, EM found cellular attachment between JE and dental calculus, conc. CHX Nyman (30-22?) split mouth. When plaque removed rather than cementum- same result. Anerud and Loe (91): Norwegian vs. Sri Lankan (dental care vs. no dental care). Norwegians with good oral hygiene had supraG calculus with no influence on attachment loss. Sri Lankans: teeth with calculus showed higher rate of AL. Ainamo (70): Correlated calculus with gingivitis. Patters (82): Looked at bone resorbing activity of calculus. Tx with citric acid removed these bacterial antigens. Cercek (83): Compared removal of subG plaque or subG plaque + calculus. Only subG removal of both resulted in clinical improvement. METHODS OF CALCULUS DETECTION: Sherman et al. (JP,90): Two clinicians determined the presence of calculus they were correct 75% of the time. If they thought no calculus was present they were incorrect 50% of the time. Buchanan (87): Radiographic calculus 43.8% sensitivity, 92.5% specificity, able to detect calculus 1/2 the time. Brown, Hancock, O’Leary, Miller, Sheldrake (JP 91, 9-9): Culture and DDFM. Non-calculus group had sig greater % of coccoid and fewer rods or spirochetes. The calculus group had higher levels of BPB and the noncalculus had higher levels of Aa. COMPLETE CEMENTUM/CALCULUS REMOVAL NECESSARY?
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YES:
Hatfield & Baumhammers (AOB 71 5-8): Initially described, endotoxin may have a deleterious effect on periodontium, irreversible morphological changes of epithelial cells when exposed to diseased roots. Aleo (JP 74 5-9): In vitro, removed cementum (endotoxin), 0.30 um/ml extract depresses cell proliferation Aleo (JP 75 5-10): Fibroblast cell attachment to healthy, cementum removed, phenol extract, but no attachment to untreated. Daly (JCP 82 5-17): LPS and bacteria found to penetrate cementum. (3-7 microns) Nishimine & O'Leary (JP,79): levels can be reduced to non-diseased level with S/RP Lopez (JP 80 5-13): Implanted root fragments. Scaled had more inflammation than, scaled & autoclaved, S/RP & autoclaved fragments, but inflammation seen in all. Concluded thermostable and cementum must be removed. Fine et al. (JP,92): associated gram- bacteria in periodontal pockets finding a high correlation between endotoxin level and % of age of gram neg. bacteria. Jones and O'Leary (JP 78, 30-1): Human, in vitro. Compared SC with S/RP which reduced the endotoxin (limulus lysate test). Concluded RP able to render Ds’d root surfaces approx as free of detectable endotoxin as healthy root surfaces of uninvolved teeth. RP teeth only had 1 ng endotoxin more than healthy root surfaces. Residual Calculus: Rabbani (JP 81, 30-27): High correlation between residual PD and remaining calculus. NSD b/t anterior and posterior teeth. The deeper the area (>5 mm) the more difficult b/c more irregular & less access and more area. Waerhaug (78): Suggested reformation of subG calculus and reestablishment of pockets in areas where calculus missed, longitudinal LM human study.
NO:
Sherman: Improvement in clinical parameters despite residual calculus Nyman et al (JCP 88, 3021): split mouth study, 2 quads S/RP, burs to remove cementum, 2 quads scaled, polished removed calculus w/o removing cementum, Clinical improvement the same, No need to remove cementum. Nakib (JP 82 5-16): Endotoxin weakly adherent, almost completely removed after 1 min brushing. Moore (JCP,86): Endotoxin can be removed with gentle washing (39%) and a toothbrush (60%) (only 1% remained). Listgarten & Ellegard (72): Epithelial attachment to calculus Soderholm: Risks of excessive cementum removal. Pulpal damage, sensitivity. Middleton and Bowers (90): Cellular cementum can form over dentin and old cementum. Hughes et al (JPR 88 5-21): LPS on SEM. LPS seen primarily on retained calculus and bacteria, only on surface area . Maidwell-Smith et al (JCP 87 5-20): Only a weak correlation exists between amount of LPS on a particular tooth and attachment loss and no correlation could be found between pocket depth and amount of LPS. Corbet et al. (JCP,93): Root debridement is best assessed on the basis of the healing response and that it should aim to disrupt plaque on and remove plaque from the periodontally-involved root surface rather than to remove part of the root surface itself. Fukazawa and Nishimura (JP,94): 10 periodontally involved roots, 5 were lightly root planed to removal superficial cementum, the other 5 served as controls, Human Gingival fibroblasts were cultured and evaluated by TEM after 4 months. In the non-treated roots, HGF failed to attach. HGF did attach to the instrumented teeth with normal morphology of health fibroblasts. Somerman et al (JPR,91): Attachment proteins in cementum- bone sialoprotein II
Maybe: Adriens, Loesche (JP 88 5-22,23): Presence of bacteria in dentinal tubules, reservoir of Recolonization, excessive S/RP alone may not be enough. Bacteria invaded the dentinal tubules up to 300 um. May need chemical debridement supplement. BL: World Workshop says excessive removal of cementum to remove endotoxin is unnecessary. RISK FACTORS OF PERIODONTAL DISEASE SMOKING
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Epidemiology: 40% of Americans in 1964 were smokers compared to List>Cntrl, Gingivitis effect: CHX = List>Cntrl Zambon, Ciancio, (JP,89): 28.9% more effective at reducing plaque than saline Axelsson, Lindhe (JCP,87): CHX better at reducing plaque, but Listerine better at reducing gingivitis Fine (JCP 85, 29-22): rinsing with Listerine as an adjunct to normal OH procedures produces an overall reduction in plaque toxicity and reduction in total plaque mass. 121
Gordon (JCP 87, 29-23): Listerine group had less plaque accumulation and decreased development of gingivitis as compared to placebo after professional prophy after 9 months. Ciancio (JP 89): Home supraG irrigation with Listerine for 6 months, sig. reduced plaque, total bacterial cell counts and gingivitis compared to the vehicle control. No sig. diff. In PD and ALOSS. Fine (JP 92, 29-33): Culture, Listerine prerinse before ultrasonic scaling showed 94% reduction n CFU’s in aerosols, 34% using vehicle. VIADENT Sanguinarine: alkaloid extract from the blood root plant Sanguinaria Canadensis , mechanism of action unknown. Alters cell wall surface so aggregation and attachment reduced. Koczyk et al. (JP,91): significant reduction of plaque, gingivitis, BOP vs. Placebo. Southard et al (JCP,87): Same as above. Mauriello (JP 88, 29-24): No sig benefit on gingivitis or plaque using dentifrice with sanguinaria or placebo. TRICLOSAN: antiinflammatory by reducing pge, no good studies. Renvert (JCP 95, 29-30) Broad spectrum nonionic antimicrobial (BOARD QUESTION), A dentifrice containing triclosan and copolymer is effective in reducing supraG plaque formation and gingival bleeding w/o causing major shifts in the salivary microflora. Modeer, et al (JCP 96, 29-36) Triclosan inhibits inflammatory mediators (IL-1, TNF) in vitro. Binney (JCP 96 10-20) Triclosan toothpaste no better that regular toothpaste. Study sponsored by competing toothpaste company. MERIDOL: Amine (125 ppm) + stannous (125 ppm) fluoride mouthrinse. Zimmerman (93): Benefits of Meridol: Decreased PlI, Decreased GI over controls. Brecx et al. (JCP,90): Meridol as effective as Listerine, but not CHX. HYDROGEN PEROXIDE H2O2: Mechanism: H2O2 releases oxygen in the presence of catalase and peroxidase. The released oxygen has some bacterial effect. Disinfectant, antiinflammatory, delay wound healing, causes tissue injury, lower BOP, bacteria same. Side Effects: Boyd (89): Showed 1.5% H2O2 to be effective in Ortho cases. Ramp (87): Chick tibias, single application of H2O2 led to decreased collagen synthesis, bone and glucose metabolism. Rees and Orth (JP,86): Oral ulcerations. PLAX
O’Mullane (JP 94, 29-31): Prebrushing rinse plaque (PBR) scores showed the biggest difference between baseline and 12 months, but was not sig different than rinsing with water. Did detect sig diff b/t PBR vs. no rinse, although not clinically sig. Binney (93): Pre-rinsing with PLAX or toothpaste slurry was no more effective in reducing pre-brushing plaque index than H2O alone. Chung (92): Confirms above. Mills (JCP 94): No difference in Plax vs. placebo clinically and in vitro in reduction of stain out to 2 weeks
DELMOPINOL Moran (92): Decreased plaque accumulation via prevention of colonization, plaque adherence. Not more effective than CHX, but has minimal side effects. Collaert (93): Topical application of 0.5% decreased plaque accumulation and delayed plaque migration and morphological complexity. FLUORIDE: Stannous fluoride appears to be a more effective antiplaque agent than sodium fluoride. Alters bacterial aggregation and metabolism, antibacterial b/c of Tn ion. Some studies indicate more of an effect on plaque than of gingivitis. Tinanoff (80)
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Perry (J West Soc Perio): Review. Fl may inhibit bacterial adsorption to pellicle-covered teeth by competing for Ca2+ ions. Comparisons b/t SnF2 and NaF have generally shown the Sn compounds to have superior antimicrobial properties. Conc in tooth pastes generally 0.1-0.2% which is effective for caries reduction but less than required to have sig antimicrobial effect (0.3-0.4%). Boyd (JCP 85, 29-4): 28 pts, double blind with cross-over. irrigation with SnF 2 in Water Pik resulted in sig improvement in clinical parameters (except ALOSS) than water irrigation group, which was reversed after the cross-over. Tinanoff (JCP 89, 29-9): SnF2 rinse decreases quantity of supraG plaque and # of CFU’s compared to placebo. Grembowski et al (JPR,93): Long term exposure to fluoridated water would appear to reduce the risk of attachment loss form 0.87 to 0.72. Hastreiter claims fluorides have no effect. ORAL IRRIGATION: Purpose: Non-specifically reduce the bacteria and their by-products that lead to the initiation or progression of periodontal disease. Hardy (JCP 82): When irrigation tip placed 3 mm sug-G got 100% penetration in shallow and deep pockets. Brownstein (JCP 90): the effect of irrigation on gingival bleeding and plaque: 1) Change in plaque composition. 2) Flushing out of the inflammation inducing factors. 3) Physical change in tissue integrity. Larner and Greenstein (IJPRD 93): Deep pockets (7-10) with calculus had less dye penetration. This was not true in 4-6 mm pockets. YES:
Lander (JCP 86): Single subG irrigation with 0.2% CHX, decreased spirochetes, fusiforms, decreased BOP Walsh (JCP 95): 0.2% CHX reduced vital micro-organisms in plaque more than CHX rinse or saline irrigation or rinse. Flemmig (JCP 95): 60 pts. 0.3% ASA in addition to regular hygiene is a beneficial adjunct in supportive care in pts with mod-severe AP. Mean PDR 0.26mm. GI decreased from 0.35 to 0.1
NO:
Silverstein (JP 88, 28-13) TCN irrigation S/RP = TCN irrigation Hugosen (78): No advantage of oral irrigation over brushing alone. Haskel (JP 86, 29-4): SubG irrigation with CHX daily for 4 weeks resulted in transient microbial and limited clinical effects. Jolkovsky (JP 90, 29-6): Professional and home irrigation with CHX helps decrease GI and PlI, but no difference b/w irrigation with CHX and H2O. Caton et al (JCP,93): Only mechanical interdental plaque removal combined with toothbrushing is effective in reducing or preventing interdental inflammation.
NSAIDS Williams, Jeffcoat (JCP 88, 3-23): Ibuprofen can inhibit alveolar bone resorption in beagle dogs above therapeutic dosages. Interferes with host inflammatory response Williams, Jeffcoat, et al (JP 89, 29-28): Rate of radiographic bone loss was sig. less in patients taking 50 mg flurbiprofen bid compared to placebo at 12 & 18 months but showed no difference at 24 months. Hawthorne Effect - patients cleaned more during 1st year b/c they thought they were getting something good. Heasman, Seymour (JCP 89, 29-29): Systemic flurbiprofen can reduce signs of exp gingivitis over a 6day period, either when used alone or as an adjunct to toothbrushing. ANTIBIOTICS Bactericidal: Penicillin, cephalosporin, metronidazole, aminoglycosides, bacitracin, vancomycin, polymixin B Bacteriostatic: Erythromycin, tetracycline, clindamycin, chloramphenicol, sulfonamides WHEN DO WE USE ANTIBIOTICS? Febrile
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LJP EOP RPP Refractory (after culturing) Post surgically
Why use Antibiotics? Nyserad: Aa invasion of epithelium and CT, S/RP unable to eradicate Aa in LJP. Mandell (JP 88 10-19): 8 LJP pts, doxycycline + surgery, effective in controlling disease and eliminating Aa. Actisite alone ineffective in eliminating Aa. Novak (JP 88 10-18): Tetracycline only (no surgery or S/RP) in early LJP was effective, 250 mg 4x day for 3-6 weeks Van Oosten ( 28-30) Case report of use of antibiotics for non-perio reasons resulted in spontaneous increase in attachment Sanders: More bone fill with bone blend and TCN Liljenberg and Lindhe: Post LJP/LJP pts tx with TCN+ pocket elimination was successful Kornman and Robinson (85): Stepwise approach to antibiotics in Aa+ pts, if BPBs present then MWF+TCN surgery also Gordon: 250 mg TCN qid, GCF = 4-8 µg/ml, serum 2.5 µg/ml (BOARD QUESTION) Socransky & (JP,93): 17 pts, tx MWF at deep sites, scaling shallow sites, used Augmentin (3), Ibuprofen (3), tetracycline (9), and placebo (2). Deeper sites and sites treated with antibiotics showed greater reduction in probing depth than shallow sites and non-antibiotic site Tetracycline was the most effective. TETRACYCLINES: Perio Bacteria Susceptibility: Aa, Pg, Bacteroides, Capno, Eikenella, F. Nuc. Inhibits collagenase, broad spectrum, inhibits protein synthesis Rare reaction to TCN therapy Pseudotumor Cerebri Can potentiate action of anticoagulants (BOARD QUESTION) Anticollagenolytic Effect Of TetracyclineS: Nip ( ) TCN and analogs inhibit collagenase. Golub (84): Mechanism: Depletes Ca++ which is required for collagenase activity. Doxycycline Substantivity Of Tetracycline On Diseased Cementum And Demirel (90): High substantivity of TCN on both cementum and dentin, up to 14 days. Baker: TCN binds to roots in vitro, inhibits bacterial growth. DOXYCYCLINE: Broad spectrum bacteriostatic, effective against G+ and G- anaerobic bacteria, liver metabolism, least affected by dairy products, reacts with (Vit K dep.)anticoagulants, oral contraceptives, photosensitivity (Gabler and Creamer 91) Perio Studies: TCN Walker (28-4) TCN in GCF after oral dosing is 4-8g/ml Slots (79): 12 refractory patients, 2 wks TCN, dramatic clinical/ micro improvements Slots and Rosling (83): 3 wks of S/RP does not reduce subG levels of Aa in LJP lesions. 3 weeks of TCN necessary to eliminate Aa, 6 LJP pts Lindhe (83): TCN long term, 50 wks, decreased spirochetes and motile rods. Kornman and Karl (JP 82, 28-5): 10 refractory pts, long term TCN on/TCN off treatment (2-7yrs), 76% of flora TCN resistant. Listgarten (78): TCN S/RP not more effective than S/RP alone Minocycline: Stains adult teeth, vertigo, not affected by food Ciancio (80): Double blind study, minocin without S/RP better than placebo with S/RP Westbury (JP 97 84-91) Minocycline induced pigmentation. Differential DX melanoma, Kaposi’s Sarcoma, Amalgam tattoo, heavy metal poisoning, racial pigmentation, Addison’s, Hemochromatosis, Peutz-Jeghers Doxycycline: (Vibramycin) increased PO absorption, increased 1/2 life Gajanan (91): Double blind, placebo controlled, Dox trial, 100mg/day for 3 weeks in disease active recurrent disease pts. Improvement in AL for treated sites, decreases in Aa, Pg, Pi, Ec, Fn, spirochetes. Kulkarni (91): Double blind study, increased PALevel and 40% decrease in path flora with doxy
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Pascale (86): DOX 3-10 µg/ml in sulcus, 2.1-2.9 µg/ml serum Mandel (86): Doxy effective in LJP pts with surgery Treatment of Refractory Periodontitis: Walker and Gordan (93 JP): 30 subjects, 3 month post-treatment Clindamycin treated group (150 mg qid 10 days) gain of attachment 2.1mm, Augmentin (250 mg tid 14 days) group 1.4mm gain in attachment. Clindamycin group stable for 21 months Augmentin 15 months Collins, Offenbacher, Arnold (JP 93): 30 pts, treated with augmentin for 2 weeks, 6 povidone Iodine rinses during this time also with CHX rinses. Results: At 34 months , > 1 mm attachment gain in 41.2% of the sites. Assume Pg and other bacteroides responsible for RP. Gordon, Socransky (90): Scaling and clindamycin decrease active sites for 8% to 0.5%. Magnusson: Augmentin with non-surgical- Stabilized 12 months, PD decrease approx. 2.5mm, 1-2 mm attachment gain. Implant Placement Dent, Olson, Farish, Bellome et al (JOMS 97): Higher implant failure rate in patients who did not receive preoperative antibiotics. Failure rates 4.0% Abs, 1.5% No Abs). Used PCN 75%. LOCAL DELIVERY SYSTEMS/FIBERS METRONIDAZOLE: Giodano (92): 20% MET in ethylcellulose fibers, 2x14 days, decreased surgical need in 1.2-2.4 teeth/pt. TETRACYCLINE: Multi-Center Study (JP 95): Quadrants treated with S/RP alone, TCN alone, S/RP + TCN, and S/RP + 2 TCN fibers. Fibers did tend to decrease F.n., P.g., P.i., and C.r. No significant clinical differences were seen though. Rapley & Killoy (JP 92 28-17): TCN GCF levels can reach concentrations of 1300µg/ml, at the same time serum level not over 0.1µg/ml thus only possible side effect is allergy, probably does not effect birth control pills, staining of teeth. Goodson (91): 107 pts, 25% TCN in ethyl vinyl acetate copolymer monolithic fibers, S/RP +fibers vs. Fibers alone, placed 10 days, TCN conc. in GCF was 650 µg/ml, better with S/RP +fibers at 3 mos, no difference between S/RP + fibers at 12 mos. Morrison: SEM with fiber therapy, TCN penetrated 10 µm into root Ciancio, Cobb (JP 92): TCN fibers with MWF surgery, 3 months post-op favored TCN quadrants in pocket reduction & 6 months in attachment gain but #'s not significant 0.47 mm gain PD and .09 mm Attachment. Kerry (JADA, 94): TCN fibers conc. in GCF 1,590 um/ml for 10 day period, mean pocket depth reduction 3.0 mm in deep sites and 1.5 mm in moderate sites. multicoated teeth same improvement as single rooted teeth. Wilson, McGuire Greenstein, Nunn (JP 97): Questions long-term effectiveness of S/RP+TCN fiber in treating periodontal disease. More recession and less AGAIN (1.23 mm/0.66 mm)S/RP +TCN fiber (than S/RP alone (0.58 mm/1.09 mm). MINOCYCLINE: Jones (92): 51 AP pts, 2% mincing ointment with syringe+S/RP vs. S/RP vs. NT, MINO + S/RP better than S/RP, NT. Also: Van Steenberghe (93): Decreased Pg, Pi, Aa 2-12 weeks POT, decreased PD 3.1 vs. 2.1 control. PENICILLINS: Yamagami (JP 91, 29-32): Ofloxacillin in PT-01 fiber, water soluble, vs. control, better clinical improvements BOP and PD with strips. What is the difference between Augmentin, amoxicillin, and ampicillin? Augmentin: Amoxicillin + clauvulanate potassium Ampicillin: Extended spectrum penicillin Amoxicillin: Synthetic analog of Ampicillin. PENICILLINS: Perio Bacteria Susceptibility: Pg, Pi, Bacteroides, Capno, F. Nuc. B-lactamase sensitive, G+/- cocci, spirochetes, anaerobes
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B-lactamase (penicillinase) resistant: Nafcillin, oxacillin, methcillin, dicloxacillin, cloxacillin Extended spectrum: Ampicillin (rash common), Amoxicillin, carbencillin, not penicillinase resistant PENICILLIN ALLERGY Only specifically determined for benzylpenicillin. This does not bind strongly enough to proteins for an allergic reaction, but a major degradation product, benzylpenicilloyl (BPO), causes responses. BPO is the major antigenic determinant. IgE response to BPO causes urticaria. IgE to minor determinants causes urticaria and anaphylaxis. IgG against BPO may have a protective role. No IgG has been demonstrated against minor determinants. PENICILLIN ALLERGY SKIN TEST A BPO-polylysine conjugate is used for skin tests for the major determinant. Diluted penicillin G is used to test for minor determinant allergy. Detects only IgE mediated allergy. A negative skin test does not exclude allergy. The test itself might induce allergy. Other penicillins cross-react with pen G. CLINICAL USE OF PENICILLINS Magnusson (89): 21 RPP pts, Augmentin 250 mg tid for 14 days, active sites decreased from 14% to 7%. METRONIDAZOLE Flagyl, G(-) Anaerobes (Pg, Pi, Bacteroides, Fn), ETOH interaction, metallic taste. doesn't affect A.a (facultative). Possible mutagen. Loeshe (92): Sig. reduction in PD, PAL need for surgery with Flagyl, best used after S/RP. (92): Decreased need for surgery, decreased spirochetes with metronidazole and S/RP. Shin: Effective in ANUG. Lundstrom (84): Effective in refractory cases. Winkler (89): Effective in HIV-P,G. COMBINATIONS: Metronidazole and Amoxicillin Van Winklehoff (92): LJP, RP, AP pts, 250 mg MET + 375 mg AMOX, synergistic effect on Aa, Pg, Pi, eliminated Aa, Pg. Metronidazole and Augmentin Rams (90): MET + AUG 250mg tid for 7 days, Eliminated Aa, improved clinical parameters. MISC Erythromycin and Seldane = arrhythmias Chloramine T: Slow release Chloride ions, bactericidal Pseudomembranous colitis treatment: Vancomycin 250-500mg qid for 2 weeks. SBE Prophylaxis Dajami et al (JAMA, 90): AHA recommendations. Amoxicillin 3 g 1 hr before, 1.5 g 6 hrs. after first dose. Penicillin allergic: EES 800mg 2hr before, 400mg 6 hr post Clindamycin: 200mg 1 hr preop, 150mg 6 hr POT Special regimens: Ampicillin 2g IV 30mins pre, Gentamycin 1.5 mg/kg IV before, Amox1.5g/kg 6 hr POT Vancomycin 1g IV over 1 hr , 1hr preop. Tzuckert (86): 1.36 deaths/million/year attributed to antibiotics administered to prevent SBE, 0.26 deaths/million/year due to SBE of dental origin. Barco (JP,91): Non-streptococcus bact frequently found in perio are now implicated in endocarditis and are not affected by systemic antibiotics. Amount of microbes may not be as important as ability to adhere, this may be where antibiotic helps. use CHX rinse. BACTEREMIA Wank (JP 76 30-23): No difference in bacteremia between brushing, flossing, and initial therapy. Before and during brushing, floss and toothpick had increased anaerobes in blood. Carrol & Sebor (80): Bacteremia with less than frequent flossing 86%, routine flossing eliminated bacteremias.
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Silver (JCP 77, 30-24): Toothbrushing can cause bacteremia in periodontal diseased patient, good OH reduces this chance. Blood culture b/f and during brushing (+) and related to amount of inflammation. Lothus (JP 91 30-25): SubG irrigation of CHx or saline same bacteremia before and after S/RP. Reinhardt et al. (JP,82): Tap water irrigation used in ultrasonic scaling did not appear to be significant causative agent in postoperative bacteremias in healthy individuals with healthy periodontium. Waki et al (90): Bacteremia after S/RP 18.5% Winslow (65): Increased incidence of bacteremia with increased periodontal disease Otten (): 40% incidence of bacteremia after removal of a partially impacted tooth. Wikesjo: Bacteremia possible after suture removal, also King (88): 5% incidence of bacteremia after suture removal. ANTIBIOTICS AND GRAFTS: See Alloplastic/Synthetic Grafts. Haffajee (JCP 95): 4 adjunctive systemic agents in tx of periodontal infections. 30 days. 98 subjects txd with MWF, scaling. DNA probes taken at 6 sites at 2 month intervals. Pts placed on either Augmentin 250mg tid, tetracycline 250mg tid, ibuprofen 400mg tid, or placebo. Overall ALG 0.34mm, PDR 0.62mm. Subjects with antibiotics had more attachment level gain (0.57mm) vs. ibuprofen, placebo 0.02mm. Pg, Bf, Pi, Pm were reduced in greater amounts in the antibiotic pts.
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INITIAL THERAPY AND RE-EVALUATION S/RP Rationale: To create a biologically acceptable root surface that is compatible with the health of adjacent periodontal tissues. Biologically acceptable = Smooth, hard, and clean. Objectives: O'Leary 1) Biologically acceptable root surfaces 2) Resolving inflammation 3) Reducing pocket depths 4) Facilitating oral hygiene procedures 5) Improve or maintain attachment levels 6) Prepare tissues for surgical procedures Limitations: Anatomy of roots, Depth of Pockets, Position of teeth, area of mouth, size of mouth opening / cheeks, bacterial invasion of tissue and or root surface. Stambaugh (IJPRD 81, 30-28): Complete calculus removal with pockets > 3.73 mm is unpredictable, maximum instrumentation 6.21mm. Hygienists 30-40 min/tooth. Curette Efficiency = 3.73 mm, Curette Limit = 6.21 mm. Jones and O'Leary (JP,78): 19 % of periodontally involved teeth still had calculus which was only detected after extraction. Most commonly found at the CEJ, root flutes and line-angles. Bower (JP,79): Furcation access of curette is limited due to furca entrances of 1st molars : 58% were < 0.75mm and 81% were < 1.0 mm and Ave. curette is 0.75 - 1.1 mm wide. Rateitschak-Plus (JCP,92): SEM, 29 of 40 surfaces cleaned, 75% of base of root surfaces not instrumented. Nagy (92): After 5 curettes do not reach deeper than regular curettes, mean curette efficiency 1-3.5mm Rabbani et al. (JP,81): Correlation between % of residual calculus and pocket depth. Loos et al. (JCP,89): In sites of > 7 mm regressed after initial tx, Overall 25% of molar furcation sites demonstrated loss of attachment compared to 7% for non-molar sites and 10% of molar flat-surface sites. Waerhaug (JP,78): Incomplete plaque removal rates: BOARD QUESTION Pocket Depth IPRR > 5 mm 89% 3 - 5 mm 39% < 3 mm 11% Other notables from the article: -Surgical elimination of pockets greater than 3 mm is the most predictable method for adequate subG plaque removal -Regrowth of subG plaque is a slow process which may take up to months or even years Cementum Removal with Hand Curettes: Coldiron (JP 90, 30-6): Complete cementum removal at 20-70 strokes. 90 minutes/quadrant to instrument pt w/ mod pdtis. Healing Time Post S/RP Proye (JP 82, 30-17): Substantial PD reduction w/i 4 weeks with single episode of RP. Biphasic response: 1 week-gingival recession, 3 weeks-attachment gain 0.52 mm. Morrison (JCP 80, 30-27): 4 weeks Badersten (JCP 84): 4-5 months in 4-7 mm PD's, 5-9 months in 7-12 mm PD's Kaldahl (JP 88): 1 year AAP World Workshop says 4-6 weeks, but gradual repair and maturation may occur 9 -12 months. Healing after S/RP Waerhaug (JP 78, 30-15): S/RP then extracted up to 7 mo. JE reformed in 7 days. Plaque front moves 2 m/day. If good supraG plaque control no subG plaque formation. New dentogingival junction in 2 weeks.
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Waerhaug (JP 78, 30-16): Plaque to fiber distance 0.5 to 3 mm 11% success calculus removal. Listgarten: LJE reforms post S/RP, Epithelium in 7 days, collagen maturation at 4 weeks Hughes, Caffesse (JP 78, 30-2): Human. The relationship of the bottom of the pocket to the MGJ may change during the hygienic phase, however, the position of the MGJ with respect to the CEJ will not change as a result of initial therapy. If no bone present under MGJ, or the pocket extended to the MGJ, there was an increased chance of decrease in crevice depth. Caton and Zander (JP 79): Healing by LJE , Histometric eval 2 monkeys, created defects, treated experimental with S/RP repeated 3, 6, and 9 months. killed Found LJE in both control sites and experimental sites. Muller et al. (JCP 86, 30-19): Darkfield. SupraG cleaning, then 1 side supraG RP, 6 mo. Clinical change related to change in flora. Excellent supraG plaque control had profound favorable effects on shallow sites, supraG plaque control cannot stop recurrence in deep pockets. SupraG plaque accumulation led to subG changes.
OHI vs OHI + S/RP: Tagge, O’Leary (JP 75, 30-14): RP + OHI more effective than OHI alone. Healing After Curettage Stone, Ramfjord, et al (66): Peak mitosis at 12-24 hrs, CT peak 2-3 days, Epithelial attach at 5 days, cells come from residual epithelial attachment in crevicular lining. RECOLONIZATION AFTER S/RP Tabita (JP 81, 30-30): SubG plaque is reformed after 14 days, despite effective supraG control (not mature or attached). Heinrichs (85): After S/RP, significant decreases in coccoid, spirochetes, motiles, in deep/shallow pockets. Insignificant reductions in bacteroides. Listgarten (JCP,78): Decrease in micro (motile rods/spirochetes) up to 25 weeks with S/RP with or without TCN. Slots (JP,79): Up to 6 months a decrease in spirochetes and capnocytophaga was evident. Mosque Listgarten (JPR,80): cocci 21 days, motile organisms 7 days, and 42 days spirochetes Magnusson et al (JCP 84, 30-18): Deep pockets (8mm) not reduced following instrumentation, decrease in spirochetes maintained with good oral hygiene, return in 16 weeks from baseline without it. By controlling supraG plaque, the development of subG plaque is markedly reduced. Effects on Clinical Parameters Morrison (JCP 80, 30-26): Initial therapy can reduce PD and increase AL: assess need for surgery after initial therapy (4 weeks) Initial PD 1-3mm 4-6mm 6+ mm
PD Change - 0.17 mm - 0.96 mm - 2.2 mm
AL Change NSD + 0.23 mm + 0.91 mm
Badersten, Nilveus, Egelberg (II) (JCP 84, 30-31): Clinical. Ultrasonic=Hand. S/RP/OHI q3mo 1yr. F/U 2 yr. Clinical improvement continued up to 9 mos after start. Plaque & AGAIN up to 3 mo. GI, BOP, PD & REC up to 9 mo. Wait 9 months post IT for Sx eval. Badersten, Nilveus, Egelberg (I) (JCP 81, 30-29): Clinical. ADV Pdtis, ½ hand, ½ ultrasonic. 12 mo. No diff b/t ultrasonic and hand instruments, great improvement in clinically w/ OHI & RP in 5 mo but after that little improvement. Removal of LPS: Smart (JCP 90, 30-12) Endotoxin on surface of roots. Scaled teeth have similar levels as healthy teeth
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McCoy, et al (JP 87, 30-4): Human. Concentration of endotoxin greatly reduced (but not eliminated) by RP in vivo, retoxificaiton occurs w/i a short time (up to 12 weeks) after RP procedures. Limulus lysate test. Effects on Mobility: Ferris (JP,66): 25% reduction in tooth mobility after root planing Rateitschak (JP,63): 14% reduction in mobility. Selipsky (DCNA,76): 23% reduction in mobility. S/RP verses Cavitron Cavitron better than S/RP: Leon and Vogel (JP 87 18-19): Non-surgical approach, decrease microbes and reduce GCF, Cavitron better in class II + III furcas. Dragoo (IJPRD,92): Modified Cavitron tips more effective than hand instruments (4.65mm verses 3.45mm) Matia & Bissada (IJPRD,86): Mand furcations tx w/ S/RP + OHI, open vs. closed, curette vs. ultrasonic. Ultrasonics better than hand instruments in narrow (RP>Cavitron Modified Tip Copulos, Low et al (JP,93 ): modified tip reduced instrumentation time vs. curettes 3.9 min and 5.9 mm respectively. Takacs (JP,93): Use of sonic scalers and ultrasonics with ball tip performed the best in furcations, EVA performed poorest. Ultrasonic vs Sonic Scalers: Baehni (JCP 92, 30-13): Changes related to length of instrumentation. In vivo NSD ultrasonic vs. sonic. Lowered spirochetes, raised coccoid. In vitro ultrasonic better due to cavitation effect. POWER-DRIVEN SCALING AND POLISHING INSTRUMENTS Cavitron: Magnetostrictive, and Piezoelectric effects, handpiece contains a wire coil producing a magnetic field when current is applied, the handpiece insert is nickel-cobalt alloy stack which acts as a transducer which shortens (in the electromagnetic field) by one-thousand of an inch and back to its original length at a high frequency. CAVITRON Infection control: Larato (JP 67, 30-9): 3,000 % increase in bacterial aerosol during Cavitron use, with still 230% 35 minutes after treatment. handpiece not autoclavable
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TITAN-S Operates at 2,500-7,500 CPS Gellin (JP 86, 30-11): Titan-S Sonic scaler versus curettes, found very similar, best when used in combination. PROPHY-JET Sodium bicarbonate blaster, Galloway and Pashley (87): Can erode dentin and cementum, minimal changes in enamel, uses sodium bicarbonate as abrasive powder. Bernstein (JP,87) - Prophy jet removes stains faster and is close to abrasiveness of the curette 27.09 um vs. 10.68 um Gillman et al. (JP,86): Cavitron and prophy-jet detoxify root surfaces allowing growth of fibroblasts. ROTARY INSTRUMENTS Schwarz et al (89): OFD with hand inst. -vs.- rotary diamond burs. 8 pts, 20 teeth: advantages of either, hand better in mesial/distal furcations. Rotary instruments removed a lot of tooth structure, but more efficacious in fissures, grooves, indentations. Parashis (JCP,93): Use of rotary diamonds for root instrumentation via an open flap resulted in furcal surfaces with significantly less residual calculus than furcations treated with hand instruments (closed or open approach). Residual calculus : Closed Rp 70%, Open RP 35%, Rotary Instrument 5%. Follow up study of furcation opening showing the same trends. 2.4 mm was threshold for narrow furcation. S/RP in Health Claffey and Shanley (JCP 86): Thin (2.0mm thick 0mm Attachment loss. Thin or thick BOP sites gain attachment. PD 7 mm big AGAIN. Lindhe, Nyman, Karring (JCP 82, 30-3): S/RP in normal sulci of monkeys q2weeks for 6 mo resulted in 0.39 mm of AL. S/RP IMPROVED WITH SURGICAL ACCESS Brayer and Mellonig (JP,89): 114 single rooted teeth, 4 operators with different experience levels experienced operators removed more calculus in moderate to deep pockets > 4mm. Open approach helped both operator groups. Fleischer, Mellonig (JP 89, 30-5): 61 molars with same 4 operators, 68% of teeth calculus free even with open approach and experienced operator. The deeper the pocket, the more calculus left on the root. More experienced practioners removed more calculut in both open and closed flap procedures. Poen flap tx allowed more efficient S/RP regardless of practioner experience. Total calculus removal in furcations utilizing conventional instruments may be limited. Badersten, Nilveus, Egelberg (III) (JCP 84, 30-32): No difference in effects noted b/t single vs. multiple instrumentations. Single rooted teeth: maintainable by nonsurgical therapy: curettes/Cavitron, single vs. multiple scalings or operator variability played no role. Caffesse, Sweeny, and Smith (JCP 86, 30-33): S/RP w & w/o flap surgery, % of Root Surface Free of calculus after extraction. CalculusCEJ, groove, fossa & furcations. Probing Depth 1 -3 mm 4 -6 mm > 6 mm
NO:
S/RP alone 86.4% 43.2% 32.3%
S/RP with flap 86.0% 75.7% 50%
Wylam, Mealy, Mills, Waldrop (JP, 93) Residual plaque and calculus using curettes only : Closed root plane : 54% Open flap curettage: 33% Furcations same , need different means to clean- ultrasonics, burs, chemo, no difference with respect to PD >90% calculus left in furcations Schroer et al. (JCP,91): Facial of Grade II molar furcations with closed RP 0.60 mm gain in attachment, and open 0.45 loss of attachment. 16 month study.
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Papillary Reflection with headlights: Reinhardt (85): 80.8% accretion free with Papillary Reflection and Headlights 29.0% accretion free with Papillary Reflection only 0% accretion free with Closed Sc/ RP DETECTION OF CALCULUS Sherman and Hutchens (JP 90, 30-37): SEV Pdtis, S/RP + OHI multiple sessions prn. 75% right if both investigators said calculus was there, but 50% right if both investigators said it was absent. High sensitivity, low specificity. LOSS OF TOOTH STRUCTURE Ritz & Hefti (JCP,91): Ultrasonic 11.6 um 100p with 12 strokes Sonic 93.0 um 100p Curettes 108 um 500p diamond bur 118 um 100p Zappa et al. (JP,91): After 40 strokes, between 0.143-0.343 mm were removed depending on the force. ROOT SMOOTHNESS/ ROOT ROUGHNESS Rosenberg and Ash (JP 74 30-1): Smoother roots did not have more or less plaque accumulation or inflammation than rough roots. Khatiblou (JP 83 30-5): Horizontal grooves placed in roots did not effect healing after MWF compared to S/RP teeth. Leknes et al. (JP 94): dogs, high speed diamond burs or sharp curettes viewed with SEM, more plaque accumulation on rough surfaces. Leknes, Lie, Selvig (JP 94, 9-23): Clinical. Attachment loss greater on grooved surfaces than nongrooved surfaces. Grooves facilitate plaque growth, hide from defense mechanism, impede OH. Sx Tx with grooves less successful. Vacek and Gher (IJPRD,93): Cementum variations 11.5%, Pebbled cementum, 94% anomalies interproximal. Oberholzer, Rateitschak (JCP 96, 30-8): Human. Open S/RP MOD pdtis, test sites roughened w/ diamond, no improvement over smooth in clinical attachment (6 months). NON-SURGICAL STUDIES Badersten Articles (Highlights) 1) Single Rooted teeth only. Studies not applicable to molars 2) Clinical Parameters up to 9 months 3) Ultrasonics = Curettes 4) Operator experience not a significant factor 5) No controls 6) Continued bleeding sites 7) Regression Analysis 8) Predict disease activity 5 yr. PD >7mm (50%), >7mm bleeding and increase in > 1mm PD (80%) 9) A single episode instrumentation = several appointments (3) 10) Deep pockets didn't progress to further attachment loss Claffey (90): 3½ yr. > 7mm 50% LOA, Increase attachment loss 1 mm 66%, + BOP 87% LOA MISC
LAL: Limulus Amoebocyte Lysate, test for endotoxin, PPT when combined with the blood of a horseshoe crab, false +s common. (Wilson and Moore (85)) Westphal Extraction: Hot phenol/water Westphal (52), save aqueous portion, dialyze against pyrogen free H2O, concentrate by dialysis against propylene glycol and ultracentrifugation. Endotoxin penetrates 5 microns into cementum.
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Cercek: no improvement in PD or AL by home care alone. Breninger et al. (JP,87): Evaluated by SEM, the stainable material used to determine residual endotoxin, the majority of stained deposits were composed of adherent fibrin and instrumentation debris. XI. SURGICAL THERAPY WHY DO SURGERY? Preserve teeth in health function and esthetics. Rationale for surgery: Therapeutic objectives include: (1) Regeneration (2) Conservative Therapy (3) Access for Debridement (4) Pocket Reduction (5) Pocket Elimination More Conservative Therapy: Pihlstrom & McHugh (1981 32-19): Pts had full-mouth S/RP (3-4 2 hrs. appointments), 1/2 mouth MWF + maintenance every 3-6 months. 4 years follow-up. For 4-6 mm pockets, S/RP was as effective as surgery. At 4 years, MWF had greater attachment gain and PD reduction. At 10 years no significant changes in S/RP and surgical sites. > 7 mm greater gain attachment with surgery. Lindhe et al (1982): 15 pts with split-mouth S/RP and S/RP + MWF. Maintenance q 3 months, followed up for 2 yrs. Sites initially gained attachment, except initially shallow sites (6mm) responded better to surgical therapy in PD reduction and attachment gain. S/RP only took twice the time. critical probing depths 2.9-4.2 mm Knowles: In deep defects the best procedure is MWF, significant pocket reduction, and attachment gain for 8 years, baseline was at initial eval. Furcations do not respond to non-surgical therapy Loos and Nylund: Teeth (furcated) with S/RP only, rebounded at 1 yr., 25% of Furcation invasion lose attachment. Badersten: Non-surgical therapy works, but in non-molar teeth only. Nordland, Garrett, Kiger, Vanooteghem (JCP 87, 30-35): Furcations with initial pocket depth > 4mm had poorer response to non-surg therapy verses flat molar and non-molar sites initially >4 mm. LJP Patients Kornman: LJP responds poorly to S/RP alone. Improve Compliance with Recall: Beckers No evidence to support pocket elimination makes teeth easier to clean, maybe more accessible, but not easier. TOOTH LOSS STUDIES UNTREATED disease Becker 79 Buckley 84 Loe 85
Duration Loss rate 3.2 yrs 0.04/pt/yr 10 yrs 0.08/pt/yr 15 0.13/pt/yr 0.11/pt/yr
Loss rate
TREATED disease
0.36/pt/yr
Oliver 69
0.25/pt/yr
Hirshfeld+Wasser 78
22yrs
0.14
McFall 82
19yrs
Becker 84
6.5
Time
10yrs
AVE 0.25
AVE
0.09 Meador and Lane: 90% of surgical pts were stable, 60% of pts tx’d non-surgically were stable
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LOCAL ANESTHETICS AND EPINEPHRINE Anesthetic Action: Binds to Ca2+receptor, blocking the Na channel which prevents signal conduction Action of Epi: Activates a-adrenergic receptors to cause vasoconstriction, and activates b-receptors to cause cardiac stimulation and bronchial dilation. Increases HR, force of contraction, systolic pressure. Decreases diastolic pressure. MAXIMUM DOSAGES Epinephrine: Healthy Patients0.2 mg/appt 11 carpules 1:100,000; 5½ carps 1:50,000 Epi) Cardiac Patients 0.04 mg/appt 2 carp. 1:100,000 0.018mg Epi/carp1:100,000, 0.036mg/carp 1:50,000. (BOARD QUESTION) Catecholamine levels: Resting adrenal medulla releases 7µg/min Epi, stress releases 280 µg/min. Contraindications. for Epi: Pheochromocytoma (medulla tumor), uncontrolled hypertension, arrhythmias and hyperthyroidism. Epinephrine given to patient taking Beta Blocker can result in transient hypertensive and bradycardic episodes (BOARD QUESTION) Anesthetics
Lidocaine: 3mg/lb, 36 mg/carp, max dose 300mg 8 carps Marcaine: 0.6mg/lb, 9mg/carp, Max dose 90mg 10 carps Prilocaine (Citanest plain): 2.7 mg/lb., 72 mg/carp, Max dose 400mg 5½ carps 36 mg of lidocaine in 1.8 cc of 2% solution (BOARD QUESTION) Contraindications for local: Methemoglobinemia (Can be enhanced with amide locals, Substitution for ferric ion on hemoglobin molecule = brown blood. Allergy to bisulfites (preservative)- used to be methylparaben
Lidocaine decreases myocardial excitability and decreases force of heart contractions (BOARD QUESTION) Intra-arterial injection Pain and ischemia distal to injection. Confusion, convulsions, respiratory arrest, arrhythmias. Treatment, stop injection, do not remove needle, inject 10-20 ml of .5% procaine, leave IV in place, transport to medical facility. (BOARD QUESTION) Buckley (JP,84): 10 pts, split mouth, cyanomethemoglobin, 1:50,000 Epi improves hemostasis over 1:100,000 Epi. Baab (77): Pt loses 16-592 ml blood aver 134 ml/quadrant, cyanomethemoglobin to determine, >500ml loss give fluids Landen et al (87): Marcaine significantly reduces post-op pain. Is the amount of exogenous Epi something to be concerned about in dental pts? Yes: Lipp (Reg Anesth 93): Looked at exogenous and endogenous plasma levels of Epi during dental tx under local anesthesia. Tx begun on an unanesthetized area produced little change in plasma Epi levels, suggesting total Epi levels are more a reflection of exogenous rather than endogenous Epi. Also suggests that endogenous Epi response due to stress was not as significant as exogenous injected Epi. HTN pts: Hemodynamic instability results in greater and faster increases in systolic pressure when Epi is used. Hypertensive meds may also interfere with the storage, release, and biotransformation of Epi. Previous MI pts: Epi speeds up the repolarization of calcium channels and further alters the refractory period, predisposing the ischemic area to re-entrance arrhythmia and fibrillation. No: Cheraskin (JADA 58): BP and pulse monitored in ext. cases. Local anesthetic without vasoconstrictor is less effective and results in greater stress which causes an increase in release of endogenous Epi. This endogenous Epi causes greater cardiovascular changes than the exogenous Epi. Davenport et al (JP,90): Lidocaine with/without 1:100,000 Epi in HTN pts. No effects on BP or HR. Lidocaine without Epi had inadequate anesthesia and hemostasis in 7/9 procedures. BASIC SURGICAL PRINCIPLES
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SULCULAR VS REVERSE/INVERSE BEVEL INCISIONS Cattermole & Wade (JCP 78 31-3): No difference between linear and scalloped incisions at three weeks, except that linear incisions have greater inflammation and slower initial healing. Smith, Echeverri, Caffesse (JP,87): Sulcular incisions are comparable to MWF as measured by gain in attachment and PD reduction. Thus the removal of crevicular epithelium is not of critical importance. (BOARD QUESTION) Litch et al (84): Half of crestal and subcrestal incisions did not completely remove pocket epithelium Pippin: Healing of the MWF, sulcular epithelium degenerates and reforms in 7 days. Kon, Caffesse (31-4): Beveled incisions heal better than perpendicular when using vertical with FTF. VERTICAL RELEASING INCISIONS Kon et al (IJPRD 84 31-4): Healing of beveled vs. perpendicular vertical releasing incisions. Beveled or "slanted" healed faster and was less detectable. Lynch (JP,88): Mandibular vertical releasing incisions allow access, should not be made distal to 2nd molars. Morman and Meier (79): 31 dental students, punch wounds at radicular and mid-axially, mid-axial is less resistant to trauma due to less collateral circulation. PAPILLA PRESERVATION TECHNIQUES Takei (JP,85): Papilla preservation technique, incisions are made from the palate and papilla are pushed through the embrasure space for access. The tissue must be thick (2 mm) and the embrasure wide. Murphy (IJPRD 96) Papillary triangle SPLIT THICKNESS VERSES FULL THICKNESS FLAPS Staffileno (JP,74): Supports use of split thickness flaps for less resorption, sooner osteogenesis, minimal apical movement of attachment apparatus at 60 days verses FTF. Must have thick CT or acts as denudation. Tisot & Sullivan (JDR,71): Abstract, monkey study, disulfine blue dye, photos, More vascular disruption with split thickness flaps Wood (JP 72 33-25): Split thickness flaps heal slower with more bone loss than full thickness flaps (0.98 vs. 0.62 mm) BOARD QUESTION Levin et al. (JOP,77): dogs, full and partial flaps adjacent at 15 and 90 min, healing faster in partial thickness and faster procedure. PERIOSTEAL RELEASING INCISION Corn (1962): Periosteal Seperation Technique- eliminate pockets, minimal marginal osseous exposure reducing resorption of bone, release of frenum and muscle pull and predictable increase in vestibular depth. LASERS Light Amplified by Stimulated Emission Radiation ND-YAG neodymium-yttrium-aluminum (Affects mostly pigmented tissue) Trylovich et al (JP,92): Nd:YAG, Unerupted 3rds, lased and cultured fibroblasts and SEM evaluation. decreased amount of flat fibroblasts in lased, endotoxin tx root segments vs. non-lased and endotoxin treated groups. Alteration of cementum surface made it unfavorable for fibroblast attachment. Morlock et al. (JP,92): Kansas city Mo (Killoy group), used as adjunct to root planing, physical changes in root surfaces not amiable to fibroblast attachment. Killoy: Nd-Yag has a wider band of necrosis than the CO2 laser, also burns root surface, melts HA no fibroblast attachment. Block: Lasers alter the surface of implants Cobb et al (JP 92 31-26): Nd:YAG, laser-induced root surface alterations appear directly related to energy levels and time exposure and has the potential for suppression or eradication of subG microflora. CO2 - highly attracted to tissues of high water content. Rossman et al. (JP,92): Retardation of Epithelial migration, monkeys. irradiation of experimental side resulted in delayed epithelial downgrowth along the root surface and more CT attachment. control seen 14 days, experimental 28 days. Israel et al (JP,95): 2 pts, used laser to de-epithelialize the flap to enhance CT attachment 1/2 CT and repair cementum.
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ELECTROSURGERY Krejci and Kalkwarf (JCP 87 31-30): Limit contact to soft tissue only, short contact with bone is ok, move tip quickly to avoid burning tissue. Wound healing is not adversely affected. Can't use on pacemaker pts, around implants. Slight recession expected with troughing incisions, Electrode contact with cementum inhibits reattachment. (BOARD QUESTION) Cortical penetrations Mellonig Aids to revascularization, Buser for GBR VASCULATURE IN SURGERY Cutright (JP,69 31-8): Proliferation of Blood vessels in Gingival wounds Day 1: Withdrawal and blockage of cut ends of the vessels at wound margin Day 2: New sprouts, club-shaped stubs at bottom of wound. Day 3: Short Capillary loops forming, arising from the cut surfaces of existing vessels which anastomose. No regeneration at angles of the wound. Day 5: Increased capillary loops with dilation of one limb. Corners of the wound show revascularization. Day 7: General contour of gingiva reestablished, floor and edges show completion of capillary loops Day 9. Capillary loops almost reach height of normal loops, density less than normal. Day 11: Further restoration of normal pattern and size, density still not equal to normal gingiva. Baab et al (JP,77): 30 pts, Flap surgery, blood loss assessed cyanomethemoglobin, range was 16 - 592 ml (Ave. 134ml) ; duration rather than type of anesthetic seemed to have the only correlation with blood loss. > 500 ml think IV Morman and Ciancio (JP,77): 8 pts, different flap designs, IV sodium Fluorescein then photographic system to determine diffusion. The following concepts in flap design: 1) Length: width ratio should not exceed 2:1 2) The base should be broad enough to include major gingival vessels 3) Minimal tension should be created in suturing and tissues should be managed gently 4) Partial thickness flaps to cover avascular sites need to have enough blood vessels included in them Morman et al (JCP,79): 31 dental students, contralateral punch wounds in mid-axial and mid-papillary 1) Ischemia occurred coronal to the wounds 2) Collateral circulation from the PDL vessels to marginal gingiva was insufficient to maintain tissue vitality 3) Circulation was oriented in an apical-coronal direction in the mandible and maxilla 4) Mid-axial gingival tissue is less resistant to trauma, has less potential of collateral circulation 5) The use of horizontal releasing flaps should be restricted to preserve blood supply 6) Double pedicle bilaterally based flap is unsound due to blood supply. Mclean et al (JP 95 31-11): Dogs, Fluorescein angiography, vascular changes following mucogingival flap (early healing of flap was extravascular diffusion until actual circulation restored): 1) Raising a flap initiates a significant vascular embarrassment 2) Lack of circulation at the most coronal portion of the flaps lasts for at least 3 days but persists for 7 days at the interproximal areas. 3) Flap diffusion recovers sooner than flap circulation 4) No apparent differences between horizontal mattress and interrupted suturing techniques circulation absent near sutures. ANTERIOR ESTHETICS Takei (JP,85): Papilla preservation technique, incisions are made from the palate and papilla are pushed through the embrasure space for access. The tissue must be thick (2 mm) and the embrasure wide. Frisch: Curtain procedure Beagle (92): Described surgical technique for papilla reconstruction, case report 28yo, 6-0 silk sutures, split thickness flaps. DELAYED (Altered) PASSIVE ERUPTION
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Coslet et al (77): Diagnosis and classification of eruption, 12.1% of pts exhibit this to some degree. Classification Type 1=excessive gingiva (A normal bone and B bone at CEJ), Type 2 is normal gingiva, A and B. STAGES OF PASSIVE ERUPTION Gottlieb and Orban: 1. Base of sulcus and JE on enamel, JE all on enamel 2. Base of sulcus on enamel and JE on both enamel and cementum. 3. Base of sulcus at CEJ and JE on root, JE all on cementum. 4. Base of sulcus and JE all on root. JE all on cementum below the CEJ. SUTURE MATERIALS Absorbable: Suture Raw Material
Plain Gut
Absorption
Strength
Tissue Reaction
Knot
Handling
Uses
rapidly healing mucosa avoids suture removal as above slower absorption subepithelial submucosa surfaces, vessel ligation
Sec urit y
Sheep or Beef intestine
enzymes & macrophage s complete in 70 days
4 - 10 days
++++
+
+
as above treated with chromic salts Coated Vicryl Polyglactin 910 coated with polyglactin 310 and Ca ++ stearate Nonabsorbable: Surgical Silk Protein fiber of silkworm coated with silicon prote in Nylon monofilament polyamide polymer Gore-Tex expanded polytetrafluor o ethylene
as above complete in 90 days slow hydrolysis complete in 60 - 90 days
10 -14 days
+++
+
+
20 -30 days
++
+++
++++
Local inflammator y response in 1 - 2 yrs
90 -120 days
++++
+
++++
mucosal surfaces
slow hydrolysis
+++
+
++
++
skin closure
none
++++
+
++
++
GTR
Chromic Gut
SUTURE TECHNIQUES Nelson et al. (JP,77): Interrupted sutures vs. continuous. No difference in healing, interrupted had slightly better flap adaptation with the continuos suturing tending to displace each papilla in a mesial direction. Antoni et al: Monofilament sutures have less bacterial wicking, less inflammation. Lily et al. (OS,72): More bacteria associated with silk sutures, polyglycolic acid sutures (Vicryl) had no bacteria, tissue response occurred with other monofilament sutures. Newell and Brunsvold: (85) Vertical (long papillae) or horizontal (short papillae) mattress sutures to prevent facial tissues from being pulled interproximally. 137
Complications with sutures: Brunsvold, Redding, Kornman (Int J oral Max Imp,91): Suture granuloma by leaving a piece of silk suture behind. SUTURE REMOVAL TIME Hiatt et al at (68): Dog study. Remove sutures at 7-14 days (except if you’re using a membrane) Time
Force Applied to Flap
Results
2-3 days 7 days 14 days 1,4,6 Mon.
225 gms 340 gms 1,700 gms 1,700 gms
flap separation from bone and root flap separation form bone and root suture pulls through gingiva suture pulls through gingiva
PERIODONTAL DRESSINGS Advantages of Dressings 1. Helpful with APF’s, crown lengthenings and covering exposed bone 2. Reminder to the patient not to chew in the area 3. Can stabilize a FGG Disadvantages of Dressings 1. Healing is not improved 2. Possible plaque trap, doesn’t allow for CHX to contact tissues 3. Contraindicated when coronally positioning a flap 4. Dressing can get under a flap, it can be loose and not add to clot stability. Sachs et al. (JP,84): Rationale for dressings: Retention of APFs, Stabilization of FGGs, protect denuded bone, graft retention? PerioCare Dressing: Ingredients: Magnesium oxide, zinc oxide, Ca(OH) 2, vegetable oils, ethyl cellulose, resins, lanolin. Barricaid: Light Cured: Polyvinyl ethyl siloxane, a polymer of methylmethacrylate. Smeekens (92): No difference between Barricaid and eugenol dressing in wound healing, more microulcerations with eugenol. Gilbert (JP 94): In vitro study of Barricaid. Cured dressing does not adversely effect fibroblast growth. Uncured dressing is lethal to cells it is in direct contact with, but an ingrowth of normal cells was seen at 5 days. After the 40 sec recommended curing time, some polymerized material still remains interproximally. Checchi (JP 94): 24 pts with APF surgery. 1quad received dressing, the other quad did not. According to the patients, there was no additional relief of discomfort in quadrants with dressing. POST OPERATIVE COMPLICATIONS Pack & Haber (JP 83 31-35): Incidence of infection after periodontal surgery 1%, no difference in the incidence of infection with antibiotic coverage. Infection highest after osseous surgery Curtis & McLain (JP 85): Incidence of postop complications: 94.5% had none or minimal POT complications. Increased duration of procedure resulted in increased POT pain. Murphy: Complications with GTR: Pain 16%, perforation 4%, infection 4%. Mathews & McCulloch (JP,93): Survey the pain perceptions of surgical vs. non-surgical tx. Pts. had significant differences between tx types, post-op pain, swelling, interference with eating, having a restoration placed in a surgical area, and prior periodontal therapy. WOUND HEALING VASCULAR Cutright (JP,69): Proliferation of Blood vessels in Gingival wounds Day 1: Withdrawal and blockage of cut ends of the vessels at wound margin 138
Day 2: New sprouts, club-shaped stubs at bottom of wound. Day 3: Short Capillary loops forming, arising from the cut surfaces of existing vessels which anastomose. No regeneration at edges of the wound. Day 5: Increased capillary loops with dilation of one limb. Corners of the wound show revascularization. Day 7: General contour of gingiva reestablished, floor and edges show completion of capillary loops Day 9. Capillary loops almost reach height of normal loops, density less than normal. Day 11: Further restoration of normal pattern and size, density still not equal to normal gingiva. SOFT TISSUE Kon (JP,69): Full Thickness Flap 0 hour: Thin blood clot over exposed bone and CT 2 days: increased flap vascularization/ vasodilation. Rete pegs flat 6-7days: Increased inflammatory reaction, flap still prone to separation, blood clot replaced by immature CT. 7 days: Osteoclastic activity reaches a peak at day 7. 12days: Flap is reattached to bone and tooth, osteoblastic activity predominates at day 12. 23-31: Bone reformed at crest and buccal septum, organized CT. 55-85: Periodontal tissues reconstructed, DGJ renewed, buccal plate is rebuilt. Thick clot impairs healing. DENUDED BONE Costich and Ramfjord (JP,68): Leave exposed bone of 10pts, 3-4 mm apical to alveolar crest 1) No pts complained of pain, 2) Sequestration and bone resorption was present 6 wks after surgery, 3) post-surgical inflammation extended into the periodontal membrane Ramfjord and Costich (JP,68): Exposure of periosteum same as above: 1) Exposure of periosteum on the alveolar process without flap coverage results in severe inflammation with bone resorption 2) The degree of bone resorption following periosteal retention is almost equal to that seen with denudation 3) As thick a layer of CT as is possible should be left over the periosteum if the area is not going to be covered with epithelium Wound healing Intervals Lindhe: More graft fill in q 2 weeks recall vs. q 2 months HEALING IN THE PRESENCE OF PLAQUE Yumet, Polson (JP,85): 4 squirrel monkeys, Healing in the presence of plaque, get marked epithelial downgrowth into an incisional wound after inflammation with a proposed loss of CT. Nyman (77): 5 types of surgery, no POT professional cleanings, OH returned to baseline @ 6 months, in Attachment loss and PD regardless of surgical method used. DIETARY FACTORS AFFECTING HEALING Protein, Fe, Vita C: Important for epithelial barrier function. Vogel et al (84): Zinc: Stabilizes membranes and decreases lysosomal enzyme and histamine release Vit C: May alter PMN function , needed for collagen synthesis (cross-link process) Fe (Iron): Collagen metabolism, may alter macrophage function and PMN Protein: epithelium barrier Folic Acid: epithelium barrier. Collagen metabolism Calcium: decreased may alter Calcium/Phosphate ratio Pauling: Vit C good for wound healing Vogel (JP 86 14-20): Showed that subclinical deficiencies of Vit C, zinc, and iron may increase the permeability of epithelium, generally reversible. However, megadosages of Vit C did not increase resistance to gingivitis/periodontitis. 139
Leggott (JP 86 14-21) With good OH vitamin c deficiency does not result in severe periodontal pathology. Vitamin C deficiency does relate to gingival inflammation. Depletion of Vitamin C can lead to increased gingival bleeding (BOARD QUESTION) Siegel (82): Conditional oral scurvy due to vitamin C withdrawal Granulation tissue removal Lindhe and Nyman (JCP,85): Split mouth 15 pts. MWF/ OFD/ S/RP. Granulation tissue removal in conjunction with flap surgery is not a critical measure for promotion of proper healing of the periodontal tissues. Saliva Contamination Bodner (92): Saliva components i.e. enzymes, IgA, etc. are important in wound healing. Rat study Wikesjo (JP,90): Dogs, Saliva contamination of the root surface does not adversely affect healing. CRATERING Jenkins et al. (JP,90): OFD pts, at 1 month 30% had craters or clefts of 1.8-1.6 mm deep, at 6 months craters reduced to 0.7mm. Tissue forming is a crevice not a LJE Newman: 3 mo pot inverse bevel procedures, Decrease in PD, increase AL but good gingival architecture not always obtained, pts maintained these areas OK DENTIN HYPERSENSITIVITY ETIOLOGY: 15,000 dentin tubules per mm 2 Theories of Dentinal Hypersensitivity: Dowell (JCP 83 16-24) 1) Transducer- " Synaptic-like" relationship between terminal sensory nerve endings & odontoblastic process 2) Modulation- Odontoblasts may become injured & release neurotransmitting agents modulates nerve fibers 3) Gate control and vibration- deals with how pain responses are interpreted. 4) Hydrodynamic- fluid movement within the dentinal tubules. (Brannestrom): Absi, Addy (JCP,87): Patency, diameter and # of tubules affect sensitivity proportionately. Pashley (JE 86 16-28): Amount of bacteria and products that can migrate into the tooth depends on thickness of remaining dentin, surface area of dentin exposed, smear layer, potency of bact products, rate of pulpal blood flow. TREATMENT: Knight (93): Methods for decreasing hypersensitivity include mechanical and chemical obliteration of dentin tubules.: Mechanical: best in descending order: Sharp curettes, dull curettes, ultrasonics, plastic instruments. Chemical: 1.09% NaF, 0.40% SnF2, 0.14% HF, 3% monohydrogen mono-potassium oxalate, glycerin, sealant 6% ferric oxalate, toothpaste 5% KNO3, light cured dental resin. SEM analysis showed most obliteration of tubules were sharp curette and light cured resin. Fogel and Pashley (JCP,93): SEM; Smear layer created by root planing is acid-labile, did not reduce dentin permeability, Potassium oxalate occluded the tubules and was acid resistant. Butler Protect: 3% monohydrogen mono-potassium oxalate. K makes nerve less excitable, oxalate combines with Ca to form crystals and block tubules. TOOTHPASTE Sensodyne: Minkoff (87): 10% strontium chloride, significantly decreases dentin hypersensitivity compared to control toothpaste. Collins (JP 84 16-25) Toothpaste study, compared Protect, Protect with fluoride and Sensodyne. All relieved sensitivity no sig difference. Kuroiwa (JP 94 16-26) Brushing with a non-abrasive dentifrice or without a dentifrice will prevent hypersensitivity. Occludes tubules with organic pellicle containing materials. TOOTHBRUSHING
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McAndrew (JP 95): Toothbrushing alone was most effective in occluding dentinal tubules and should not precede or follow dietary acid application and separate from mealtimes. IONTOPHORESIS: Forces fluoride into dentin by setting up a charge gradient. Lutins (84): Less hypersensitivity to controlled mechanical pressure/temperature in iontophoresis treatment group. Brough et al (JADA,85): all methods , 2% NaF and distilled H20 with and without Iontophoresis were the same FLUORIDE Gel-Kam 0.4% SnF2 Mazza (Bowers favorite) high concentration Gelcam 1.2%?? effective at decreasing sensitivity Tinanoff (80): SnF2 reduces plaque, but does not affect gingival health. GI and plaque score did not change sig, but CFUmg reduced 30%and total CFU reduced 50%. Perry (J West Soc Perio): Review. Fl may inhibit bacterial adsorption to pelliclecovered teeth by competing for Ca2+ ions. Comparisons b/t SnF 2 and NaF have generally shown the Sn compounds to have superior antimicrobial properties. Conc in tooth pastes generally 0.10.2% which is effective for caries reduction but less than required to have sig antimicrobial effect (0.3-0.4%). Boyd (JCP 85, 29-11): 28 pts, irrigation with 0.02% SnF 2, sig. improvement in clinical indices, better than OHI+H2O irrigation. Hastreiter (89): No effect on plaque, gingivitis, perio except with radiation and ortho decalcifications INFECTION CONTROL BOARD QUESTIONS Activated glutaraldehyde is most effective disinfectant for cold sterilization 2% glutaraldehyde requires complete rinsing. Bleach requires exposure for 10 minutes. Spore tests should be done weekly. Dry heat sterilization requires 160 degrees for 60 minutes. Herpes virus can survive for 2-4 hours on environmental surfaces. CAVITRON Infection control: Larato (JP 67, 30-9): 3,000 % increase in bacterial counts in air during Cavitron, with still 230% 35 minutes after treatment. handpiece not autoclavable GINGIVECTOMY Contraindications: intrabony pockets beyond the MGJ, or narrow AG, highly inflammed tissues, risk of caries, irregular pocket depths, esthetics a concern. HISTORICAL: Fouchard 1742 - Described a procedure and instrumentation for removal of excessive gingiva Pickerill 1912 - Coined term gingivectomy Kronfeld 1939 - Claimed bone to be not infected, thereby no need for bone removal, gingivectomy more popular Goldman (OS 50, 33-1): Described the gingivectomy 45° bevel to establish physiologic contours of tissues and to remove periodontal pockets, gingival overgrowth. Glickman (JP 56, 33-2): Described the unembellished gingivectomy, no preop therapy Kramer (92): Advocates the use of gingivectomy to treat intrabony defects.
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Proestakis et al (JCP, 92): Gingivectomy vs. MWF, split mouth design, There was no significant difference in the healing response in infrabony pockets between Gv and MWF. The bone gain was not predictable in either case. Healing after Gingivectomy: Engler & Ramfjord (JP 66, 33-3): Epithelialization: Tritiated thymidine in monkeys, epithelial cells migrate b/w polyband and CT after a delay of 12-24 hrs , most activity 2 mm from wound margin, reaching tooth in 5-7 days, Epithelium migrates at 0.5mm/day, it takes 1 week to cover a 3mm defect, 3-5 weeks to reestablish DGJ. Ramfjord and Engler (JP 66, 33-4): Connective Tissue: Same M&M as above, acute inflammation observed 2 hrs post op, epithelial labeling reached peak 1 day after surgery, CT labeling peaking on day 3, CT healing started 0.3-0.5 mm under wound surface, but spreads to rest of supracrestal area once epitheliazation is complete. Functional arrangement & collagenous maturation of connective tissue requires 3 - 5 weeks . Stahl (JP 68, 33-5): Humans re-epithelialization at 7-14 days. CT repair continuing for 28 days. Listgarten (JP 72): JE reestablished at 12 days POT, heals by extension of basal layer of oral epithelium apically between gingival CT and tooth. BOARD QUESTION Moskow (JP 77, 32-27): Monkey, histo. Interdental creaters treated w/ GV, curettage and flaps 11yr. All 3 worked at crater elimination. Wennstrom (JCP,83): Regeneration of Gingiva following surgical Excision, Keratinized gingiva consistently regenerated following surgical excision of the entire portion of the gingiva. Blood Loss Gingivectomy: Hecht and App (JP 74): Split mouth, one side infiltration the other a block w/ 2% lidocaine 1:100,000 Epi Block: mean blood loss, 19.3 ml, mean operating time 24.5 min Infiltration: mean blood loss 6.7 m., mean operating time 20.5 min Gingivoplasty: Goldman (JOS 50): Gingivoplasty includes the establishment of physiologic gingival architecture to maintain health. Festooning of the gingiva to obtain interdental grooves is important for food spillways. Indications: 1) Thickened gingival margins which remain inflamed 2) Fibrotic, bulky tissue 3) Improper gingival contours following curettage or gingivectomy 4) Areas of interdental cratering OPEN FLAP CURRETAGE/DEBRIDEMENT ENAP (Excisional New Attachment Procedure) Yukna (JP 76, 32-31): ENAP procedure in 5 monkeys, pocket reduction 5-2.8mm, 1.6 new attachment by LJE Yukna (JP 80, 32-32): 5 year follow-up post ENAP, 1.5 mm attachment gain maintained although PD increased, mean "new" attachment decreased, compares favorably to MWF (0.5mm). Curettage: Stone, Ramfjord (JP,66): Epithelium regeneration mainly from remaining cells of epithelial attachment and crevicular lining. Ramfjord, Nissle etal (JP 68, 32-25): One of the first split mouth studies, SubG curettage vs. surgery (OFD, gingivectomy) After 5 years most pts with curettage gained attachment, Surgery had greatest PD reduction but also loss of attachment. Stahl, Weiner et al (JP 71, 32-26): Romoval of crevicular epi not consistently achieved by curettag/RP. Epithelialization of crevice complete by 1 week v. 2-4 weeks w/ GV. Curettage reduced inflammation but returned in 8 weeks. Caton and Zander (JP 79, 32-28): Monkeys, Coronal attachment gains and increased resistance to probing following RP and curettage is due to long junctional epithelium formation. 142
Echeverria, Caffesse (JCP 83, 32-30): S/RP plus curettage does not predictably result in improved clinical parameters over S/RP alone in the treatment of shallow, suprabony pockets. Litch: You leave sulcular epithelium when you do inverse bevel incisions. Chemical Curettage: Kalkwarf et al (JP 82, 32-29): Sodium hypochlorite provides uniform and predictable pocket lining removal without anesthesia as well as antimicrobial effects. Forgas and Ground (JP 87): S/RP plus antiformin-citric acid curettage = to S/RP alone. OPEN FLAP CURRETAGE/OFD Ammons & Smith (DCNA 76, 32-2): REVIEW. Stimulates regeneration, inverse bevel initial incision, sulcular epithelium and granulation tissue removed with a curette. Lindhe (85): Granulation tissue removal not necessary for clinical success. (BOARD QUESTION) Ellegaard B & Loe (JP,71): With OFD full regeneration of intrabony lesions occurred in 72% of 3 -wall defects, 45% of 2 wall defects, and 40% of combined 3 and 2 walled defects. Not all re-entries. HEALING AFTER OFD Froum et al (JP,82): 2mm recession, 1.4mm A Level gain, 1.2mm osseous fill, 0.8mm crestal resorption, LJE formation these findings were repeated by Stahl, Froum, et al (JP,82) with the LJE formation. Listgarten, Rosenberg, and Lerner (JP 82): Rats, at as early as 3 weeks CT replacement of LJE after OFD. This has never been repeated with no real proof that CT and Cementum was removed during the procedure. Creeping attachment Kohler and Ramfjord (OS 60): 15 specimens 0f 14 pts. OFD, block section hopeless teeth. Results: 1) Flaps healed with no loss of attachment, 2) Foreign body (calculus, remnants of gauze, tooth fragments). Caton, Nyman, Zander (JCP 80): Monkeys, No new attachment occurred in monkeys treated with MWF, Autogenous graft, alloplastic ceramic graft, or root planing/curettage all formed a long junctional epithelium. Steiner, Crigger, Egelberg (JPR 81): No new attachment with conventional replaced flap surgery, healing by LJE. sometimes used as the control for the Cole et al (80) study using CA root chemotherapy. Karring, Isidor, Nyman, Lindhe (JCP 85, 32-14): Monkey study. Induced pdtis 50% bone loss, crowns reduced, RP, cementum removed, submerged lateral pedicle. New bone 2 mm. The epe and granulation tissue derived from the bone and gingiva must be excluded in order to obtain new fibrous attachment w/o root resorption. Attachment formed from the coronal migration of the PDL cells when the epi was excluded. HEALING FOLLOWING FIBER RETENTION PROCEDURE Stahl (JP 77, 32-24): Rat study. Removal of cementum & CT fibers result in LJE or deepened crevice with JE apical to preop postion. MODIFIED WIDMAN Ramfjord and Nissle (74): Described Original Widman Flap: 1 mm FGM, reflect beyond MGJ, curette tissue, APF, 1916, limited bony manipulation. MWF marginal scalloped incision parallel tooth axis, sulcular incision, then horizontal to remove tissue. FTF minimally, leave as much interproximal as possible. Bony contouring for IPX papilla adaptation. Good access, esthetics, optimal root coverage, LJE. Good procedure when minimal recession is desired. Ramfjord (77): 7 yr. follow-up, 105 pts, MWF compared favorably with pocket elimination surgery. Renvert, Nilveus, Egelberg (JCP 85, 32-22): S/RP vs. MWF and CA root treatment. 6 month results. CA with surgery was more effective in tx intraosseous defects than S/RP even though no sig difference. MWF HEALING Caton, Nyman, Zander (80): Monkey study showed no regeneration, LJE only Bone Denudation (Pushback) Procedure Wilderman, Wentz, Orban (60): Described healing after bone denudation procedure, generates attached gingiva
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Healing:0-2 days Clot formation. Polyband 2-10 days max osteoclastic, 10-28 days max osteoblastic, 28-185 days functional repair. Regeneration of all but 1/3 of bone. Complete regeneration of keratinized, alveolar mucosa. Long Term Effectiveness of Periodontal Therapy Meador (JP 89): Stability of tx over 22 yrs (mean 7.4 yrs). OFD 95%, MWF 91%, FO 71.6%, Nonsurgical 63.6% OSSEOUS SURGERY Osseous Resection: Pro: Olsen (85, 33-27): 12 pts, 5 yr. follow-up APF with and without osseous, initially the same, but long term osseous had maintained pocket reduction while APF alone had soft tissue rebound and increased inflammation (2.3 times as many 4+ bleeding sites). 6 month study done by Smith, Ammons, and Van Bell. Kaldahl (92): flap with osseous has long term maintainability and stability. Schluger (OS 49 33-10): Osseous resection leads to more stable and more maintainable dentitions Lindhe (84): 14 yr. study. Sites where FO was performed had less residual pocket depth. Only 0.8% had >2mm LOA. Selipsky (DCNA 76 33-14): Mobility back to baseline after 1 year POT, 0.6mm circumferential supporting bone removed after osteoplasty and ostectomy as an average of 6 sites per tooth, max 1.5mm. Bu and Li bone less important for tooth support than interproximal bone. (BOARD QUESTION) Con: Becker: Pts treated with pocket elimination without maintenance had recurrent disease. World Workshop: Osseous resection is indicated for 1) Thick bony ledges, Tori. 2) Tx of class 1 furcations. 3) Shallow 2 wall craters. 4) Shallow 1 wall (No GTR). 5) Crown lengthening. Physiologic Architecture: Schluger (OS 49, 33-10): Opinion paper of 10 yrs observation, Pocket elimination as the goal of surgery and since soft tissue form and depth ultimately depends on hard tissue, physiologic osseous contours must be attained to assist in pocket elimination. Ochsenbein: Bone does not influence the morphology of the gingiva, but rather the CEJ and interproximal spaces. Confirmed by Wirthlin (87) World Workshop: States we should not remove excessive bone to produce physiologic architecture. CLASSIFICATION OF INTRABONY DEFECTS Goldman &Cohen (JP,58): Classification of infrabony pockets Three osseous walls: A) Proximal, buccal, and lingual walls TX: curettage/ GV B) Buccal, mesial, and distal C) Lingual, mesial, and distal Two osseous walls: A) Buccal and lingual walls (crater) TX: osseous therapy B) Buccal and proximal walls C) Lingual and Proximal walls One osseous wall: A) Proximal wall (hemiseptal) TX: osseous therapy B) Buccal wall C) Lingual wall Combinations A) 3 walls + 2 walls B) 3 walls + 2 walls + 1 wall C) 3 walls + 1 wall D) 2 walls + 1 wall Four osseous walls (circumferential)- Buccal, Lingual, mesial and distal Tal (JP 84 3-16): 100 mandibles, 4.1% incidence of intrabony defects, 2 walled defects most common (50%) also when inter-root distance increases 2.1-4.1, so does incidence of intrabony defects. Karn (JP 84 3-15) Classified defects as moats ramps craters trench etc. OUTCOME VS DEFECT MORPHOLOGY Renvert et al . (JCP 85): 51 pts, many combinations of osseous defects, Surgery of OFD, RP/SC, CA (3 min):
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results: Tx outcomes based on the # of walls of osseous defect, the defect circumference, and the number of tooth surfaces involved showed little or no relationship to bone fill. Steffensen & Weber: (JP,89) Most defects with an angle less than 45 o showed a gain of bone (31% fill) while largest defects angles showed a loss. OSSEOUS Techniques Ochsenbein & Bohannan (JP,63): Palatal approach to osseous surgery. Advantages: elimination of reverse architecture, less denudation of buccal radicular surfaces, and less buccal recession and furca exposure. Ochsenbein & Bohannan (JP,64): Crater Classification: A. Class I Crater: 2-3 mm, thick B & L walls; TX: Remove palatal wall of deformity B. Class II Crater: 2-5 mm, wide orifice and thinner wall abrupt slope to base: Tx: Remove palatal some buccal C. Class III Crater: 6-7 mm, concavity with sharp drop to broad, flat base D. Class IV Crater: variable depth with extremely thin buccal and palatal walls- base wider buccolingually Tibbets, Ochsenbein (DCNA,76): Lingual approach to osseous resection, watch for lingual artery/nerve, mylohyoid ridge. Rationale: 1) 25o lingual inclination, thus crater more lingual, 2) Lingual embrasures wider than buccal, 3) Reduction of lingual bone is osteoplasty vs. ostectomy from the buccal, 4) Buccal is usually overtreated, 5) Lingual furcation is more apical than buccal furcation, 6) Lingual CEJ's are lower apically on the tooth and since bone follows the CEJ, natural slope lingually. OSSEOUS SURGERY: WOUND HEALING Wilderman, Wentz, Orban (JP,60): dog study: Epithelial migration finished after 10 days. Bone formation greatest at 21-28 days. Bone resorption even with periosteum in place. Preparatory phase (0-2 days) Osteoclastic phase 2-10 days. Osteoblastic phase 10-28 days. Maturation / functional repair 28-185 days. (BOARD QUESTION) Where does granulation tissue come from? Pennel, Wilderman (JP 67 33-21): Clinical, Mean bone loss with osseous 0.54 mm, (range 0 to 3.8 mm) 82% loss 48 hours Golub et al (Current Opinion 94): Anticollagenolytic effect Terranova (JPR 86, 34-19): Human epi on dentin slabs. TCN 50-100 mg/ml for 5 mins, followed by application of FN could lead to attachment of fibroblasts and decreased attachment of epi cells due to binding of LM. TCN & CA reduced epi attachment. Terranova et al (JP 87, 34-20): TCN promotes fibroblast adhesions and growth. PDL cells migrate toward FN which is enhanced when dentin tx’d with TCN. Gingival epi cells had increased proliferation and migration when dentin tx’d with LM. 1st to use AFSCM (assay for specific cell migration). Stabholz et al (JP 93): TCN-HCL at 50 mg/ml had a greater antimicrobial activity than CHX for 22 days. 50 mg TCN displayed antimicrobial activity out to 14 days; CHX only for 24 hours (BOARD QUESTION) Smith Caffesse (JCP 87, 34-21): Dog. Use of combination of FN and LM in new attachment procedures not justified. LM may inhibit LM. Guided Tissue Regeneration: Parashis and Mitsis (JP,93): No additional effect of tetracycline root preparation on GTR in the treatment of Class II furcation defects. Application articles: Hanes et al (JCP,91): 5 min immersion of CA (pH 1) gave much better smear layer removal than 0.5% (5 mg/ml) TCN Wikesjo et al (JPR,86): Bovine teeth, immersion 1-10% TCN solution (10-100mg/ml) gave the best results. Demirel et al (JP,91): Used human dentin and cementum, doxycycline, 50 mg/ml solution inhibited bacterial growth for 7 -14 days, 100 mg/ml inhibited growth for 14 days. Desoxycolate: Assad, Dunlap (JP 87, 30-7): Findings suggest desoxycholate/plasma combination enhanced in vitro fibroblast attachment to Ds’d root surfaces. Antiformin: Lasho (JP,83):
a) Solution of hypochlorite, sodium hydroxide & sodium carbonate (Nebraska) b) Very caustic agent (pH 13-14) c) Originally used for chemical curettage, destroying pocket epithelium d) No known damage to the CT e) Used to detoxify root- endotoxin removal f) Applied for 5 min, then neutralized for 30 sec with citric acid
Fibronectin: Terranova et al (JPR 86): TCN-HCL and fibronectin as treatment produced a four-fold increase of # of attached fibroblastic cells over untreated slabs. Caffesse et al (JP 87, 34-25): Faster healing with the combination of CA and FN enhancing cellular proliferation. Alger et al (JP,90): Histology, Tx of human roots with TCN or TCN + FN during periodontal surgery did not result in new attachment. The addition of fibronectin actually appeared to inhibit CT attachment. Ripamonti et al (JPR 87, 34-22): Potential for CT attach and bone regeneration is enhanced if planed and CA tx’d roots are additionally tx’d with specific attachment glycoproteins and plasma factors.
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Peltzman, Bowers, Reddi (JP 88, 35-14): Human bilateral furcations on Mand molars, AUTOG vs. AUTOG + FN. AGAIN equivocal for both groups. FURCATION MANAGEMENT Furcation Classifications Goldman: Incipient, Cul de Sac, Through and Through Glickman: Grade: 1= detect 2=moderate 3= through & through 4= Exposed and can see through Hamp: Degree: 0= no Horizontal penetration 1= < 3mm penetration 2= >3mm penetration 3= through & through. Ramfjord: 0= no penetration 1= < 2mm penetration 2= >2mm penetration 3= through & through. Tarnow and Fletcher: Class 1, Subclass A 1-3mm Vertical Component Class 2, Subclass B 4-6mm Vertical Component Class 3, Subclass C +7mm Vertical Component Lindhe: 1/3, >1/3 but not through and through, through and through. Hamp based treatment on Lindhe’s classification. Anatomy Herman and Gher (83): Attachment area of roots. Root trunk 31%, MB 25%, P 24%, DB 19% Ross and Evanchik (81): 29% of all molars had fused roots, 35% max 24% Mand Hou and Tsai (JCP 94): 33% of all teeth with fused roots; 42% max, 24% man Prevalence and Distribution Tal (JP,82): Furcation involvement 85% of 100 pts (untxd south Africans) FI increases with age, 1st molars most common. Tal (JP,82): Correlation between depth of furcal defects and distance from the CEJ and alveolar crest, 5-6 mm suspect CL III Ross and Thompson (JP 80 18-20): 615 molars from 72 perio pts, 90% FI in maxilla and 35% in mandibular, only 22% of max furcations could be diagnosed solely with X-rays. Larato (JP 70 18-13): 305 Mexican dry skulls, FI increases with age, 1st molars most common (max more than Mand), buccal more than lingual/ palatal. Incidence related to length of time in mouth, decreases as more posterior except premolars. Svardstrom (JCP 96 1093) Highest frequency of furcation involvement is the distal of MX 1 st molar (53%). Lowest frequency of furcation involvement is the mesial of the MX 2 nd molar (20%) Etiology
Kalkwarf & Reinhardt (DCNA 88, 18-14):Review 1. Anatomic factors: carious lesions, restorations, furcation morphology-width, shape, root trunk length 2. Enamel projections: role as contributing factor uncertain 3. Occlusal trauma: still may be controversial Waerhaug (JCP 80, 18-16): Plaque is the main contributor, subG plaque even in areas where no supraG plaque was evident, GI and PI do not reflect actual level of destruction of furcation, loss of attachment did not increase with increasing mobility.
Contributing Factors to Furcation Involvement: (1) Root Concavities: Bower (JP 79 18-15): Furcation root surface anatomy
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1. Max 1st molar teeth furcal aspect of root concave 94% MB, 31% DB, 17% P deepest concavity was in the MB root- mean concavity 0.3 mm furcal aspects of buccal roots diverge toward the palate in 97%, divergence 22° 2. Mand 1st molar teeth furcal aspect of root was concave 100% M, 99% D deeper concavity on M root (0.7mm), D root (0.5mm) concavity presence of more cementum Gher and Vernino (JADA,80): Max 1st premolars - groove furcation side buccal root 78%, 1st Max molars concave facial side of MB, Mand have M and D concavities. (2) Cervical enamel projections Masters and Hoskins (JP 64 9-21): CEP Mand 28.6%, max 17%, 90% of Mand furcations associated with CEP’s. (BOARD QUESTION) Grade I - CEP very slightly extending from CEJ Grade II - CEP approaching furca Grade III - CEP extending into furca Leib, Berdon, Sabes (JP 67, 9-22): CEP’s: maxilla: I>III>II, Mand. I>II>III. No correlation between CEP presence and furca involvement. 22% maxillary molars and 25% mandibular molars, 4% are class 3s. Hou and Tsai (JP,87): 1. CEP’s in all molars 45.2% 2. CEP’s in molars with furcation involvement 82.5%, Mand 1st molar most common (all other studies suggest CEP’s more common in 2nd molars), 1st Max, 2nd Man, 2nd Max 3. Chinese 2X more prevalent than Caucasian population Swan and Hurt: Significant relationship between tooth surfaces with grade II and III furcations and CEP’s, (3) Accessory Pulp Canals Gutman (JP 78): 28% in furcation region; 24% in furcation only (BOARD QUESTION) Lowman (OS 73 20-8): 59% Navy study treat perio 10-12 weeks after endo treatment Vertucci 46% Burch and Halen: 76% (4) Bifurcation Ridges Everett (JPR 58): bifurcation ridge is present 73% Mand 1st molars running M to D at the midpoint of bifurcation (5) Root Trunk Length (6) Width and Location of Furcation Entrance Wheeler (Text 68): Furcation entrances, location from CEJ Max 1st molar Man 1st molar mesial 3mm buccal 3mm buccal 4mm lingual 4mm distal 5mm Bower (JP 79 18-15): 1. Mean M-D width max 1st molars was 7.9 mm, Mand 1st molars was 9.2 mm 2. 81% of all furcations have entrance diameter 1.0 mm, 58% the diameter was 0.75mm or less. 3. Extremely low correlation between M-D width of tooth and furcation entrance diameter 4. Blade face width of the curettes tested were within 0.75 mm to 1.10 mm . Hou and Tsai (94): Furcation entrance means Max 1st molar Max 2nd molar Man 1st molar Man 2nd molar Buccal 0.74mm 63mm Buccal .88mm .73mm Mesial 1.04mm .90mm Lingual .81mm .71mm Distal 0.99mm .67mm
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Diagnosis Zappa et al (JP,93): Using Ramfjord and Hamp indexes, Overestimation of furcation defects Mealey et al (JP,94): Bone sounding with anesthesia significantly improves the diagnostic accuracy of furcation invasions as compared to standard probing techniques. (Vertical and horizontal) If no anesthesia, tend to underestimate by 1-1.5 mm. (BOARD QUESTION) Kalkwarf (DCNA,88): Diagnosis not complete until surgical access. TREATMENT MODALITIES FOR FURCATIONS: S/RP, furca obliteration, GV, APF, Osseous, tunneling, root amp, bicuspidization, hemisection, GTR Non-surgical therapy Loos et al. (JCP,89): In sites of > 7 mm regressed after initial tx, Overall 25% of molar furcation sites demonstrated loss of attachment compared to 7% for non-molar sites and 10% of molar flat-surface sites. Badersten: Non-surgical therapy works, but in non-molar teeth only. Nordland (87): Furcations with initial pocket depth > 4mm had poorer response to non-surg therapy verses flat molar and non-molar sites. 0.5mm loss in 24 months Leon and Vogel (JP 87 18-18) Compared hand and ultrasonic scaling in furcations Class I No difference between modalities Class II and III ultrasonic scaler better. Parashis (93) Calculus removal in furcations best with open scaling and rotary diamonds (BOARD QUESTION) Bower (JP 79 18-15) Width of furcation entrance is too narrow for most scalers Tunnel: Little (JCP 95): 18 pts with 5 max and 13 man furcas txd by tunneling. Adjacent teeth were used to evaluate bone loss. After 5 yr., 3/18 had developed root caries. No difference seen in CAL or bone loss when compared to adjacent teeth. Hellden, Steffensen et al (JP,89): 149 teeth with Grade III furcations at 3 yrs, 75% caries free. Hamp, Nyman, Lindhe (JCP,75): Tx of teeth with furcations revealed the following 5 yr. results: 1. 44% of the teeth were extracted during initial treatment 2. 50% of the remaining teeth received root resections , one root preserved 64% of the time ,none of the teeth were lost in 5 yrs 3. Tunneling procedure had root caries 4/7. Root Amputations: Consider implants, may have better long term success Langer et al (JP,81): 10yr, 100pts, results are as follows for resected teeth: 38% of resected teeth failed by 10 yr. mark (62% success rate), 15.8 % in 5yr. Of the failures: 1. 47% (greatest number of teeth) failed due to root fractures (BOARD QUESTION) 2. 26.3 failed to progression of perio, most were maxillary molars 3. 18.4% failed to endo 4. 7.9% failed due to cement washout Erpenstein (JCP,83): 3 yr. hemisections, 6/34 failed due to endo, 1 failed due to perio. Suggests favorable prognosis for hemisections, but these resections were sometimes done without surgical access and no osseous recontouring was performed. Carnevale et al (IJPRD, 91): 500 teeth with either root amps or hemisections. Overall 5.7% failures, highest being caries and root fractures, 97.6% of these teeth were treated for periodontal reasons, only 0.6% had recurrence of periodontal breakdown. Buhler (IJPRD,94): 337 cases, 7 yr. period of hemisection, reported failure rate of 13.1%. Klavan (JP,75): Mean 38 month follow-up study of primarily DB root amps. Only 3/33 teeth showed an increase in mobility after the root amp. The removal of one of the roots of a maxillary molar does not increase the mobility of the tooth in normal function or contribute to increased PD. Splinting does not seem to be necessary. FURCATIONS - LONG TERM MAINTENANCE STUDIES
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Pearlman (JP, 93): 172 pts classified similar to Hirschfeld and Wasserman with similar breakdown of results. Finding was that even in the well maintained group, there were more molars lost with furcation involvement over those without involvement. Hirschfeld, Wasserman (JP 78 19-17): 22 yr. maintenance study of 600 pts. 1. 31% of teeth with original furcation invasion were lost 2. Breakdown of teeth lost according to groups WM 19.3%, D 69.9%, ED 84.4% 3. Average overall tooth loss by patient groups WM 0.68, D 5.7, ED 13.3 4. Order of tooth loss: Max 2nd, Max 1st, Mn 2nd, Mn 1 st (BOARD QUESTION) 5. 300 lost no teeth, 199 lost 1-3 teeth, 76 lost 4-9 teeth, 25 lost 10-23 teeth 6. Mortality of teeth correlated more closely to case type rather than type of surgery 7. Periodontal disease is symmetrical PATIENT PERCENTAGES Well Maintained 83%, Downhill 12.6%, Extreme Downhill 4.2% (BOARD QUESTION) Ross and Thompson (JP 78 18-20,21): 100 pts treated with 387 furcas,. Conservative treatment only OFD, no resection (BOARD QUESTION) or osseous treatments, 5 yr. Minimum follow up, 88% of teeth were functioning after 5-24 yrs, (BOARD QUESTION) radiographs were the only diagnostic tool of success. Max FI three times that of Mn. Max furcas detected most frequently by radiographs, MN furcas detected most frequently by clinical exam. McFall (JP 82): 100pts in maintenance for 15 yrs. 57% of teeth with initial furcation involvement were eventually lost (BOARD QUESTION) with 25% being lost in the well maintained category. Avg. overall tooth loss: WM 0.68, D 6.7, ED 14.4 Goldman, Ross (JP,86): 211 pts, 15-34 yrs with maintenance. 1. Furcation teeth lost WM 16.9%, D 66%, ED 93% 2. Avg. overall tooth loss: WM 1.0, D 5.8, ED 14.2 Becker studies (JP 89): No therapy group: 31% furcations became involved at second exam 5 yr. 22% furcations got worse at 5 yrs. Therapy w/maintenance: 22% furcations became involved at second exam 5 yr. 12% furcations got worse at 5 yrs. Kalkwarf, Kaldahl, Patil (JP 88 18-22): 82 pts, 1394 furcations, teeth were tx with CS, RP, MWF, F/O teeth were extracted, resected, hemisection, if bone loss past apex or bony architecture not corrected. 2 yr. - F/O had less breakdown than other tx , but several more teeth taken out in the group 5 yr. - Less breakdown with F/O (4.1%) although overall the other therapies haven’t caught up with total extractions BL: FO does better if one can create a positive architecture otherwise the MWF or OFD may be the better treatment as far as tooth loss goes Wang (JP 94 19-28): 24 pts 8yr study with 3 mo recalls. Molars with initial mobility showed greater LOA than ones without mobility. Molars with furcation involvement also showed greater LOA over this time period than molars without furcal involvement. Summary of the above studies stresses the importance of maintenance in pts with FI and that the majority of tooth loss occurs in a minority of pts. BONE GRAFTS GOALS OF OSSEOUS GRAFTING: Schallhorn (JP 77, 35-1): Review 1. Pocket reduction/elimination 2. Restoration of lost alveolar process 3. Regeneration of functional attachment apparatus GREATEST INDUCTIN POTENTIAL WITH ILIAC AUTOGRAFTS. Advantages: reconstruct lost periodontium, idealistic therapy, reverse disease, tooth support, better esthetics and improved function. Disadvantages: longer tx, autograft disadvantages, availability of graft material, more post-op visits, lost post-op tx eval, $$, multi-step, recurrence.
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FUNCTION OF A BONE GRAFT 1. Provides viable cells, hip graft best 2. Osteoinduction form bone in a non-bone forming site (non-orthotopic site) Hip, DFDBA best 3. Osteoconduction form bone in a critical size defect 4. Epithelial exclusion 5. Clot enhancement (Polson and Proye in CA studies) 6. Space maintenance. Don’t pack material too tightly need space for vascular ingrowth 7. Enhance cementum formation 8. Enhance formation of new attachment PROPERTIES OF AN IDEAL GRAFT 1. Viable cells 2. Osteoinductive 3. Osteoconductive 4. Physically stable 5. Replaced or incorporated by host DFDBA is not resorbed No mechanism for resorption of Type I collagen. Eventually turned over with collagen metabolism. Hip bone lasts 3-5 years. 6. Safe 7. Unlimited Supply 8. Enhance new attachment 9. Clinically effective INDICATIONS FOR GRAFTING 1. Deep intraosseous defects which cannot be adequately treated by other methods 2. To retain a critical tooth 3. Juvenile periodontitis 4. To reduce post op recession PROBLEMS WITH GRAFTING 1. Additional time 2. Logistical problems of donor site and material quality 3. Post op care 4. Longer post-op treatment evaluation time RESPONSES TO GRAFTING Active Bone Formation: Bone cells survive and form bone. Possible only with iliac fresh graft Osteoinduction: BMP proteins etc. which induce chemotaxis of mesenchymal cells/ bone precursor cells Osteoconduction: Lattice which allows migration, resorption, bone formation (collagen matrix important for bone formation). Bone Principles Endochondral vs. Intramembranous Urist (CO 67): Bone induction principle cell differentiation caused by physiochemical effect of one tissue on and in contact with another. BMP is protein derivative from mineralized matrix tissue. Earliest deposits of new bone in 24-26 days. Reddi (OCNA 87): 3 phases of bone induction, 1. Chemotaxis - activation and migration of mesenchymal cells aided by fibronectin (anchorage to cell matrix), 2. Mitosis and proliferation of mesenchymal cells. 3. Differentiation and mineralization of cartilage followed by vascular invasion, and osteoblast differentiation, followed by matrix mineralization in 10-12 days.
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Types of Grafts:
1. Autograft Same Individual Cortical bone chips, Osseous Coagulum Bone Blend Cancellous bone 2. Allograft Genetic Difference/ Same Species 3. Xenograft Different Species 4. Isograft Identical Twins (Nyman) 5. Alloplast Synthetic 6. Syngenisograft Allograft Between Blood Relatives 7. Brephoplasiograft Fetal Tissue. Graft: Tissue/organ for transplant/implantation, living tissue. Implant: Material placed under mucosa/periosteum or within bone for functional, therapeutic, esthetic purposes, inert tissue. Transplant Denotes living tissue e.g. iliac crest
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AUTOGENOUS AND ALLOGENIC BONE GRAFTS Study
Bone Type
Defect Type
mm Of Increase
Eval Method
Schallhorn, Hiatt et al (JP 70, 35-15)
Fresh/Frozen Iliac Autographs
Crestal
2.57 mm
Sounding/Re-Entry
1-Wall 2-Wall Furcations Crestal
3.75 mm 4.18 mm 4.50 mm 2.06 mm
Sounding/Re-Entry Sounding/Re-Entry Sounding/Re-Entry Re-Entry
Infrabony Furcations Infrabony
3.62 mm 3.30 mm 3.44 mm
Re-Entry Re-Entry Sounding/Re-Entry
Furcations Crestal
0.7 mm
Complete Fill Rare Sounding/Re-Entry
Intrabony
2.1 mm
Sounding
Schallhorn, Hiatt, (JP 72, 35-20) Hiatt, Schallhorn (JP 73, 35-9) > Fill With More Walls Dragoo, Sullivan (JP 73, 32-17)
Frozen Iliac Allograft Intraoral Autografts Fresh Iliac Autograft
Hiatt & Schallhorn (JP 73, 35-9): Intraoral transplants of cancellous bone & marrow in perio lesions. 40 pts/166 human defects autogenous bone from tuberosities, healing ext sites and edentulous areas. Mean of 3.44 mm fill reentry. Surface area of cancellous bone more desirable than cortical bone. Occasional sequestration seen. Adequate soft tissue coverage & large area of vascular bony walls imp for success. Furcation less predictable. Greatest fill came from defects with the most walls. Equivocal Results: Peltzman, Bowers, Reddi (JP 88, 35-14): Human bilateral furcations on Mand molars, AUTOG vs. AUTOG + FN. AGAIN equivocal for both groups. Renvert (JCP 85, 35-13): Human clinical, 1 yr f/u. Healing after tx of perio intraosseous defects. III. 19 pts/53 defects with PD > 6 mm. Used CA with or without autogenous bone. Used stents with standardized probings. Limited differences are noted. 1.1 mm probe gain. NO histo, all clinical measurements, no re-entry and 3 different operators. Both therapies resulted in approximately 1 mm gains in probing attachment and probing bone levels. PD 1.9 mm Bone levels: CA 0.8 mm CA + Autog 1.4 mm ILIAC GRAFTS Most osteogenic material yet. Problems include: difficulty in obtaining graft, root resorption (keeps going), morbidity,2nd surgical site, sequestration, $$. Hiatt (JP 78, 36-31) Root resorption (1-20%). Dragoo, Sullivan (I) (JP 73, 32-17): 13 pts, 4 histo, grafted with fresh autogenous iliac marrow, 1 case was ankylosis, 2.1 mm increase by sounding, 2 months cementum, 3 months PDL, osteoblastic activity > 2 months and < 8 months. (0.7 mm crestal bone) 1.03 mm new CT, 1.34 mm new epi attachment. Dragoo, Sullivan (II) (JP 73, 30-18): 4 cases, 7 teeth with root resorption (2.8% root resorption), 250 autogenous fresh iliac bone grafts. Detected at 3 weeks. Rads should be taken monthly. Burnette (JP 72) Root resorption occurs most frequently at 2 months post-operatively. Schallhorn & Hiatt (JP 70, 35-15): Iliac transplants in perio tx. 52 pts/182 autogenous iliac cancellous & marrow implants into 1-, 2-, 3-wall, furcation and crestal defects. Some were fresh and some were frozen. Reentry. 2-wall defects filled. Crestal mean increase if 2.57 mm, 7/8 furca 100% fill. Avg. Increase bone height 3.33 . 1-wall 3.75 mm, 2-wall 4.18 mm. 2 cases of root resorption from fresh grafts. Schallhorn (JP 72, 35-16): Lecture. Post-op problems assoc. w iliac transplants. Recommends prophylactic use of antibiotics, sequestration is most common problem, don't overfill, root resorption may be due to viability of cells. Cover. Important to evaluate and monitor pt's plaque control. Root resorption may be related to mobility.
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Piatelli, Degidi, Marchetti, Scarano (IJOMI 97): Case report, block resection following recurrence of tumor. Nonvascularized iliac block graft may be used to augment the deficient mandibular ridge prior to implant placement. RAMUS AND SYMPHYSIS GRAFTS Misch (IJOMI 97): Ramus and symphysis grafts are associated with low morbidity, minimal resorption and heal in 4-6 months. Ramus Graft - min pt concern for altered facial contour, lower incidence of incision dehiscence, decreased complaints of postop sensory disturbance and proximity to posterior mandible recipient sites. Symphysis Grafts - potential for thicker grafts with increased cancellous component. ILIAC ALLOGRAFTS Not used today due to strong possibility of disease transmission Schallhorn & Hiatt (JP 72, 35-20): 1st report, greatest osteogenic potential of any graft material, crestal bone apposition potential (mean 2.57 mm). Results not as good as with autogenous iliac grafts but still very good (3.07 mm bone fill overall, intrabony = 3.62 mm, furcations = 3.30 mm). CORTICAL BONE CHIPS: Nabers and O'Leary (JP 65, 35-5): 1st published case in US. 8 case reports. Cortical bone chips obtained during ostectomy and osteoplasty (2-4 mm) used as successful graft material. No histo, just probing depth reduction: disadvantage: sequestrum of large particles and low osteogenic potential. However Nabers (JP 72) showed histo 57 months post-op of with new vital bone. Langer (JP 81, 35-19): Human case report. 5 yr histo eval, reentry at 3 months, root Fx and block section at 5 yrs. Early reentry of autogenous grafts for evaluation and physiologic recontouring is possible without significant compromise to the ultimate success of the graft. Long term clinical success with cortical bone. Friedlaender (76): Cortical bone less antigenic than cancellous bone (tested in rabbits) Urist et al (70,73): Cortical bone has a higher concentration of bone inductive proteins. Kucaba and Simpson (JDR ,78): max tuberosity is questionable source for autogenous bone grafts, little marrow. HISTO OF AUTOGENOUS GRAFTS Moskow, Karsh et al (JP 79, 35-10): Histo of single case of grafted cancellous intraoral bone, 28 wks after grafting, showed fibrous encapsulation with a LJE, repair not regeneration. New bone was found but the epi interposed b/t it, new attachment present at base of defect. Moskow used to clean roots with soap b/f putting in graft—this would leave surface coating on tooth that would be the death of fibroblasts. BOWERS: “BONE NOT PREPARED CORRECTLY.” Wound Healing in autogenous bone grafts Sullivan and Dragoo (76) 1) new bone seen at 7 days 2) Cementogenesis 21 days 3) New PDL at 3 months 4) By 8 months functionally oriented fibers but maturation may take up to 2 years OSSEOUS COAGULUM: Robinson (JP 69, 35-6): Osseous coagulum (burs and blood) reentry 6 pts, smaller particles more effective in resorption and replacement, osteogenesis and fill of furcations. Overpack the defect. BONE BLEND: Difficult to harvest enough bone for grafting Diem & Bowers et al (JP 72, 35-7): Describes technique. Bony fragments can be reduced to useable consistency using an amalgam capsule w/ trituration for ~60 secs to consistency of a slushy mass. Eliminates problems association w. ossious coagulum. Froum (JP 75, 35-8): Human histo. 1st human histo. 3 cases osseous coagulum/BB placed in intrabony defects on anterior teeth, block sections 6, 9 & 13 wks. Perio remodeling of graft, regeneration of bone and cementum, marked increase in cementogenesis at graft sites and variations in parallel or functional orientation of PDL, 2.4-3.4 mm osseous fill.
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Froum et al (JP 76, 36-29): Osseous Coagulum/Bone Blend gain 2.98 mm (70% fill) vs. OFD .66 mm fill (21% fill) Lekovick (91): Periosteal grafts vs. OFD in Mand Class 2 furcas, more horizontal fill, attach gain PD reduction with graft Hiatt and Schallhorn (75): Intraoral cancellous bone (3.4 mm bone fill) Also Rosenberg (71): 400 pts. Froum (1975): equally effective as iliac marrow. Schallhorn, Cushing: Extra-oral cancellous bone(iliac) Froum et al (JP,75): Histo intrabony defects with autogenous bone-blend, new cementum, bone, PDL. Ahl (1980): Zaner, Yukna (JP 84, 36-2): 300-500 m (380 m) sized particles optimal to permit 100 m space for vascularization, minimize macrophage response, promote osteogenesis. EXTRACTION SOCKET: Evian (JP 82, 35-11): 2 phases of bone regeneration: 4-8wks - progressive osteogenic phase with proliferation of osteogenic cells and immature bone formation. 8-12 wks - mature bone present and osteoblasts and osteoid are in less quantity that at 4-8 weeks. A core removed at 8-12 weeks contains a combination of both types of tissues. The healing socket can be used form 8 to 12 weeks after extraction. (BOARD QUESTION) Sohren (79): Fatty marrow in retromolar/ tuberosity region. The best place to obtain bone for graft is healing extraction site 8wks max, 12 wks Mand BOWERS FAVORITE Bowers bone grafts are ok in extraction sockets if the socket is not intact Boyne healing of extraction socket can prove anything depending on where you take the biopsy, if you want to get a sample that shows healing, take it from the bottom or sides. If you want to show no healing, take it from the middle. BONE SWAGING PROCEDURE Ewen (65): “Bone Swagging”, no flap Zubrey, Kozlovsky (JP,93): Human Histological case report, new bone was seen, however epithelial migration between the tooth and graft area was seen but not to the base, no evidence of new cementum with disorganized PDL fibers, probing depths were reduced but that didn't necessarily mean regeneration had taken place. LONG-TERM RESULTS, AUOGENOUS GRAFTS Nabers (INPRD 84, 35-12): No histo, 1-, 2-wall defects most 7-9 mm defects radiographic documentation up to 25 yrs. Criteria for success: uncomplicated MxHx, pt understanding of procedure, proper Dx, occlusal adjustment PRN, aseptic technique, proper initial prep, Ab coverage, flap design, defect prep, root prep, vascularization improvement, proper graft placement, suture for primary coverage, dressing change and H2O2, post-op rads, possible tissue recontouring to eliminate food impaction and maintenance. Don’t probe 6-9 months. Langer (JP 81, 35-19): Human case report. 5 yr histo eval, reentry at 3 months, root Fx and block section at 5 yrs. Early reentry of autogenous grafts for evaluation and physiologic recontouring is possible without significant compromise to the ultimate success of the graft. Long term clinical success with cortical bone. CORONAL FLAPS Gantes (91): Class 3 furcations, citric acid and coronally positioned flaps with moderate results. Gantes (88): Coronal flap and DFDBA vs. coronal flap. 30 defects. Similar results for both 1.6 vs. 1.5mm attach gain with 44 and 43% complete closure. Questionable results. Garrett (90): Coronal flap and DFDBA vs. Dura mater and DFDBA, 31 defects, 2.2mm vertical fill for both, Coronal flap and DFDBA had 2.7mm horiz fill vs. 1.8mm for Dura mater and DFDBA. 56% complete closure with coronal flap and DFDBA vs. 20 for Dura mater and DFDBA. XENOGRAFTS Neilson (JP 81) Bovine bone Vs. Autogenous both did fairly well. DFDBA/FDBA
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Developed at Naval Dental School. Navy Tissue Bank started to deal with injuries from the Korean War. Freeze drying allows the water in the tissue to move directly from the solid state to vapor bypassing the liquid state (sublimation). Lyophilization synonymous with freeze drying. Preparation of Bone Grafts Urist AAA bone = Autolyzed, Antigen extracted, Allogenic Harvested, ground, demineralized with 0.6 N HCL, methanol + chloroform extracts, wash with phosphate buffers/enzyme inhibitors, final grind, sifted, (Sublimation) freeze drying Reddi: HCL demin, ethanol + anhydrous diethyl ether, final grind, freeze dried. Musculoskeletal Transplant Foundation: Procession of DFDBA 1) Cortical bone harvested in sterile manner-long bones-cortical less antigenic 2) Rough cut- 500 um to 5 mm efficiency of defatting bone and decalcification 3) 100% Ethyl alcohol 1 hour to remove fat, inhibits osteogenesis, inactivates virus 4) Frozen (-80 o C) for 1 to 2 weeks, analyzed bact cultures, serology, antibody assays 5) Freeze drying - remove 95% H20, kills all cells, reduces antigenicity 6) Ground to particle size 250 - 750 um, below 125 um foreign body response 7) Washed 100% ethyl alcohol to remove chemicals (permeon, nonionic detergent) 8) Decalcified with 0.6 N HCL to remove Calcium, leaves bone matrix and expose bone protein 9) Washed Sodium Phosphate Buffer to remove residual acid 10) Re-freeze dried 11) Vacuum sealed. FDBA:
Mellonig (1976): 1st large scale study, 6 month reentries in 971 defects. 64% of defects 50+% fill (24% complete); 24% partial fill Sepe, Bowers, et al (JP,78): FDBA (100-300 µm) placed by 53 periodontists in 109 pts with 231 sites189 re-entered @ 1yr > 50% fill in 60%, (67% without furcations, furca had poorer response) better with intramarrow penetration & 1° closure. Altiere et al (JP 79, 36-31): Lyophilized bone allografts (FDBA) vs. control OFD, showed no significant difference. note the allograft was subject to 3 million rads of radiation. ANTI-BONE GRAFT Yukna, Sepe (1980): FDBA + TCN (4:1) in LJP patients, - 98% defects (61/62) 50% fill - mean bone increase 2.8 mm; 72% defect fill Sanders, Sepe et al (JP 83, 35-22): Large scale Navy, 48 dentists, 381 sites comparing FDBA and FDBA/autogenous (bone blend mostly); 50% fill 63% defects w/ FDBA vs. 60% of Sepe & Bowers (JP 78). > 50% fill 80% of combination graft sites (FDBA + autog) also better success with antibiotics 85% vs. 38%, lesser results with RCT teeth. Horning favorite. Evans and Yukna (JP 89, 35-23): 10 JP pts with bilateral defects. No controls. TCN locally and systemically can be used safely with allografts and alloplasts in the treatment of osseous defects associated with LJP. Reentry. FDBA, Periograft (HA), Synthograft (-TCP) all 65% fill.
DFDBA: “Superior grafting material in use today” Bowers, 1989 Urist (65): DFDBA in heterotropic sites will form bone (rabbits, intramuscular), hypothesize BMP in bone matrix. Urist (67): Freeze drying of cortical bone graft induces new bone formation and enhances osteogenic potential Urist and Strates (71): demineralization is necessary because bone mineral blocked the effect of the chemical inductive agent Libin (1975): 3 cases with FDBA, 4 mm mean clinical attachment, 4-10 mm new bone on reentry. Harakas (84): DFDBA induces the host stem cells to differentiate into osteoblasts Quintero, Mellonig (JP 82, 35-26): 27 defects in 11 pts grafted with DFDBA (250-500 m)and reentered 4-6 mon. 1-wall defects gained 2.6 mm (61%), 2-wall 1.8 mm (62%), 3-wall 2.9 mm (73%), overall 2.4 mm (65%). More walls=more bone. Mean probing attachment gain of 1.9 mm. DFDBA has some potential for osseous regeneration. Some crestal apposition. No controls Mellonig (JP,84): 47 defects treated with either OFD or DFDBA, re-entry:
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50% fill 78% defects w/ DFDBA Treatmen t
PD
REC
AGAIN
OFD
2.86 mm
1.3 mm
1.5mm
DFDBA
3.1 mm
0.2 mm
2.9 mm
bone fill
> 50% fi ll
1.3 mm (38 %) 2.6 mm (65 %)
40% 78%
Garrett (JP 88, 35-29): Tx of intraosseous perio defects w combined adjunctive tx of CA, bone grafting, & placement of collagenous membranes. All clinical. 25 defects/21 pts. DFDBA + dura mater and CA. Limited success with TX. Gain 1.8mm year. Dura resorbed too fast. Limited success may be explained by the difficulties in obtaining adequate wound closure in most human situations. Dura mater may transmit disease. Creutzdeldt-Jacob. OSTEOGENIC POTENTIAL: BOWERS FAVORITE Mellonig, Bowers, Bailey ( JP 81a, 35-1): Critical size calvaria guinea pigs, tested osteogenic potential of: autogenous, osseous coagulum, autogenous bone blend, DFDBA, and FDBA implanted in nylon chambers and placed in calvaria, used strontium 85 (concentrates in new bone and can be used as a measure of the rate of new bone formation. Results: the rate of new bone formation in the presence of DFDBA increased rapidly from day 14 to 28 then declined. This was much more rapid than other graft materials. The following order for materials: DFDBA>>Osseous Coag=Oss BB>FDBA>control. Mellonig, Bowers, Cotton (JP 81b, 35-25): Same M&M as above except determined new bone formation histology with the above mentioned graft materials and in guinea pig calvaria. The results again showed DFDBA>Oss Coag=BB>FDBA. Bone formed with DFDBA 1 st and increased rapidly from 14-28 days. Mellonig et al (80): composite grafts studies (DFDBA/OSS Coag, DFDBA/BB, FDBA/OSS Coag, FEBA/BB) with SR 85 model no difference was noted in rate however the Histo Mellonig (82) showed the DFDBA composites did better than the FDBA composites. Schmitz, Hollinger (Clin Orthoped & Related Res 88, 34-26): Rabbit, critical size defects. Biodegradable copolymer of polylactide-polyglycolide (PLA:PGA) combined with DFDBA & implanted into rabbit calvarial defects produced significantly greater volume of bone than control defects tx’d w/o polymer and DFDBA. PLA:PGA copolymers may provide acceptable carrier vehicle that provides for immediate stability conducive to repair of the craniofacial skeleton. Hollinger (Clin Orthop & Rel Res 91, 35-31): Histo studied 4 different DBA (Demin Bone Allograft) bone preparations in skull holes in rats. Endochondral & Intramembraneous antigen extracted, autolyzed, allogenic (eAAA & iAAA) bone and DBM (Demin Bone Matrix) and control. DBM resulted in the most bone formation. But all better than empty control. DBM similar to DFDBA. FACTORS IN DETERMINING OSTEOGENIC POTENTIAL Age of donor: Jergesen et al (Clin Orthop 91, 35-43): Animal study. DBM in rat model varying age of recipient and donor. Bone induction decreases with increasing age of the recipient animal and increases with decreasing age of the donor. Nyssen-Behets (Arch Orhtop Trauma Surg 96, 35-42): Human DBM, various age donors, implanted in subQ pouches of athymic mice for 28 days. Sig lower alk phosp activity in implants form the old donors vs. young donors. There appears to be a tendency to decreased osteoinductive capacity in bone from older donors. Particle size Residual Calcium some residual calcium may be helpful 1-2%. Schwartz (JP 96): Not all tissue banks follow same procedures, osteogenic potential of different batches of DFDBA vary greatly. Gender not a factor in osteogenic potential
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HUMAN BONE OSTEOINDUCTION AFTER PROCESSING (TISSUE BANK) Yes: Schwartz, Sommers, Mellonig (NOT PUBLISHED YET!): Human DFDBA 7 F, 20 M (age 15-50), 107 batches, 108 Nude mice (athymic 75% chance doesn’t recognize Ab), blinded eval 6 wks. R: 8-, 8-low, 7 good, 4 excellent, donor gender doesn’t play role, donors should be < 50yrs. (xenograft but doesn’t respond like one b/c athymic mouse). Testing: Zhang, Powers, Wolfinbarger (JP 97): Zhang, Powers, Wolfinbarger (JP 97): HISTOLOGY STUDIES: HENAH Studies (BOARD QUESTION) Middleton , Bowers (JPR 90): Histo evaluation of submerged roots. 1) New cementum formation was cellular in nature (98%). 2) Cementum formation 100% DFDBA grafted, 53.1% non grafted. 3) Cellular cementum can form over exposed root surfaces, dentin, or old cementum. Bowers et al (89a, 36-34): Submerged vs. Non-submerged roots, no regeneration in non-submerged roots, while submerged roots had new attachment, new bone, new cementum. 0.75 mm new attachment in submerged teeth. Bowers et al (89b, 36-25): Submerged vs. Submerged w/ DFDBA, new attachment, bone, cementum occurred more frequently in the grafted sites. Grafted 1.76 mm 1.96 mm 1.88 mm
New attachment New bone New cementum (NSD)
Non-Grafted 0.76 mm 0.80 mm 1.48 mm
Bowers et al (89c, 36-26): Non-submerged vs. non-submerged w/DFDBA, non-grafted sites showed a LJE downgrowth on the entire exposed root surface and often apical to the notch while the grafted sites showed regeneration of new cementum, bone, and CT fibers. BL: With a graft there was 1.24 mm of new bone cementum and PDL (this is in addition to the mean defect depth of 3.69 mm, therefore, had mean of 5 mm of repair and regeneration. Control sites healed by LJE. Reynolds & Bowers (JP 96, 37-40): Histo from phase III of HENAH studies. Compare fill w/o graft and amount of attach. 72% sites residual DFDBA 6mo biopsy but greater new attach 1.7 vs. 0.2, bone 2.33 vs. 0.2, cementum 1.7 vs. 0.2 and PDL. DFDBA is incorporated into new bone and produces more new attach vs. empty control. Comparison Studies: Carraro (JCP 76, 36-28): Intraoral cancellous bone autografts in the treatment of infrabony pockets. More favorable healing in intrabony pockets when bone grafts are used especially in the 2-walled defects (2.88 mm vs 2.18 mm). In one-walled defects there was no difference in healing between grafting vs. debridement-only. Hiatt, Schallhornn (JP 78, 36-30): Human bone and marrow allograft, autograft, and nongraft periodontal regenerative procedures. Consistently found regeneration of bone, cementum and a functional pdl in the successfully treated graft sites when compared to the non-grafted sites. Unable to demonstrate immunologic responses to transplants of allogenic cancellous bone & marrow. No resorption except for fresh iliac crest. Listgarten, Rosenberg (JP 79, 36-32): Osseous allografts w/ & w/o S/RP, Overall, the grafted sites did better clinically and histologically than the nongrafted sites. The lack of oral hygiene in this study population could account for less than optimal results obtained when compared to other studies and points out the importance of this through adequate maintenance of our surgical patients. Tendency for JE to proliferate apical to alv crest in all specimens, and new attachment only at base of defect. Stahl, Froum Kushner (JP 83, 36-33): Human, grafting citric acid 1 year, Autogenous best, followed by DFDBA, then synthetic filler. Citric acid didn't appear to improve the success of the treatment. "New
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attachment" can be obtained on root surfaces previously covered by calculus. (2 cases) Need close proximity of PDL cells. Rummelhart (1989): DFDBA Vs. FDBA No difference, bone fill DFDBA 1.7mm (59%) vs. FDBA 2.1mm (66%). Mellonig (IJPRD,84): DFDBA vs. OFD Probing depth reduction similar approximately 3.0 mm, Recession: 0.2 mm DFDBA 1.3 mm OFD Att gain: 2.9 mm DFDBA 1.5 mm OFD Bone fill: 2.6 mm DFDBA (65%) 1.3 mm OFD (33%) Barnett, Mellonig (JP,89): FDBA vs. Porous hydroxyapatite (Interpore 200), bone fill with FDBA was better (2.1mm 66%) than. Porous hydroxyapatite (1.3mm 42%) (BOARD QUESTION) Bowen, Mellonig (JP,89): DFDBA vs. PHA (Interpore 200), bone fill DFDBA 2.2mm (61%) vs. PHA 2.1mm (53%) Oreamuno, Lekovic, Kenney et al (JP 90, 36-23): DFDBA Vs. PHA PHA better Graft Material DFDBA PHA (Interpore 200)
PD reduction 3.3 mm 4.3 mm
Attachment gain 2.1 mm 2.9 mm
Bone fill 2.4 mm re-entry 3.3 mm re-entry
Grafts with Growth factors: Hollinger, et al (JOMFS 89, 34-31): Baboon, bovine osteogenin placed in calvarias. Increased osteogenesis when osteogenin used, controls healed with more fibrous CT and less bone. OG may accelerate bone formation and needs bone derived matrix. Doll, Towle, Hollinger, Reddi, Mellonig (JP 90, 34-32): Long-Evans rat, critical calvarial defects. HA healed w/ dense CT, Osteogenin + collagen bone, control soft tissue. OS + collagen produces excellent results and holds great potential for clinical use. (HA binds too strongly to be effective carrier for OS. Bowers, Felton, Middleton (JP 91, 35-23): Human histo, teeth indicated for extraction: DFDBA + osteogenin resulted in more regeneration and new attachment than DFDBA alone, Collaplug, or collaplug plus osteogenin. Becker et al (JP 92): dog study, immediate extraction sites for Implants augmented with either 1) ePTFE alone, 2) ePTFE with FDBA, 3) ePTFE with PDGF/IGF. Results were: ePTFE with DFDBA highly variable and may have hampered results, remember that human DFDBA was used in a dog (Xenograft), ePTFE and the ePTFE with PDGF/IGF were statistically significant in Antigenicity of Allogenic Bone Grafts Quattlebaum, Mellonig et al (JP 88, 35-27): Antigenicity of freeze-dried cortical bone allograft in human perio oss defects. 20 pts, 49 serum samples assayed for presence of anti-HLA AB's against donor antigens. No donor specific anti-HLA AB's detected. FDBA could be regarded as material lacking clinically sig antigenicity. Reduces challenge. Not like transplant b/c replaced. Freeze-drying reduces antigenicity (no HLA antibodies) Mellonig and Levy (1984): Bone particles below 125 µm can induce a significant foreign body response. Sandpath and Reddi (83): Antigenicity of bone is via Type 1 collagen in the bone matrix. Optimal particle size is 74-420µm Dragoo & Sullivan (JP 73, 35-18): Low incidence of resorption (2.8%), can use curette to prevent it. Friedlaender et al (JBJS,84): 9/43 pts receiving large FDBA developed anti-HLA antibodies. Graft Particle Size Always look at particle size in studies, too small, no vascular ingrowth, too big bone sequestrates. Just right 300 µm. Zaner and Yukna (JP 84, 35-2): Examined particle size of autogenous bone obtained by different means bone/blend: 210 x 105 m; Hand chiseled largest particles, most variable: 1559 x 784 m; and High speed hand piece: 351 x 198 m, low speed hand piece: 299 x 527 m, FDBA: 551 x 306 m. Minimum pore size b/t particles of >100m (0.1 mm) is needed to allow proper vascularization and bone formation. Material in 300-500 m best. Size of 380 m would permit a 100 m space for vascularization. Mellonig and Levy (Abs): Optimal particle size of DFDBA is 250µm-750µm. Less than 125µm causes inflammatory response.
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Bhaskar (OOO,71): Pore size of range of 100-200um is considered optimal for endothelial and fibroblastic ingrowth. The space between the particles may be just as important as the size of the particles themselves. Shapoff, Bowers, Levy, Mellonig & Yukna (JP 80, 35-21): Monkey femurs, Particles of 100-300 µm + marrow had better results than 1000-2000 µm + marrow. (BOARD QUESTION) Fucini, Quintero, Gher, Black, Richardson (JP 93, 35-34): Human IPX 2-, 3-wall defects. Small vs. Large particle size. Small particle group (250-500 um) had defect fill of 1.32 mm (38.6%) vs. the Large particle group (850-1000 um) had fill 1.66 mm (34.9%) No significant difference. GRAFT SAFETY Points to tell patients Used since 1951, in perio since 1969 2 million grafts have been done There have been no reports of antigenicity or rejection No adverse effects like root resorption or ankylosis OTHER COMMON RISKS Dying from flying 1 in 22,000 Dying from an automobile 1 in 8,000 Buck (Clin Orthop & Rel Res 90, 35-30): Freezing alone results in HIV-risk of 1/8 million. 1/3 chance present in bone if pt tests HIV (+), 3/5 chance present in bone after freezing, 1:1.67 million chance of graft containing cultivable virus from unrecognized HIV (+) pt. 1/3 3/5 1.67 million = 1:8 million. Russo (1995) Revised risk of transmitting HIV through DFDBA 1 in 2.8 billion. 1:22,000 chance in airplane crash 1:8,00 in auto accident Mellonig, Prewitt, Moyer (JP 92, 35-35): Demineralization and treatment with a virucidal agent inactivates HIV in spiked and infected bone. Resnick (JAMA 86, 35-27): Viral infectivity is undetectable within 1 min of alcohol treatment. Stability and inactivation of the HTLV-II/LAV under clinical and lab environments. Exposed to quaternary ammonium chloride, alcohol, NA hypochlorite, nonionic detergent and acetone. Exposing the virus to different temperatures reduced infectivity . 0.5% Na hypochlorite, 70% alcohol, 0.5% nonidet-P40, and 0.08% quaternary ammonium Cl for 10 min and 1:1 mix of acetone-alcohol were effective in reducing virus to undetectable levels. Virus can survive up to 15 days at room temp and 11 d at 36 C. HIV not as fragile. Tissue Bank effective protocol. Prewitt (91) says ethanol completely penetrates. Mellonig (91): Effects of irradiation and ethylene oxide on osteogenic potential are unknown. Zislis (89): Ethylene oxide alkylates bone; shuts down osteogenic potential. Marx (JOMFS 93, 35-36): Lecture. Concern over transmission of infectious diseases (HIV, Creutzfeldt-Jakob disease, Hepatitis B & C) Bank accredited by AATB. If bone can be cultured after freezing the bone, it will not be inactivated by other usual procedures used in tissue banking, such as washing and freeze-drying. Creutzfelt-Jacob neurologic disease affecting primarily the cerebral cortex and basal ganglia in adults under 30 years of age, have been reported following use of dura allograft. Keep recd, obtain consent. Moran et al (JP,94): reported that irradiation up to 3 Mrads does not destroy the osteogenic potential of DFDBA Towle: X-radiation decreases osteogenic potential. Prewitt (90): Irradiated chips had no osteogenic potential, whereas irradiated whole bone had some osteogenic potential. Simmond (NEJMed 92, 35-33): HIV sero(-) Pt as donor. HIV (+) and retested samples. Vascular organs all (+). Freeze dried tissue or bone and avascular (corneas) all (-), but some at large untested. Retest after 8 weeks. Need to improve recd keeping. Shigeyama (JP 95, 35-39): Lab comparison of BMP biologic activity between fresh bone and DFDBA. Similar ability to stimulate cell attachment. DFDBA retains proteins with biological capacity, and BMP with osteogenic potential but with lower potential. DFDBA has ability to influence cell behavior but looses some with processing.
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Ijiri (J Orthop Res 94, 35-29): In rats. BMP w and w/o collagen through ethylene oxide and gamma. Rad of Collagen or BMP. 2.5 rads produce no bone. Ethylene oxide 29 C 5 hrs reduce bone but not much. Can irradiate BMP but not collagen. Tissue Bank Requirements 1. Donor must be free from infections, malignancies, auto-immune diseases, diseases of unknown etiology, severe trauma 2. Tissue must be taken within 24 hours 3. Tissue must be procured under sterile conditions 4. Sterility testing is done throughout procurement process. Lifenet now only accepts donors under 50 years of age. In the future, all DFDBA may be tested osteogenic potential BONE GRAFT HEALING Angiogenesis: Paralker(91): Endothelial cells of capillaries may respond to growth factors, important for bone formation. Ankylosis of FDBA/DFDBA: Bowers, Mellonig et al: Low incidence. Rabie (J Dent Res 96, 35-41): Critical defects in rat parietal bone, filled w/ IM (intramem) bone graft, DBM alone (cortical bone) DBM-IM bone or left unfilled. DBM & DBM-IM healed w/o intermediate cartilage stage, and IM did not. Type of bone making up graft material will determine type of regenerative process induced. ANTIBIOTICS and BONE GRAFTS Systemically: Sanders, Sepe (JP 83, 35-22): Navy study, FDBA vs. FDBA/ Bone blend coag, Better results with antibiotics (TCN) and complete closure over graft. Mixed with Graft: Evans and Yukna (89): 10 LJP pts, 4:1 ratio of TCN to ß-TCP, HA, FDBA, at reentry HA was better than ß-TCP, however all 3 worked well. Pts were also on Doxycycline 100mg/day for 10 days POT. Mabry and Yukna (JP 85 10-23): LJP pts, TCN mixed in FDBA + systemic vs. no TCN, significant bone fill 2.8mm, and resolution of defects using local and systemic TCN with FDBA. (BOARD QUESTION) Drury and Yukna (91): FDBA +sterile H2O vs. FDBA + 10ug/ml TCN in baboons, TCN + bone had 35X bone fill as bone alone. Terranova, Wikesjo: Suggest 50 mg/ml TCN reconstitute with graft. Sommerman (88): Low doses (100mg/ml) inhibit fibroblast attachment. Fibroblasts were flattening and spreading. ANTI-GRAFTING Becker (JP 96) DFDBA is dead bone, slowly resorbed should not be used around implants Altiere et al (JP,79): Lyophilized bone allografts (FDBA) vs. control OFD, showed no significant difference. *Note: allograft subjected to 3 million rads of radiation. Xiao (JP 96 1233) Study of DFDBA results using antibodies to osteocalcin, decorin, biglycan (bone proteins) DFDBA encapsulated by fibrous CT. Becker (IJOMI 95 25-12) 2 Dog study. Immediate implants, all with membranes. Compared DFDBA to autologous bone. Autologous best (95% regeneration), membrane only (80%), DFDBA (75%), control (37%). Anti-DFDBA. 12 week study, small n Becker, Becker, Caffesse (JP 94, 35-37): 2 extractions on 7 pat. One filled DFDBA, other with autog. 3-13mo biopsy. DFDBA caved in with particles at bottom buried in CT, no calcification or osteoblastic activity. Interfere in healing. Autog hard, viable bone, + calcification. DFDBA no bone, interference. Mellonig & Towle (JP 95, 3538): Rebuttal: Critique previous article. Why ext and not perio defect. Ext heals spontan. Comparisons at different time periods. Deep biopsy on DFDBA but surface on autologos. No eval of healing interference. Conclusions are not facts.
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ALLOPLASTIC /SYNTHETIC GRAFTS Ideal properties of alloplastic implant materials: Biocompatibility, non-allergenic, non-carcinogenic, non-inflammatory, sufficient porosity to allow bone conduction-growth of bone into and around the implant, ability to stimulate bone induction, resorbability with replacement by bone, radiopacity which permits radiographic visualization, withstand sterilization procedures, easy to obtain and inexpensive, and stable to variation in temperature and humidity. (AAP Periodontal Literature Reviews) Why use alloplastic implant materials: 1) Unlimited quantity 2) No additional surgical site 3) Nonantigenic 4) No disease transmission SYNTHETICS: Osteogen: Porous crystalline calcium phosphate, resorbable Corsair (92) Periograf: Durapatite nonporous HA, Yukna, Ganales (86): Human histo of 4 pts, no osseous regeneration. Perioform: Calcium phosphate cement which crystallizes in vivo as HA. NON-CERAMIC IMPLANT MATERIALS:
1) Calcium Sulfate (Plaster of Paris): Shafer & App (JP 71): Used in human tuberculosis bone defects, intent to stimulate osteoblasts, provide bulk to support the flap, prevent apical downgrowth, resorbs quickly, in rough form arsenic can be identified. Sottosanti (Compend 92, 36-1): Add sterile medical grade CaSO4 hemihydrate to hydrated DFDBA so CaSO4 is 20% by volume. CaSO4 helps bind the graft to prevent loss. Mix CaSO 4 separately and place over graft as a barrier and extend 2-3mm onto the surrounding bone. Case reports indicate that CaSO 4 retards epith and he shows nice clinical response but there are no long term controlled clinical studies and no histo. 2) Polymers: a) HTR (hard tissue replacement polymer): (PHEMA) polymethylmethacrylate core with polyhydoxylethyl methacrylate and calcium composite, micropores, nonresorbable, granular and molded forms, barium for radiopacity, hydrophilic thus ease of use, electrically charged to promote osteogenesis ? Shahmiri (93): Fibrous encapsulation. No evidence that it has osteoinductive properties. Stahl, Froum & Tarnow (JP 90): Healing by LJE, connective tissue adhesion, limited bone formation Kwan et al (IJPRD 90): Severe inflammatory reaction has been reported to material Yukna (JP 90,36-24): May result in some decrease in PD & gain in clinical attachment. Pts with intraosseous defects, radiographs, stents, and HTR. 6 month re-entry. HTR had 60.8% defect fill with greater reduction in pocket depth and increase in attachment then FPD (32.2%). b) Polylactic acid: Meadows et al (JP 93): c) Polyglycolic acid d) Proplast: Radell & Cassingham, (80): Two polymers: PTFE & pyrolytic graphite, pore size 100-500 um, used in alveolar ridge augmentations 3) Calcium Carbonate: Yukna (JP,94): Porous material- removal of organic material from the genus Porites coral, Well tolerated, resorbable, bone ingrowth 4) Porous Hydroxyapatite (non - ceramic), composed of porous, crystalline clusters OsteoGen: Corsair (92): mean fill of intrabony defects 2.26 mm, 51% fill 5) HA Cements Perioform Tetracalcium Phosphate Cement (HAC)
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CERAMIC MATERIALS: 1) HYDROXYAPATITE A) NON-POROUS HYDROXYAPATITE (Durapatite), coral particles sintered. Periograf: Galgut (JP,92): Not much difference. between control sites except 4 yrs in deep sites. Calcitite 4060 Orthomatrix HA-500 Animal studies: Biocompatible, not osteoinductive (Barney,86) , Healing by fibrous encapsulation (Boyne,82) Human studies: Rabalais et al (JP,81): 1st human study, HA enmeshed in CT, resistant to probe, defect fill HA 1.7 mm vs. 0.5 mm OFD, no difference in AL or PD reduction. 6 month re-entry. Froum (JP 82, 36-2) Histo, Durapatite (Periograf), This alloplast should be considered "a tissuetolerated foreign body fill." well tolerated, no new attachment, foreign body fill. Yukna (JP 84, 36-5): Durapatite ceramic as an alloplastic implant in periodontal osseous defects after 3 years. Durapatite ceramic particles as a bone graft material in periodontal osseous defects are at least as good as, surgical debridement alone. Yukna (JP 85, 36-9): Appears material is a biocompatible nonresorbable filler that will support a dense CT matrix over time and giving comparable results to OFD in the treatment of human periodontal osseous defects. Caution with meaned data, therefore its potential may be as autograft extender or expander. Yukna et al (JP 89): 5 yr., HA three times better than OFD (BOARD QUESTION) and more stable at 5 yrs, OFD regressed 3-5 X faster. Shepard (IJPRD 86, 36-14): Calcitite 4060, new bone associated with fibrous CT, Calcitite encapsulated by fibrous CT w/o inflammation, but no evidence of new attachment, healing with LJE. Ganales (JP 86, 36-11): Durapatite, human intrabony defects, In 17/19 of the cases, osseous tissue did not regenerate around or through the implant particles when used in human periodontal intrabony defects. Interface with tissue had existence of mucopolysaccharide "bonding zone" that was amorphous collagen free. Meffert (IJPRD 86, 36-15): Human histo, Calcitite 4060, Osteogenesis is possible within the fibrous CT surrounding the HA particles in deep intrabony periodontal defects in humans. May be function of time and dimension. Kramer (IJPRD 89, 36-21): Combination FDBA/HA graft material can be used in human periodontal defects and may obtain clinical/radiographic appearance of success. FDBA induces osteogenesis and HA induces fibrous activity. Moskow (JP 83, 36-25): Case report, Durapatite + autogenous chips, 9 wks root fxd and block section. Durapatite ceramic particles were well-tolerated by the body but no bone formation was seen around this filler, osteogenesis around bone chips. Radiographs give appearance of defect fill due to radiopaque nature of the alloplast. B) POROUS HYDROXYAPATITE: hydrothermal conversion of calcium carbonate exoskeleton of porites coral into HA (replamineform process). Interconnecting channels are 190-230m to support fibrovascular ingrowth and subsequent bone formation. Available in both solid and granular forms. Interpore 200: Stahl and Froum (JP 87, 36-19): Interpore 200, 1 yr. block sections, biocompatible, clinical attachment gain, reduced PD, bone formation in pores, no evidence of new CT attachment, closure by LJE. Evidence of osteogenesis around and within the pores of the particles at 3 mos & union with alv crest at 12 mo. Some root resorption noted. Gain of clinical attachment 2.0-4.2 mm Kenney (JP 88, 36-20) Interpore 200, Human grade II furcations Mand molars, HA greater attachment gain, bone fill, histo of new bone in pores. Gain in attach levels when compared to controls (2.08 mm).
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Lekovic, Kenney et al (JP 90): Interpore 200 + ePTFE vs. ePTFE membrane. Similar reduction of PD. Greater horizontal and vertical bone fill and less recession with combined. Kenney (JP 86, 36-10): Interpore 200, 6 months, 1st evidence of materials ability to stimulate osteogenesis w/i porous structure of implant. At 3 mo CT infiltration through pores & narrow zone of bone formation. At 6 month continued bone formation with in the pores. Krejci (JP 87, 36-18) Porous v. Non-porous HA. Grafted sites in general demonstrated more positive clinical defect changes than the non-grafted sites, with the nonporous HA being the best overall (3/12 porous HA exfoliated). Radiographs over estimated the amount of defect fill. Bowen & Mellonig et al (JP 89): NSD b/t HA and DFDBA, Bone fill HA 2.1 mm vs. DFDBA 2.2 mm. If regeneration is the goal, then DFDBA is the choice. If defect fill is the goal, then either material will work. Oreamuno & Mellonig et al (JP 90): HA greater PD reduction & gain in Attachment bone fill than DFDBA. NSD, no histo. Barnett et al (JP,89): FDBA 2.1 mm bone fill vs. HA 1.3 mm. Yukna (84, 85, 86, 89A, 89B): A summary of findings indicates that the use of HA ceramic as a bone implant material in periodontal osseous defects yields at least as good and often better results than those following surgical defect debridement alone. HA is clinically beneficial in most cases, provided it is used judiciously. Stahl and Froum (JCP 91, 36-27): Interpore 200 + Goretex, human, . Vertical lesions on hopeless teeth. Used OFD, HA and Goretex. One control with OFD only. Calc notch. Block sections. HA alone does not stimulate cementum but increases bone mass. With a teflon membrane and HA, it appears cementogenesis and bone mass was enhanced. 5/7 exp had epith attachment and new cementum was seen in the osseous crater (range 0-2.4 mm). 2) TRICALCIUM PHOSPHATE: a CaPO4 PPT from alkaline aqueous solution low temp 950°C for a short time, CaPO4 mixed with naphthalene leaving pores in evaporation, sintered to solid mass (slowly resorbable). C/P of TCP 1.5/1, bone is 1.67/1. (Synthograft) Snyder, Levin, Cutright (JP 84, 36-3): Human, TCP is a useful graft material because of its potential for osseous (clinical ave of 3 mm as did Schallhorn) repair, its availability, host acceptability, ease of manipulation and storage advantages. No residual particles at 6 months. Baldock et al (JP 85, 36-26): Histo, TCP encapsulated in CT, minimal new bone, only partially resorbed at 9 months. Bowers et al (JP 86, 36-13): Histo: Bone & osteoid around TCP, partial resorption, nidus for new bone formation. supracrestal apposition was noted in 3/4 specimens. Stahl & Froum (JP 87, 36-12) & Froum & Stahl (JP 87, 36-17): Histo 3-8 months and 13-18 months: Synthograft, TCP not osteoinductive. No osteogenesis, cementogenesis or new attachment. Healing by LJE. Slowly resorbing TCP particles act as inert fill material and b/c well encapsulated by gingival CT. Active root resorption seen immediately. Gain in clinical closure (clinical AGAIN) 2.6 & 2.3 mm respectively. Saffar (JP 90): Human histo of Synthograft, 5 biopsies, fill and resorption takes about 40 months Pepelassi (JP 91): Synthograft: Composite graft vs. OFD, 26 defects, composite had 1.9mm attach gain vs. 0.6 for control. 1 and 2mm more vertical and horizontal fill with composite graft. No complete closures. Xenografts: OsteoGraf N- 300, bovine collagen, when Boplant exposed it is recognized by body as foreign and sloughed. Nielsen et al (JP 81): No difference between Kielbone and autogenous grafts when comparing clinical gain of attachment and radiographic bone fill. World Workshop: Supports only porous HA for grafting, if regeneration objective use DFDBA, if fill objective then use HA. Studies:
Yukna (JP 89): Durapatite (Periograf) vs. OFD, 39 pts, 2mm bone fill for HA/ 0.7 for OFD, HA had less recession, less crestal resorption. Also has 12 month re-entry study. Meffert (JP 85, 36-6): Calcitite 4060 vs. OFD, 9 mo reentry, HA has potential as an alloplast in periodontal osseous defects and is well-tolerated by hard and soft tissues. HA had 54% bone fill and 0.6 mm increase in crest height for a total of 67% fill. Controls lost crest height for a 10% total fill.
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Kenney (JP 85, 36-7): Interpore 200, 25 pts, angular defects, 5mm PD or greater, had 3.6mm attachment gain vs. 1.2mm control. Implant well tolerated, and produced sig reduction POD, depth of osseous lesion and gain in AL. Stahl and Froum: HA grafted 3 teeth, block sectioned: LJE separated graft from tooth, some osteogenesis Nagahara et al (92): HA and TCP both undergo resorption (yrs), TCP resorbs more but more bone formed with HA. Allogenic vs. Alloplastic Stahl, Froum Kushner (JP 83, 36-33): Healing responses of human intraosseous lesions following the use of debridement, grafting and citric acid root treatment 1 year. Autogenous best, followed by DFDBA, then synthetic filler. Citric acid didn't appear to improve the success of the treatment. Showed that "new attachment" can be obtained on root surfaces previously covered by calculus. (2 cases) Need close proximity of PDL cells. Barnett (JP 89): No difference FDBA vs. porous HA, slightly better fill with FDBA. Bone fill: 2.1 vs. 1.3 mm PD: 3.0 vs. 1.3 mm AGAIN: 202 vs. 1.3 mm Bowen (JP 89): No difference DFDBA vs. porous HA. Histo: little osteogenic activity associated w/ either material. Glass and Mellonig (JP 89, 36-22): HA and bone inductive proteins vs. bone and BMPs, HA + BMPs no bone, Bone + BMPs grew bone. Oreamuno, Lekovic, Kenney (JP 90, 36-23): Porous HA vs. DFDBA. HA had more defect fill, less residual PD, more attachment gain than DFDBA. COMBINATIONS OF ALLOPLASTS Nery (92): 85% HA + 15% ß-TCP had more bone, new attachment than other concentrations. Shows advantages of both, slow resorption HA, osteoinduction ß-TCP. ROOT RESORPTION Ibbott (JP 85, 36-8): Durapatite. Case of root resorption with Periograf. Resorption detected radiographically at 12 months and clinically at 18 months. Froum and Stahl (JP 87, 36-17): Root resorption with TCP (Synthograft). Stahl, Froum (JP 87, 36-19): Interpore 200, LJE but osteogenesis around graft. REGENERATION GTR DEFINITIONS (1992 Glossary of Periodontal Terms) New attachment: Union of CT or epithelium with a root surface that has been deprived of its original attachment apparatus. This may include cementum, no bone, CT attachment only, or LJE. Reattachment: The reunion of epithelium or CT with root surfaces and bone such as occur after incision or injury. Regeneration: A HISTOLOGICAL TERM: Reconstruction or reconstitution of a lost or injured part. Repair: Healing of a wound by tissue that does not fully restore the architecture or function of the part. (Proper term is new attachment) Bone Fill: Clinical term only. ACCEPTED REGENERATIVE TECHNIQUES AUTOGRAFTS Extraoral Intraoral ALLOGRAFTS FDBA FDBA + Autografts FDBA + Tetracycline DFDBA
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GUIDED TISSUE REGENERATION GTR GTR + DFDBA Not fully accepted yet due to lack of histological data Alloplasts are not accepted as regenerative materials. They are biocompatible fillers only. GTR PRINCIPLES 1. Epithelium exclusion (epithelium migrates at a rate 3-5 X faster than PDL cells, Polson Proye with Citric acid, Yukna with ENAP were different approaches to exclude epithelium) 2. Space creation 3. Stabilization of clot (Loma Linda: Wikesjo) key to fiber linkage 4. Complete coverage? 5. Amplification of Growth factors and progenitor cells? CHARACTERISTICS OF SUCCESS OF GTR Machtei, Zambon, Genco et al (JP,94): 1) Age doesn't play a role 2) No difference between 1st and 2nd molars 3) No difference if initial therapy was performed or not 4) Sites with low PI, GI, and A.a. did better 5) Deeper initial PD demonstrated best results. 6) Greater # of fibroblasts on inner portion of membrane had best results THEORY Kramer: Fiber barrier theory, transeptal fibers, also supports rotary instruments prior to grafting. Becker: The wider the bone defect, the poorer the regenerative results Terranova (88): Regrowth of bone is related to the distance from root to bone. Harris: The osteogenic "gap" is 1 mm. Wikesjo (92): Membrane stabilizes graft, essential to success. Prichard: Interdental denudation technique Steffensen and Weber (89): The more acute the defect angle (radiographic) < 45º, the more fill you get Renvert/Bowers (89): Both authors said walls did not effect defect fill potential (with grafts.) Depth is key Where do the cells come from? According to Dr. Bowers, the primary source of cells for regeneration is bone with a little contribution from the PDL Aukhil et al (JCP 86 37-06): Dogs; Contact with root dentin may be necessary for progenitor cell differentiation into cementoblasts. used membrane to block cells from dentin , no Cementogenesis in this area. Melcher (JPR 86 37-07): Bone cells from rats can grow cementoblasts in rat calvaria. Iglhaut: (37-15) Bone and PDL, PDL migration at 2 wks, peak mitotic activity at 3 wks. Nyman (70s): Get ankylosis with bone, CT from epithelium causes resorption, blocked by PDL (86) All wound healing from PDL. Caton (JP 87 37-11) Cementum formation is the rate limiting step in regeneration. Aukhil (JP 87 37-10) Flap CT cannot form new cementum or fibers Areco (JP-91 37-25) PDL cells can initiate mineral-like nodules in vitro Van Dijk (91): Co-cultured cementoblasts and fibroblasts, placed back into defects = no new cementum. (Not from cementoblasts??) Aukhil (88): Tritiated thimidine PDL cells, with/without membrane. Got 200µm with both. Suggested we need membrane to allow amplified division of cells. Histologic new attachment Nyman et al (JCP 82 37-03): Millipore filter, #23, no new bone but CT/cementum found. 1st study to show regeneration possible. Gottlow et al (JCP 86 37-05): Histo of human teeth, tx’d with Gore Tex, new CT. Coined term Guided Tissue Regeneration. Factors that influence regeneration: 1) degree of gingival recession that occurs during healing
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2) Periodontal defect morphology 3) Amount of remaining periodontium Becker/Becker (87): Open probing new attachment, unpredictable results, 2.6mm gain in bone. Becker/Becker (89 37-18): Clinical improvement of Class II, not Class III furcations. Dahlin (89 ): GTR over implants grows bone. Stahl (JCP 90, 37-24) histo 9 lesions Gore-tex new cementum noted .5-1.7 mm. Stahl & Froum (JCP 91): Histo: 4 vertical lesions with DFDBA + e-PTFE reduction of probing depth, 1/4 closed with LJE, 3/4 had new attachment but not coronal to the calculus notch. Stahl & Froum (JCP 91): Histo: 7 vertical lesions, tx with porous HA and GTAM, 2/7 had LJE, 5/7 had new cementum, and increased bone mass apical to calculus notch with functionally-oriented PDL usually. Greaves, Martin (AJP 85): Malignant fibrous histiocytoma in rats at sites of implanted Millipore filters. BONE RESPONSE: Renvert: GTR effect = 0.8mm "sphere of influence" GTR DEVICES Microfibrillar collagen (Avitine, surgicell, collatape, etc.), duramater, polyglactin, polyglactic acid, coronal positioning, foil, Expanded PTFE, demin cortical plate, synthetic skin (polydimethyl siloxane) Rubber dam, interdental denudation, CaSO4 , Lambone, FGG, CTG, Periosteum, Coe Pak. GTR in Furcations (See Furcation Regeneration) Gantes (91): Class 3 furcations, citric acid and coronally positioned flaps with moderate results. Lu (JP 92 37-27): Complete circumferential adaptation of the membrane to the root is not possible, gaps will remain. Occlusal border should be placed 1-2mm below CEJ. GTR success may be more from clot stabilization than from epithelial exclusion. Pontoriero et al (JCP 88 37-16): GTR in class II furcations, 14/21 complete closure, 5/21 had residual of < 1 mm. 90% closure of Class II’s with membrane, OFD 2/21 completely closed, No reentries. GTR better than OFD in Class II furcas. Pontoriero (JCP 89 37-21): Class III, 8/21 closure with GTR, control 0/21, no re-entry, clinical probing depth only. Pontoriero (JCP 95 37-32) Buccal furcations more predictable than interproximal furcas, GTR doesn’t work in class III furcas. Lindhe et al (JCP,95): Flap management and bioresorbable membranes in class III molar furcations in dogs: -Large furcation defects can be treated provided soft tissue flaps covering membranes prevented from recession -Resolute equally as effective as e-PTFE. Anderegg et al (JP,91): 15 pts, molar furcas, GTR alone vs. GTR and DFDBA (BETTER), 6 mo reentry, combined more fill, more PD reduction, greater attach gain both horizontal and vertical. Mellonig (91): IJPDR: Class 2s, membrane better than OFD, improved HOPA/VOPA, GTR will improve clinical results, rarely complete closure. Mellonig (IJPRD 94): 13 pts with grade II furcas. Comparison of ePTFE vs. debridement-6 month reentry. ePTFE sites showed more PDR, ALG, as well as recession in man II defects. There was no difference between the 2 txs in max grade II furcas. Anderegg (JP 95): Gingival thickness in GTR. 37 pts with grade I or II max or man furcas were txd with GTR. Pts with 1mm gingival thickness only had 0.6mm recession. Less recession with thicker tissues. Lekovic and Kenney (JP,89): class II furcations, e-PTFE vs. OFD, test site showed PD reduction, gain in attachment levels of 2.86mm, vs. controls which didn’t change from preoperative levels. Nygaard Ostby (JCP 96) GTR vs. OFD. GTR has no significant advantage over OFD. No grafts were used. Metzler and Mellonig (91): GTR vs. OFD in Max II furcations, 6 mo re-entry, overall results inconsistent and unpredictable, recession 0.7mm. Furcation Morphology:
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Pontoriero (JCP 92): Beagles, the larger the furc, the less likely fill, suggests critical size to Class II or III, wider/shallower the defect is better, narrow deep is bad, i.e. poor access for debridement. The study had small Class IIIs. Lu (JP 92 37-27): Topography of root trunk, 94% had concavity depth that prevented proper membrane adaptation to root surface. The depth range from 0 to 2.25 mm, recommend that membrane be placed coronal to this area. Maxillary Furcations: Pontoriero (JCP 95 37-32) Buccal furcations more predictable than interproximal furcas, GTR doesn’t work in class III furcas. Metzler and Mellonig (JP,91): GTR vs. OFD in Max II furcations, 6 mo re-entry, overall results inconsistent and unpredictable, recession 0.7mm. Proestakis et al (JCP,92): Maxillary Premolars, very little difference between GTR and OFD controls. GTR in Intrabony Defects Cortellini (JP 93 37-29): Selected deep defects, mean gain in bone 4.3mm: 95% fill of 3-wall, 82% fill of 2-wall, 39% of 1-wall. 73% defect fill overall. Becker W. and Becker B. (JP 93 37-12) 32 pts, 33 sites. Mandibular 3-Wall Intrabony Defects by OFD and e-PTFE The initial clinical attachment was 9.7 mm (deep) with an average gain of 4.5 mm at the second examination (3 years 5 months). Recession between the 1st and 2nd examination was 1.2 mm. The average initial defect depth was 11.7 mm with re-entry at 7.2 mm or a bone fill of 4.4 mm. Average crestal loss was 0.3 mm which is made net bone gain 4.06 mm (72% when figured from the crest). The 3 rd exam (4 years 3 months) was soft tissue measurements only which showed probing depth decrease of 5.8 mm, attachment gain of 4.1 mm, and recession 1.0 mm from the initial values. When comparing these results with open flap debridement it is difficult to do with different measuring techniques and the fact that this was a unique group of deep defects. Mean of 2.5 mm with attachment gain around that same 2.5 mm figure. Even the grafted sites with Yukna,1985 with Hydroxyapatite showed 2.1 mm bone fill and Mellonig,1984 with DFDBA reported 2.5 mm of defect fill. Selvig et al (JP,93): Influence of defect configuration on healing response, Intrabony defects , no reentry, bone sounding, Results: 1) Areas of deepest probing depth exhibited greatest PD reduction and AL gain. 2) Extent of defect surrounding the tooth, # of tooth surfaces involved, or predominant wall form of the defect than any significant effect on healing. Cortellini et al. (JP,95): describes a modified papilla preservation technique for interproximal regeneration resulting in primary closure of 14/15 cases. Pushes the papillae through sutures with cross horizontal low, internal vertical high. Tonetti, Pini-Prato, Cortellini (JP, 93): Tissue gain at 4-6 wk (membrane removal) 7 ±2.2 mm, deep defects, decreased angle. Incomplete coverage (35%) and exposed membranes (72.5%) didn't significantly affect tissue gain. At 1 yr. PAL (gain) was 5.6 ± 2.6 mm and bone fill 4.3 ± 2.5 mm. The greater the amount of tissue at 4-6 wks the better PAL and bone fill, coverage of the new material was essential for success Cortellini (JP 95): Covering regenerated material with FGG after membrane removal was significant when compared to coronally repositioning. Nygaard-Ostby (JCP 96): GTR vs. OFD - GTR no sig. Advantage over open flap debridement grafts used. Long Term Stability of GTR Tissues Gottlow (JP 92): Probing attachment levels maintained at 4-5 years. McClain and Schallhorn (IJPRD,93): 5 yr. follow-up of GTR with and without CA root conditioning and composite grafts. Long term results enhanced with CA + graft, 5yr stability of CPAL. 93% stable with graft, 30% stable with membrane only. Yukna (91): OPNA does not hold up vertically and minimally horizontal (furcations). Bragger (92): Assessed tissues with CADIA, slow consolidation of tissues and mineralization. Becker, Becker (JP93) 4yrs + , 3-wall intrabony with ePTFE (see above)
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Cortellini (JCP 94): Effect of OH on long term stability of GTR. 40 defects were txd with GTR in 23 pts. For the 1st yr. pts were seen on a monthly recall basis and maintained stringent plaque control. Pts at this point averaged 4.1mm PALG. For the next 3 years, 15 pts were seen on a 3 mo recall basis and 8 pts received sporadic care. The pts seen on a regular basis maintained their PAL and exhibited lower PI and bleeding. Those seen sporadically lost 2.8mm of the PAL they had gained at 1 yr. They also showed an increase in BOP, plaque, Pg., and Pi. Study emphasizes that stability of gained clinical attachment is dependent on stringent OH> Weigel, Bragger, Lang (JCP 95 37-36): 18 pt, 4 yr. follow-up. Mean 1.27mm loss of attachment. CAL+1 mm was maintained at 12/19 sites. If the pt lost attachment in their dentition, they lost attachment in GTR sites also. The key to success was low inflammation. BACTERIAL CONTAMINATION: PTFE Membranes Selvig (JP,92): SEM. Clinical appearance of retrieved membrane may be an indication of clinical success or failure. The extent of bacterial contamination of the membrane correlated inversely with clinical assessment of attachment gain. Wang et al (JP,94): in vitro micro-organisms on e-PTFE, polyglactin 910, and collagen - no spirochetes found, strong adhesion of S. mutans, microbes incorporated in membrane are resistant to antibiotics so removal is indicated in infection. Pg, Pm and T.d found to degrade bioresorbable membranes. Simion et al (JP,94): ePTFE membranes when exposed to the oral cavity are prone to bacterial contamination in approximately 3 - 4 weeks and should be removed to prevent further bacterial infection of the underlying regenerative tissues. Note no CHX was used in these studies. Simion (JCP 95): Same M&M as above study except .12% CHX gel applied bid on one side and the other side was used as the control. The controls showed greater amounts of plaque than the test groups and the plaque was more complex in nature. In the CHX group, plaque did increase over the 4 week period and by the 4th week, complete bacterial invasion of the membrane had occurred. CHX does not prevent bacterial penetration of membranes. Nowzari and Slots (JCP 94): Perio defects and implant sites txd with ePTFE. Inverse relationship between microbial counts and PALG. Nowzari (JCP 95): 2/3 wall defects in 18 pts were treated with GTR via ePTFE. 9 pts were placed on Augmentin postop for 8 days, the other 9 pts served as controls. At 6 months, the Augmentin group showed significantly higher PALG than the control pts. When membranes were removed, the Augmentin group had significantly fewer organisms present. Sites free of pathogens on the membrane surface side gained the most clinical attachment. This study emphasizes the importance of controlling microbial pathogens in GTR procedures. Sanders, Karring (JCP 95): Monkeys. Submerged and non-submerged roots covered with ePTFE or polyglactin. Roots that were completely covered displayed new CT, bone the length of the initial defect 67-100%. Non-submerged roots showed bacterial contamination which jeopardizes formation of bone & CT (30-59%). CONCLUSIONS: Bacterial contamination reduces benefits of GTR. TISSUE THICKNESS Anderegg (JP 95): Consider thickness of KT when performing GTR. Pts with 1mm. ePTFE + GRAFT: Anderegg et al (JP,91): PTFE+DFDBA vs. PTFE alone, 30 defects, PTFE+DFDBA had 3.1mm attach gain, vs. PTFE alone 1.4. PTFE+DFDBA had 2mm more vertical and 1.5mm more horizontal fill. 27% were completely closed (4/15).Combined method decreased defect 85% of time while only 50% in the membrane only group. Lekovic et al (JP,90): grade II furcations PTFE+HA vs. PTFE alone, 30 defects, PTFE+HA had 2.9 mm attach gain vs. PTFE alone of 2.4 mm. PTFE+HA had greater vertical/horizontal bone gain and less recession. McClain and Schallhorn(IJPRD 93 37-17): GTR + GRAFT =Long term stability DFDBA + autog + GTR + C.A. = 4.0 mm mean clinical AGAIN, including furcation fill. 5 yr. follow-up of GTR with and without CA root conditioning and composite grafts. Long term results enhanced with CA + graft, 5yr stability of CPAL. 93% stable with graft, 30% stable with membrane only.
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Caffesse et al (JP,93): beagles, DFDBA in combination with e-PTFE was not adjunctive to e-PTFE alone, problem was human bone used in the dog (Xenograft), the defects healed completely in dog with e-PTFE alone, thus no improvement possible. Guillemin, Mellonig, Brunsvold (JP,93): Intrabony defects treated with either DFDBA or a combination of DFDBA and e-PTFE, results show 58% defect fill with DFDBA alone and 70% fill w/e-PTFE/DFDBA combination, however no significant differences were noted between the two treatment groups. Garrett (JP 94): Grade III man furcas txd with DFDBA alone or DFDBA + ePTFE. Both covered by CPF. No benefit was seen with the use of ePTFE. Wallace (JP 94): Grade II man furcas txd with either ePTFE alone or ePTFE + DFDBA. 6 month re-entry showed similar results as far as recession, and reduction of horizontal defect depth were concerned. The ePTFE + DFDBA group showed greater vertical defect fill and greater PALG when compared to the ePTFE only group. Mellado (JP 95 37-34) ePTFE with and without DFDBA more bone formed without DFDBA AntiDFDBA study. Rossen (NOT PUBLISHED YET!!) DFDBA v. DFDBA + ePTFE, grade III furcations sig gain horizontal and vertical bone with DFDBA + ePTFE. Schallhorn and McClain (IJPRD 94): Healing responses of >100 defects txd with combination regenerative therapy Rapid Typical Delayed % of occurrence 13% 76% 8% Membrane exposure none early early Membrane removal dissection relatively easy easy or premature needed Substance under bone-like pink, rubberlike or immature membrane at granulation tissue granulation tissue removal Resistance to probing resistant resists gentle no resistance probing Radio maturation 3-12 mos. 3-12 mos. 6-24 mos. Long term results predictable predictable, favorable, partial success favorable resolution Most Common Most difficult to predict GTR: PTFE: Haney J, Nilveus R, McMillan P, and Wikesjo U.: J Periodontol 64: 883-890, 1993.supraalveolar periodontal defect model in the dog. Results: a) Control teeth exhibited long junctional epithelium and reduced connective tissue repair. b) Membrane-treated teeth had connective tissue repair coronal to the membrane and minimal junctional epithelium. * note: this difference was only significant when looking at defect height. c) When membranes were found collapsed to the root, minimal or no bone regeneration was observed, while if the membrane allowed space adjacent to the root, substantial bone regeneration was seen. d) Three membranes became exposed and an extensive inflammatory cell infiltrate dominated and bone regeneration was minimal. e) Cementum regeneration was minimal when present (7/11 membrane-treated, 5/14 controls) f) Root resorption was common even when connective tissue was excluded by the membrane. Pontoriero (88): PTFE membrane vs. OFD, 42 defects, PTFE had 3.5mm Attach gain vs. 1.1 for controls. Not more than 6 mm deep, shallow sites. Lekovic (89): PTFE membrane vs. OFD, 24 defects, PTFE had 2.9mm attach gain, control had -0.1. Metzler (91): PTFE vs. OFD, 34 defects, PTFE had 1mm attach gain vs. 0.2 for control. More horizontal /vertical fill with PTFE. Mellonig (91): IJPDR: Class 2s, memb better than OFD, improved HOPA/VOPA, GTR will improve clinical results, rarely complete closure. GTR COMPLICATIONS Murphy (IJPRD 95 37-31): Pain 16%, perforations 4%, infection 4%, Kramer (93): Collagen bovine membranes, 2% pts experience transient localized hypersensitivity.
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Adverse 3% early, progressiv easy, premature
fragile tissue wit surface necrosis pos no resistance
Variable limited, failure, o regressio
GTR in MG Defects Techniques and Case Reports: Described by Tinti (JP 93), Shanaman (IJPRD 93), and Shih (IJPRD 94). Pini Prato (IJPRD 93): Described technique using GTR and FGG to treat buccal gingival recession. Complete coverage obtained in 3/5 pts with 4-6mm initial recession. The other 2 pts had 1mm recession remaining. Pini Prato (JP 96 1216) 4 year follow up, no difference between GTR and MG surgery. Over time, attached gingiva increases with GTR. RIDGE AUGMENTATION Allen et al (85): Classification of ridge defects: type A: apico-coronal; type B: buccolingual; type C: combined. Defect depth: mild: 6 mm. Buser (90): Uses titanium pins to gain bone/space under membrane (1.5-5.5mm). Ridge augmentation prior to implants RESORBABLE MEMBRANES Problems associated with resorbable membranes, resorption by-products, resorbs too quickly, not occlusive, too malleable, inflammation associated with resorption. Advantages of resorbable membranes, single surgery, LACTIC ACID DERIVATIVES: (1) Guidor Guidor: polylactic Acid = stability, Citric acid ester = malleability. Resorbed through hydrolysis: Lactic acid to citric acid to Kreb’s cycle, small particles = phagocytosis. (2) Vicryl Caton (JP 94): 40 pts Vicryl vs. OFD in man Class II furcas. Greater gain in attachment in Vicryl group vs. OFD. Christgau et al (JCP,95): Resorbable membranes (polyglactin) provided attachment gain similar to ePTFE Desanctis (IJPRD 96 435) Used vicryl membrane for treating buccal recession. HA used under the membrane for tenting. Got good results. I question the use of a non-resorbable graft material for GTR Gager (91): Vicryl mesh and DFDBA, 9 case reports, excellent fill. (3) Resolut Caffesse (JP 94 37-13) Dog study Resolut vs. ePTFE similar results Becker (JP 96) Human study, Resolut good for Class II furcations Cortellini (JP 96 37-39) Resolut similar to ePTFE. Lindhe (JCP 95): ePTFE vs. Resolut in Class III furcas in dogs. 5 month results showed the bioresorbable membranes performed as well as ePTFE. Simion (IJOMI 96) Gore-tex better than Resolut in GBR around implants (4) Atrisorb Polson (JP 95): 29 pts, class II defects. significant PDR, PALG at 1yr. No controls or comparison groups. Soft tissue results: PDR 2.2mm PALG-V 1.7mm PALG-H 2.5mm (5) Others Vuddhakanok (JP,93): Resorbable 50:50 polylactide:polyglycolide barrier, 7 HUMAN pts, 20 teeth, block sections, no new attachment, more bone recession than controls. Warrer (93): 25 teeth, notch in calculus, tx’d with polylactic acid + polyurethane. Got LJE between membrane. No significant regeneration. COLLAGEN (1) Bio-Gide: Resorbable collagen membrane of porcine origin (Jewish people would have problenm with animal products). Zitman, Naef, Scharer (IJOMI 97): Human study. Implants placed , grafted with Bio-Oss (deprotinized cancellous bone material of bovine origin). Bio-Gide and Gore-Tex both result in good bone formation, however, if Gore-Tex becomes exposed there will be less bone formation. GUIDOR:
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SAFETY: Olsen (OOO,82): Comparative study of polylactic acid in dressing material vs. Gelfoam for extraction sites- minimal inflammation - elicits a mild foreign body reaction- multinucleated giant cells. Myers, Autian (J. PHARM,64): Citric acid esters used as plasticizers does have the potential for blocking neural transmission when they come in direct contact with the nerve trunk. Nakamura (J Biomaterials Res, 94): Tumoriginicity of Poly-L-Lactide plates and polyethylene, 27/50 PLLA- still present for 2 yrs caused fibrosarcoma 23/50 Polyethylene- had the fibrosarcoma Article states that it is the presence of the material continuously not the material itself. The reaction was more of an irritation. So the question is how long is the material present in the same area. Verheyen (J Biomedical Res, 93): Material noted in the lymph nodes 2 yrs after implantation of Poly (llactide) plugs, deep inguinal lymph nodes retrieved from goats sacrificed at 2 yrs were swollen when compared to controls. BL: The role of crystalline degradation products of the polymer may limit the clinical application or Poly(L-lactide). Suganuma (J Applied Biomaterials, 93): Use of Polylactic acid sutures for internal fixation of mandibular fxs. No inflammatory response in 6 wks, degradation products at 12 wks show some inflammatory response When the materials degrade into small particles 2 um they elicit a foreign body response, when 40 um they did not influence a bone response. Kronenthal (75): Four stages of polymer degradation: (1) Hydration or water infiltration. Lubrication of polymer chains results in loss of membrane stiffness and increases plastic deformation "creep". Affects space-making ability. (2) Strength loss. Initial cleavage of polymer backbone decreases space maintenance. (3) Loss of mass. The material is no longer cohesive and breaks up into fragments which can elicit a foreign body reaction. This response can compromise or prevent bone formation or even result in bone resorption. (4) Final breakdown involves inflammatory reactions including phagocytosis of small particles by macrophages and multinucleated giant cells. * the risk for bacterial induced complications may continue as long as the material is physically present. RESORBABILITY: Gottlow et al (IJPRD,94): 15 monkeys showing the results at 6wks, 3,6,12,and 24 months. Healing was uneventful without inflammation or adverse tissue reaction. At six wks of healing the matrix barrier was completes integrated with no inflammation. New attachment, new cementum, and new bone were found in 6 wks and the matrix was still stable. The material was completely resorbed between 6 to 12 months. At the final stages of resorption, macrophages and multinuclear cells were present. GINGIVAL CONDITION: Laurell et al (JDR,92) : 28 pt, 32 defects, mild inflammation in one defect in 1st month of healing. gingival recession in 13/32 with 2.2 mm average (range 1-5 mm), exposure 5/32. Lundgren (JP 95): 24 defects 4 monkeys. Guidor vs. Vicryl mesh. exposure prevent down-integration new attachment
Guidor 3/12 9/12 2.2mm
Vicryl 10/11 0/11 0.8mm
NEW ATTACHMENT / BONE: Gottlow et al (JPR,92): Comparison in monkeys of Guidor vs. ePTFE. Guidor better Exposure % Bone fill New Attachment
e PTFE 21/30 87% 63%
Guidor 2/30 89% 72%
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CLINICAL RESULTS: Gottlow et al (JDR,92): 28 pts, 32 defects, 12 were class II molar furcations, 20 intrabony defects Class II molar furcations Probing depth reduction 5.6 mm to 3.0 mm, Vertical attachment gain 3.2 mm Horizontal attachment gain 3.1 mm, complete closure of 7/12 , 5 now class I. Intrabony defects: Probing depth reduction 8.9 mm to 3.1 mm, Gain of attachment mean 4.9 mm Wikesjo (93): PTFE vs. Guidor: Horizontal gain = 1.4 vs. 2.1. Laurell (JP 94): 19 man class II furcas and 47 2 or 3 wall defects txd with Guidor. Soft tissue results: PDR 3.7mm PALG-V 3.4mm PALG-H 3.3mm Recession 0.2mm Intrabony results: PDR 5.4mm PALG 4.9mm Recession 0.5mm Multicenter study (Sweden) (JDR,92): 38 pts Class II molar furcations. Hugoson, Gottlow (JP 95 37-30): 12 mo soft tissue measurements Guidor better than ePTFE PAL-H Recession
Guidor 2.1 ± 1.7 mm 0.3 ± 1.0 mm
e PTFE 1.4 ± 1.4 mm 1.2 ± 1.0 mm
MISCELLANEOUS MATERIALS FOR GTR: FREEZE-DRIED DURA MATER: Yukna (JP,92): Grade II molar defects, results were similar between FDDM and e-PTFE. COLLAGEN: Mattson (JP 95): Collagen vs. OFD, intrabony defects. Greater PDR, CALG, less recession than in OFD sites. Soft tissue results at re-entry (6 mos. to 3 yrs): PDR 3.12mm CALG 2.37mm Recession 0.75mm Black, Gher (JP 94): Collagen vs. ePTFE. No difference. Paul, Mellonig (JP,92): Use of collagen barrier membranes in grade II defects doesn’t compare to other membranes. No difference vs. control. Blumenthal (JP ,93): Humans , 12 month re-entry ,bovine collagen membrane vs. e-PTFE in Mandibular Class II defects. All parameters were similar with the exception of better horizontal open probing attachment and reduced inflammation with collagen membranes. Anderson (JP 91): Collagen vs. control in Class II furcas. Greater defect fill with collagen membranes. Blumenthal & Steinberg (JP,90): Combination of autolysed antigen extracted allogenic (AAA) bone and microfibrillar collage (Zyderm) covered with a resorbable collagen membrane showed 62.2% bone fill and gain in attachment in infrabony defects. CONNECTIVE TISSUE GRAFTS: Bouchard et al (JP,93): Mandibular class II furcations, Comparison of e-PTFE vs. CTG. The connective tissue graft cannot be recommended for furcation defects: 1) very difficult to perform, 2) Advantage of one stage lost since need a second surgical site, 3) The use of e-PTFE membranes gives better soft and hard tissue results. BIOBRANE: Flanary et al (JP,91): 15 pair grade II furcations, biobrane membrane vs. OFD, no statistical difference. RUBBER DAM: Advantages Cheap, adapts well to teeth, no suturing Disadvantages high allergic reaction rate 15%, powder acts as foreign body, no space maintenance effect, recession Salama (IJPRD 94): reports on 10 pts using rubber dam as GTR material. material biocompatible and easily adapted. space maintenance inadequate., tissue integration does not occur recession postop common. Avg. attachment level gain 3.84mm and defect fill of 4.25mm. 15% of the population allergic to latex packed with corn starch. Cortellini (IJPRD 94): 5 case reports where intrabony defects were txd with rubber dam material. 3-5mm gain in bone and attachment level were seen at 1 yr. re-entry.
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Zellin- critical size defects, thru-and-thru rat mandible, Resolut LT, GTAM and Millipore filter- good for bone marrow, GTAM least inflammatory reaction. CALCIUM SULFATE: SOTTOSANTI GTR WITH GROWTH FACTORS: Park…Genco (JP 95, 34-29): GTR vs. GTR + PDGF-BB. (1) At 8 and 1 wks greater amount of bone was seen in group with growth factor. 80-87% vs. 14-67% (2) P-GTR stimulated formation of fibrous CT in early stages of repair stabilizing the wound. CT later mineralizes into bone or cementum. MUCOGINGIVAL PROCEDURES Determination of the Mucogingival Junction: Roll technique, visual, Stains (Mallory-CT, PAS-glycogen, Weigert-elastic fibers), biopsy (Stanford intermediate zone, 600-800µm), Schillers IKI Iodine solution. Infiltration technique. MGJ histology described by Lozdan and Squier. Masticatory Mucosa: Attached gingiva, marginal gingiva, palate Lining mucosa: Covering alveolar processes, fornix of vestibule, mucosa of the floor of the mouth, ventral lingual surface of tongue, soft palate, lips, cheeks. Specialized mucosa: Dorsal surface of the tongue Gingival Thickness Soehren (JP 73 39-19) Mean thickness of palatal epithelium: 0.34 mm; Range (0.1-0.6), mean CT thickness was 0.3 mm when harvested with Paquette knife. no grafts thinner 0.75 - 1.25 to assure CT component. Also scuffs up adjacent epithelium when doing FGG. Scar epithelium adjacent to graft. Studer (JP 97 148) Thickness of palatal tissues. Thicker as you go medially, 2-3 mm. Thinnest over palatal root of MX first molar. Thickest in tuberosity area. Goaslind (77): Mean thickness of free gingiva averaged 1.56 mm increased from anterior to posterior and was directly proportional to sulcus depth. Attached gingiva average 1.25 mm, increased from anterior to posterior in the Mand arch, remained constant in the max anteriors, and was inversely proportional to AG width. WIDTH OF ATTACHED GINGIVA Bowers (63 1-11): Facial only, 1-9mm (narrowest Mand cuspid/1st pre), health consistent with less than 1 mm, but areas with no attached gingiva were inflamed. Buccal and Lingual tooth position, high frenum and muscle attachments affected amount of AG. Found an increase in width from primary to secondary dentitions. Tenenbaum (JCP 86 1-15): 331 kids (3-15) 30 pts/age group, saw no change in width from primary to permanent dentition, but did see an increase in the permanent dentition related to decrease in pocket depth. Wennstrom ( 22-26) Thickness of tissue is more important than height of attached gingiva in determining risk for recession (BOARD QUESTION) With supereruption of teeth, the width of the attached keratinized tissue increases. World Workshop says that no one can agree on how much AG is necessary, use your best judgment Ainamo & Loe (JP 66 1-14): X-sectional study, width of attached gingival increases with age Voight (78): Lingual attached gingiva, 1-8mm, more in 1st & 2nd molar (4.7mm), less in anterior (1.9 mm). When going from primary to permanent dentition AG decreased. Andlin-Sobocki (93): 96 kids, aligned teeth, saw width of KG over 2 years. How much is necessary? Lang & Loe (72 1-12): 2mm KG, 1 mm AG, necessary for inflammation persisted even in light of good oral hygiene. Miyasato et al (77): Dental faculty, dental students, areas of minimal width of KG were no more prone to inflammatory changes. Stability of width of Attached Gingiva: Dorfman & Kennedy (80): 92 pts, maintained 3-6 months, Bilateral study, one side graft, 2 yr. followup, in face of inflammation no difference in grafted side over the control. 179
Kennedy, Bird, and Dorfman (JCP 85 39-02): 5 yr. follow up to Dorfman (80), >90% of patients with minimal attached gingiva and poor oral hygiene had increased recession. (BOARD QUESTION) Maintained Patients Discontinued Patients
Control Sites -No increase in gingival inflammation -No increase in recession - Re-establishment of gingival inflammation - Increase in recession >90% (BOARD QUESTION)
Experimental Sites - increase in KG, AG - Gain in Attachment - Decrease in recession - Increase in KG, AG - Gain in Attachment - Decrease in recession
Wennstrom (87 1-13): 26 sites , 6 pts surgically deprived of KG, No difference in recession noted after 5 yrs of follow-up, 3 of controls developed recession. " inadequate AG is a result, rather than a cause of recession. Wennstrom, Lindhe (83) dogs Freedman and Salkin (JP 92 39-1) 10 yr. follow-up to Salkin study. Only 10/64 sites saw a decrease in AG. Supports previous conclusion regarding untxd defects and good OH. BL: Areas with minimal keratinized tissue in the presence of good OH remain stable over 10 yrs. CRITERIA TO DETERMINE ADEQUATE WIDTH OF ATTACHED GINGIVA Hall (77): Age, teeth involved, esthetics, sensitivity, oral hygiene, dental needs, previous dental treatment WHEN WOULD YOU CONSIDER GRAFTING OF AN AREA? It depends on the following: (1) Age of the Patient Wait Andlin-Sobocki (JCP 93): F gingiva of max/man well aligned teeth evaluated in 96 children (7-12yrs) 2xs over 2years. AG and KT increased over 2 year period. Suggests conservative approach in children of this age with minimal attached gingiva. (BOARD QUESTION) Now Maynard (IJPRD 87 39-4) graft before you have a problem, rationale for grafting in kids (2) OH of the Patient Dorfman and Kennedy (80): 92 pts FGG placed on one side vs. ungrafted side with minimal AG. Pts placed on maintenance every 3-6 mos. for 2 years. Both sides sustained PAL. Suggest that with good OH grafting may not be necessary in area of minimal AG. .Kennedy, Bird, and Dorfman (JCP 85 39-2) 5 year follow-up to Dorfman study. Compliant pts results same as in previous study. 10 non-compliant pts examined. GI in these pts had returned to baseline. The grafted sites in these pts displayed no recession, while non-grafted sites displayed addl. recession. Suggests that in pts with areas of minimal AG without consistent maintenance, FGG may be indicated. Also emphasizes importance of good OH in areas of minimal AG. Salkin (87): 39 dental students with inadequate AG (10) HARRIS DISAGREES Maynard and Ochsenbein (JP,75): Conclusions: 1) Mucogingival problems occur in children 2) Prevalence 12-19% 3) FFG should be performed prior to tooth movement 4) Grafts recommended in children with 1 mm or less keratinized tissue 182
5) Grafts would not be recommended in children with > 1mm attached gingiva or 2 mm of keratinized tissue. FREE GINGIVAL GRAFTS: WOUND HEALING Sullivan & Atkins (Perio 68,39-10): Plasmatic circulation (0-2 days), vascularization (2-8 days), organic union (4-10 days). Caffesse et al (JP 79, 39-12): Healing of FGG placed on periosteum or denuded bone: initially slower healing on bone but eventual outcome was the same. Monkey study (BOARD QUESTION) Busschop (JCP 83, 39-21) Fluorescein study on FGG placed on bone and periosteum, no healing differences Mormann et al (JCP 75, 39-20): Fluorescein angiography of FGG Results: 1 day: Marked plasmatic circulation 3 days: Increased # of capillaries, new centers of vasculature and permeation of adjacent graft tissue 4 days: Capillary blood circulation is unimpeded 9-14 days: Uniform capillary distribution Caffesse et al (87, 40-9): Citric acid does not improve clinical attachment in lateral sliding flaps Pasquinelli (IJPRD 95, 39-22) Histo of FGG revealed 4.4 mm of new bone and 4.0 mm of new attachment Oliver et al (68): Epithelialization complete by 14 days; keratinization complete by 28 days Kisch (86): Over 5 years, mobile unattached gingiva was not more prone to recession. Laterally Positioned Pedicle Flap: Grupe & Warren (56 40-1): Lateral pedicle graft with a step BOWERS Pennel et al (65): Oblique pedicle graft******** grafting pioneer Hatler Technique Slide flap over a half tooth (HORNING) Wilderman & Wentz (JP 65, 40-11): Histo: 4 stages of healing process: 1) Adaptation stage (0 hours - 4 days) 2) Proliferation stage (4 - 21 days ) 3) Attachment stage (21- 28 days ) 4) Maturation stage (28 - 6 months) 50% shrinkage of flap 25% new attachment 25% new epithelium Pfeifer & Heller (JP,71 40-12): Full vs. Partial thickness flaps. Full thickness flap (BETTER) had CT attachment in the apical 1/2 of defect and LJE in the coronal 1/2, while the Partial thickness flap had a LJE on its entire surface with no CT attachment. Citric Acid and Laterally Positioned Flaps Caffesse R (IJPRD 87, 40-9): Lateral Sliding flaps with and without CA, No difference. Oles (JP 85 40-7) Agrees with Caffesse on citric acid Double Papillae Graft: Ross et al Cohen (IJPRD,86 40-2): Double papillae graft, technique article Maynard (77): Do FGG 1st, then coronally position the tissue. Tarnow et al (86): Semilunar pedicle Robinson (64): Edentulous ridge pedicle Connective Tissue Grafts: Langer & Langer (83 39-23): subepth. CT graft 2-6 mm of root coverage Edel (74) actually first Raetzke (JP 85 40-8): CT graft placed in an envelope or pouch, (pita pouch) 5/12 achieved total root coverage, 80% coverage, gain attachment 3.5mm, Grafts blended harmoniously with neighboring tissues by 17 days.
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Harris (JP,92 40-10): CTG with partial thickness pedicle graft (double papilla graft), complete root coverage 24/30, mean root coverage 97.2% Used TCN to etch roots. Important factors in success pedicle size, previous FGG, plaque control Harris (JP,94 40-4): 100 defects 97.7% Mean root coverage of above technique. Allen A (IJPRD,94): CT using supraperiosteal envelope, 84% root coverage. Bouchard et al (JP,94): CT with and without the epithelial collar. Gingival coverage was better with the epithelial collar 94% vs. 65% with out, without however did have better color blending. Subpedicle Connective Tissue Grafts: Nelson (JP,87 39-27): Double papilla technique, suture mesial and distal papilla together. Subpedicle connective tissue graft; donor trap door approach, Results: 3mm or = < 100%, 4 to 6 mm = 92%, 7 to 10 mm = 88%. Free Rotated Papilla Autograft Tinti (JP 96 p1016) Split thickness incision, deepithelialize papilla, remove and rotate over area of recession, crossed sling suture, coronally position flap. Questionable methodology (BOARD QUESTION) Coronally Positioned Graft: Bernimoulin(75): Coronally positioned graft First to describe BOWERS Caffesse (JP 78 40-13) advocated FGG before a coronally positioned flap Allen & Miller (JP,89): coronally positioned flap (requires minimum of 3 mm of keratinized. tissue apical to defect and minimum thickness of 1 mm), Class 1 recession. (BOARD QUESTION) What was the success rate Laney et al (JP,92): No advantage of coronally repositioning of a FFG. (BOARD QUESTION) Harris and Harris (JP,94): 20 isolated Class I defects, mean root coverage 98.8% Mucogingival Surgical Methods Comparisons Jahnke (JP 93 39-19): FGG vs. Subepithelial CTG, CTG better than FGG (BOARD QUESTION) Laney (JP 92 39-19) FGG vs. 2 stage coronally positioned flap equal in root coverage Caffesse (JP,80 40-6): Coronally positioned FGG vs. Lateral Pedicle. No sig. difference in predictability and root coverage at 3 yrs POT. Mucogingival vs. GTR Pini Prato (40-14): Compared GTR vs. FGG/CPF. Good results with GTR in covering recession greater than 4.98 mm Tinti (JP 93 40-15): TR membranes can treat M-G defects. Pini Prato (IJPRD 95 40-16) Guidor in tx of buccal recession 65% defect coverage Cortellini (JP 93 40-17) Histo of recession tx’d by GTR Resulted in new bone, cementum and CT Roccuzzo (JP 96 40-18) Gore-tex and Guidor equal in effectiveness in treating buccal recession (BOARD QUESTION) Shih and Allen (IJPRD,94): GTR in mucogingival defect, 86% root coverage. Pini Prato (IJPRD 93): 5 pts with 4-6mm recession txd with GTR + FGG. 3/5 complete root coverage. The other 2 had 1mm of gingival recession remaining. Trombelli et al (JP,95): 24 pts. treated mucogingival defects with ePTFE, fibrin/fibrinogen, TCN (100mg/ml), found that mean % root coverage 71.7%. (BOARD QUESTION) Onlay Graft Siebert (CCDE 93 39-26) Thick onlay grafts to reconstruct deformed ridges Soft Tissue Ridge Augmentation: Langer (IJPRD 89 39-28) uses CT grafts to reconstruct deformed ridges Allen et al (JP 85 39-27): Use of HA for localized ridge augmentation. Scharf and Tarnow (IJPRD,92): Modified Roll Technique, Split thickness from palate and repositioned and sutured in the buccal. Papilla Preservation: Takei (JP 85 31-5) Papilla preservation 184
Murphy (IJPRD 96) Papillary triangle for papilla preservation in GTR procedure. Used only on palate, purse string suture technique. Holmes if cut off papilla, will grow back 50% of the time. HORNING FAVORITE!!!!!!!! Beagle (IJPRD,92): Split thickness flap from the palate, sutures (6.0) suspends tissue between teeth, a broad interdental space is the best for lack of tissue trauma. Anterior Esthetics: Tarnow et al (JP 92 31-33): Effect of distance from contact point to crest of bone in the presence or absence of interproximal papilla. 1) 5 mm or < the papilla was present 100% of the time 2) 6 mm papilla was present 56% of the time 3) 7 mm or > the papilla was present 27% of the time. Allen EP (DCNA,88): Mucogingival Surgical Procedures to Enhance Esthetics 1) Excessive gingival display with insufficient clinical crown length 2) Asymmetry of gingival margins 3) Improper relationship of gingival margins 4) Flat marginal contour 5) Localized marginal tissue recession 6) Localized alveolar ridge deficiency Vestibular extension Bergenholtz (JP 73 39-8)): Lip switch procedure for vestibular extension buccal mucosa to bone, periosteum to lip Robinson (JP 64 39-6): Periosteal fenestration technique at the MGJ. Bone was denuded, healed like attached gingiva. Technique an alternative to grafting?? Corn (JP 62 39-5) Periosteal separation technique to deepen vestibule Allen (JP 67 39-7) Eval’d vestibular extension sx radiographically gain in vest 2.7 mm AG 2.3 mm. Bohannan (63): Vestibular extension procedure, increase 1.5 mm, unpredictable Creeping Attachment: Matter (JP 80 39-14): 5 yr. study of FGG’s, less than 3 mm. Of creeping attachment occurred between 1 month and 1 year Listgarten, Rosenberg, and Lerner (JP,82): Rats, at as early as 3 weeks CT replacement of LJE after OFD. This has never been repeated with no real proof that CT and Cementum was removed during the procedure. Rats have continuously erupting teeth. Dorfman (82) Described coronal creeping attachment in grafted sites (BOARD QUESTION) Bell et al (JP,78): creeping attachment of 0.89 mm or 28%. ROOT SURFACE MODIFICATION Reasons to Modify 1) Surface demineralization 2) Irregular surface that impedes epithelial migration 3) Removal of endotoxin, antibacterial effect 4) Inhibit colonization of root surface aerobes and anaerobes from plaque of periodontally involved teeth in vitro (Daly, 82) 5) Widened dentinal tubules 6) Exposure of inductive proteins. IN VITRO STUDIES Pitaru and Melcher (JPR 87): porcine root slices, EDTA, Human Gingival Fibroblasts. The collagen exposed by demineralized cementum may regulate the physiological organization of CT cells and enhance the strength of attachment of fibroblasts to the tooth during early stages of periodontal wound healing. CITRIC ACID
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Demineralizes peritubular dentin 7-10 µm in depth, exposes collagen fibers in root, detoxifies. Garret: Exposes fibers of dentin/cementum to get anastomoses with flap Polson and Proye (83): Fiber linkage key to success, does not occur without demineralization, monkey study Gottlow: No new CT with CA Tanaka (89): Use of CA to remove all debris and bacteria from partially scaled teeth Animal Studies: Dogs: Garret, Register & Burdick, Ririe & Crigger, Nilveus & Egelberg: All showed it was possible to get CT attachment to previously diseased roots. Monkeys: Polson & Proye, Nyman, Isidor: Minimal or no enhancement Human Studies: Cole (80): 9 human teeth, notch in calculus, CA 5 min, New CT, Some bone, AL 2.1 with CA / 1.5 without CA no one has repeated, 1st to describe a notch in calculus. Dragoo: 21 human blocks, no bone, no CT, no advantage of CA over open flap curettage. Albair (82): 5 min CA, extracted teeth, No CT attached to non-CA treated teeth, CT attached to old cementum, new cementum, but not dentin of CA treated teeth. Chaves (92): Citric acid use does not enhance the results of S/RP i.e. presence/absence of bacteria in humans. Technique: Trombelli (JP 95): Topical application to root surfaces. Morphologic alterations of cementum and dentin are related more to the application interval than concentration. 1 vs. 4 min. 10 vs. 100mg. Sterrett and Murphy (93): Optimal CA concentration is 25-30%, pH 1.55, for 1 minute. Register and Burdick (75): Optimal pH is 1, 3 minute application. Wen (92): Paint it on for more smear layer removal, more demineralization. Miller: Burnish until milky white appearance. Sterrett, Murphy (JCP 95): CA lightly rubbed or burnished has significantly more tufting with greater depth. FIBRONECTIN High molecular weight glycoprotein, cell surface binding (calcium chelator) Caton: Effects upon healing with fibronectin Caffesse: MWF 1.7 attach gain vs. MWF +CA +FN 1.9 attach gain ?significant Terranova (86): In vitro fibroblast attachment enhanced with fibronectin, decreased with laminin Wikesjo, et al (JCP 88, 34-27: CA & TCN enhance CT repair of furcation defects, but root resorption & ankylosis are prevalent. FN did not enhance CT repair & slightly decreased resorption & ankylosis. CA>TCN Terranova, et al (JP 89, 34-28): FN + basic-FGF slightly more chemoattractant than b-FGF alone for PDL cells. TETRACYCLINE AS ROOT CONDITIONER Max binding of TCN at 50mg/ml or greater. Alger (J Perio 1990): human study showed TCN application as root conditioner to enhance new connective tissue attachment. TCN alone was better than TCN + fibronectin. Labahn (92): TCN 100mg/ml vs. CA, CA opened tubules better. Demirel, Baer (91): In vitro, tooth soaked in Doxy 3 mins, 100mg/ml had antimicrobial effects persisting to 14 days Claffey (87): PDL response to Tetracycline was greater than CA in beagles. Wikesjo (86): Release of Tetracycline up to 48 hours post application with biocidal activity, reservoir for TET 2 days. Lafferty, Gher et al (JP 93 34-18) SEM of root surface treated with CA or TCN-HCl for 5mm, exposure and removal of smear layer, devoid of debris, and network of collagen fibers. CA and TCN produce similar root surfaces after conditioning. TCN from capsules may introduce fillers and other sediment. DOXYCYCLINE AS A ROOT CONDITIONER Demirel (91): 100mg/ml inhibited Aa, Av, Pg on root surfaces in vitro.
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PERIDEX as a root conditioner Alleyn et al (JP 91): CHX impairs fibroblast attachment to dentin in vitro (impacted 3rd molars) Stabholz (93): CHX vs. TCN (100mg/ml), CHX had no long term antimicrobial effects 1-6 days POT. Antiformin Sodium hypochlorite, Na(OH)2, Sodium carbonate ROOT SURFACE BIOMODIFICATION (with GTR) CITRIC ACID with GTR McClain and Schallhorn (93): 5 yr. follow-up of GTR with and without CA root conditioning and composite grafts (DFDBA + autogenous bone). Long term results enhanced with CA + graft Handelsman (91): 17 pts reentry at 9 months, CA with GTR = no enhancing effects Kersten et al (JP 92): CA with e-PTFE in intrabony defects. No statistical difference. More recession in CA treated defects. TETRACYCLINE with GTR Machtei (91 abs): Adjunctive effect with TCN root conditioning and GTR Parashis (93): PTFE membranes vs. PTFE + TCN100mg/ml, 6 pts, bilateral Class 2 Mand molar furcas. No sig. difference with TCN. SAFETY: Blomlof (JCP 95): Monkeys. Long time etching (3 min) at low pH impaired periodontal healing. Short time etching appeared to promote CT formation despite low pH. Why Extract teeth? Furcations, severe intractable pain, root fracture, non-functional/severe disease. SUPPORTIVE PERIODONTAL THERAPY COMPLIANCE Wilson (JP 84): 16% full, 49% erratic, 34% non-compliant the longer the maintenance interval the more compliant compliance overall very poor (BOARD QUESTION) Wilson (JP 87 41-22) Compliant pts lost no teeth, Erratic group lost all the teeth. Wilson (JP,93 41-31): Using compliance improvement methods was able to increase complete compliance from 16% to 32% at the expense of the non-compliant group. Becker, Karp (JCP 88 41-26): Surgery patients are more compliant with maintenance, better if good self image, self confidence Johansson (JCP 84 41-16) Possible to maintain perio status despite poor compliance by the patient. Pts didn’t use supplemental cleaning aids. Mendoza (JP,91): 36% compliant, 48% dropped out the first year; 30% failed the first recall Checchi (JCP 94): 38% completely compliant the 1st yr., only 20% completely compliant at 4 yrs. Highest drop out rate occurred from the 1st to the 2nd year. Derbyshire: Pt needs and motivation must be determined Rayant and Sheiham: No relationship between perceived susceptibility and behavior. Kuhert and Rachske (88): Both 5 visit (short), and 2 visit (long) OHI were equally effective in improving pt OH at 12 weeks and 48 months with recall every 3 months. Rosenstock " Health Belief Model"- perceived seriousness, perceived susceptibility, perceived barriers, perceived benefit, Demetriou et al (JP,95): Compliance 14 yr retrospective study in Europe, 27.4% complete, 14.4% erratic TYPES OF MAINTENANCE Schallhorn (JADA 81 41-6): preventive, trial, compromised, post-treatment Untreated Periodontal disease: Marshall-Day (1955): 5.2 teeth over a ten year Becker et al (JP,79): Mean loss was 0.36 teeth/PT/year Lindhe, Haffajee et al (JCP,83): Swedes: 11.6% sites measured more > 2mm, 37% lost 2mm, 78% lost > 1mm Americans: 3.2% lost more than 2 mm, 4.3% gained more than 2 mm
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Maintenance and Non-Surgical Treatment Caton (82 41-11): Patients well maintained following S/RP at 3 month intervals (actually closer than 3 months). Axelsson, Lindhe (JCP, 81 41-8): After 6 yrs, pts receiving q 2-3 mon maintenance had control of perio vs. once/year maintenance. Anti-GP maintenance Periodontist should be involved in maint. Caton et al. (JP,89): Oral hygiene reduced interdental inflammation, but subG scaling in addition to OH decreased the interdental inflammation to greater extent than OH alone, repair occurred within 4 weeks and was the same for 4 months Axelsson (JCP,91): Pts with q2-3 month recall had control, pts on 1 year recall (Back to GP) did not have control. Maintenance and Surgical Treatment SWEDES: OH MOST IMPORTANT Nyman (JCP 77, 41-4) Surgery in plaque infested dentitions, one session of OHI and periodontal disease recurred Nyman (JCP,75 41-2): Reverse bevel surgery, q 2 weeks verses 6 month maintenance (considered failed surgery) Shorter, the better. Rosling (JCP,76): Regenerative surgery, SPT q 2 wks on 12 pts gained 2.8 mm of bone, SPT q 1 yr. on other 12, deteriorated. Rosling (JCP 76 41-3): Different types of surgery all successful with good oral hygiene and close recall. Lindhe, Nyman (JCP,84 41-14): Tx of advanced disease can be maintained over 14 years. Wennstrom (JCP 93 41-15) Regular dental patients lost very few teeth over 12 years. Attachment lost most frequently on the buccal surfaces Lindhe (75): 75 pts with "severe" perio, surgery including tunneling, root resection, maint 3-6 months, no teeth lost over 5 years. MICHIGAN: MAINTENANCE Q3 MONTHS MOST IMPORTANT Ramfjord (JCP 87 41-25) OH not critical if patients are maintained q3 months Knowles et al (JP,79): Modified Widman, Curettage, pocket elimination: all stable for 8yrs with 3-4 mo recall. Split mouth study design, Problems: No furcations, measured at line angles, pooled data. Morrison (82): Gingivitis not related to PD and AL in 7 yrs maintenance of 78 Michigan study pts. ARIZONA: Becker. (BOARD QUESTION) Perio treatment SPT 0.11 tooth lost per year Perio treatment No SPT 0.22 tooth lost per year No Perio Treatment No SPT 0.36 tooth lost per year
41-18 41-17
TEXAS: Nabers (88 41-28): 1535 pts, Ave. tooth loss was 0.29 teeth/pt/12.9 yrs. 444 teeth lost in 164 pts (due to other factors) Splinted patients lost a lot of teeth. 74% of patients had surgery. 15.9% required retreatment. Meador (85): 620 pts treated with surgery/non surg over 22 yrs, surgical pts were 71.1% stable, non-surg pts 54.8% stable RETROSPECTIVE STUDIES: % of Patients in Group
Average tooth loss/Patient
Study H&W 78 McFall 82 (41-32) Goldman et al 86
tooth / yr. 0.08 0.14 0.16
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(41-33) How well does maintenance prevent gingival inflammation? Suomi, Greene (JP,71): Large scale study (1248pts), showed oral hygiene and professional prophy @ multiple times during 3 yrs resulted in less radiographic bone loss, PAL, GI, and PI than matched controls. Morrison, Ramfjord (JP,82): Gingivitis was not related to PD and PAL levels in 7 yrs of maintenance MAINTENANCE INTERVALS Lovdal (61) Three month maintenance, showed decreased tooth loss regardless of OH. (BOARD QUESTION) Lindhe & Nyman (1975): Patients on 3-6 months interval maintenance for 5 years lost little or no further attachment. Failure to contol supraG plaque following Sx may result in an extremely rapid rate of loss of clinical attachment. Hirschfeld & Wasserman (1978): 600 pts 4-6 months interval for 22 years. Most patients lost very few teeth. Listgarten (JCP 82. 41-12, 20, 21, 6-11) Used DDFM to set recall interval, didn’t work well. Also found that most gingivitis lesions did not progress to periodontitis Westfelt (JCP 83 41-13) Studied different recall intervals, q2 weeks best, increasing recurrence of disease with increasing maintenance intervals Ramfjord (JCP 87. 41-25) OH not critical if patients are maintained q3 months Magnusson et al. (1984): Microbiota returns to baseline after treatment within 4 months if good OH is not accomplished. Greenstein (92): Return of flora to baseline at 9-11 weeks. When is it Necessary to re-treat? Chace (JP 77, 41-5): 1) BOP 2) Increase in pockets 3) Radiographic bone loss 4) Increase in tooth mobility Are vertical defects more prone to bone loss during maintenance? NO! Pontoriero (JCP 88 41-36) Sites with angular bony defects are not particularly susceptible to recurrent periodontitis. Prognosis vs. Outcome McGuire (JP 91 41-30 19-27) Prognoses more accurate for single rooted teeth. Prognosis best for good category. Prognoses for other categories switched between categories a lot. Very conservative estimates. SupraG Plaque Control Effects on SubG Flora: YES: Katsanoulas (92): Professional supraG plaque control can effect subG bacteria (spirochetes/motile rods via darkfield). Seigrist & Kornman, Smulow supports. Dahlen (92): 2 yr period, supraG scaling, caused a reduction in Pg, Aa, Fn, Selenomonas, marked change in composition of flora. McNabb et al. (JCP,92): SupraG cleaning 3X / week for 12 weeks showed a decrease in subG microbiota. Waerhaug ( 27-14) SupraG plaque determines subG NO:
Kho (85): SupraG plaque control on deep pockets, 8 pts, prophies with supraG scaling failed to alter quantity and composition of the subG flora after 18 weeks. Listgarten (78): Effects of scaling on subG microflora, 6 pts, 8-25 weeks, Darkfield exam: no changes in coccoid, rods, spirochetes.
MISC: Kornman (JPRes 86, 8-6): Prevent disease by: 1) eliminating all detectable plaque 2) reduce plaque below individuals threshold for disease 189
3) alter plaque composition such that periodontitis will not develop. Patient Satisfaction: Kalkwarf & Kaldahl (92): 80-90% of patients were willing to repeat therapy, didn't know what kind of surgery performed. 2nd molar most commonly lost during maintenance. IMPLANTS PRINCIPLES Branemark (JPD 84 24-1): Concept of osseointegration, direct connection between living bone and a load carrying implant at the LM level Albrektsson (IJOMI 86 20-21): Proposed changes for the criteria for implant success, 1) immobile, 2) no periimplant radiolucency, 3) < 0.2 mm bone loss after the first year loading, 4) no pain, infection, neuropathies, paresthesia, 5) minimum 85 % success at 5 years and minimum 80% success at 10 years. Meffert (87): Biointegration, LM direct biochemical bone to implant surface interface, confirmed at the EM level. Weiss (86): Fibro-osseous integration, i.e. the interposition of healthy dense connective tissue between the implant and bone. Must have blade or spiral shaped implants for this to work. IMPLANT SIZE Langer, Langer (IJOMI 93): 5.0 mm diameter Branemark, self tapping good for areas of inadequate bone height, poor bone quality, immediate placement in previous failure sites or extraction sites. Bahat (IJOMI 93): Studied implants placed in the posterior maxilla of varying bone qualities. Length of the implant was especially important in Type IV bone situations. The longer the implant the greater the success. Type IV bone and 7 mm implants 14.3% failure Type IV bone and 10 mm and above implants, 1.6% failure rate Saadoun (IJPRD 92) Titanium screw vs. HA cylinder. Implants placed in both maxilla and mandible, anterior and posterior. Overall 8 mm implants were only 56.9% successful. Implants > 12 mm had close to 100% success IMPLANT SURFACE AREA Daniels A screw increases the surface area by 7%, plasma spray increases surface
area by 6X
BONE QUALITY Bone Types: Lekholm and Zarb: I II III IV
Homogenous cortical bone Thick cortical bone with a marrow cavity Thin cortical bone with dense trabecular bone of good strength Very thin cortical bone with low density trabecular bone of poor strength
Truhlar, Orenstein, Morris (JOMS 97): Multi-center examination Type 2 bone predominated in the mandible and type 3 in the maxilla. Patents classified as healthy, had a lower proportion of type 1 and 2 bone than those with mild systemic disease. Males showed similar levels of type 1 compared with type 4 bone with females had more type 1 than type 4 bone. Jaffin and Berman (91): Branemark fixture failures by bone type: Type Bone I, II, III 190
Mand 2.6 %
Max 3.6 %
Total 3%
IV
26 %
44 %
35 %
Friberg Jemt, Lekholm (IJOMI 91) Failure rates associated with type four bone in maxilla and type 1 in the mandible. Most fixtures were lost in the maxilla advanced resorption IMPLANT SUCCESS RATES Overall Misch Need 25% bone to implant contact minimally for success Adell (IJOMI 90 24-18) Long term follow-up on Branemark implants. 700 patients, 4636 implants 95% continuous pros stability 5-10 years in maxilla. 99% for mandible Individual fixture success rate MX 8492% MN 86-98%. Albrektsson (JP 88 25-20) Success rates of non-Gothenburg placed implants. MX 84.9%, MN 99.1% Partial Edentulous Patients Pylant, Triplett Retrospective of titanium implants MX 89.3% and MN 87.8%. Single Implant Restorations Jemt, Lekholm (IJPRD 90) at 3 years 91% success, 1 mm more bone loss than standard implants. Jemt et al (IJOMI 91) multi-center study showed 2.8% failure at one year. Ekfeldt (IJOMI 94) 98 single unit Branemark implants ranging from 1 year out to 5 years. 98% success rate. Overdentures Quirynen et al (JCP 91) Implants in function a mean of 1 year. 1% failure in the MN. Jemt (IJOMI 92) 1 year follow-up of 92 patients with overdentures in severely resorbed maxillae (16%). failure rate at 1 year (84% success rate). Note Approximately 70% of the implants were 7 mm in length. Hemmings (IJOMI 94) 25 patients 5 year data 91.2% success rate. Fixed Prostheses: Jemt (IJOMI 91) 2199 implants, (73% MN) overall success rate 99.5% for prosthesis, 98.1% fixtures. Hemmings (IJOMI 94) 25 patients 5 year data 88.6% success rate. Partial Bridges Quirynen et al (JCP 92): 6 year period, failure rate 5.9%, cumulative rate means down but can be replaced it is still considered a success.
if bridge breaks
Implants in Posterior Jaw Jemt (IJOMI 93 25-16): Cumulative success rate 97% for fixtures, 100% for prostheses Nevins and Langer (IJOMI 93): Maxilla 652 implants >99% prosthetic success, 95.2% implant success Mandible 551 implants 97% prosthetic success, 95.5% implant success Bahat (IJOMI 93): Examined implants placed in the posterior maxilla with an average loading time of 30 months. 63% of implants placed in type II/III bone with the remainder placed in type III/IV bone. Overall failure rate 4.8% Type IV failure rate 5.5% Type II/III failure rate 4.6% 7 mm failure rate 9.5% 10 mm + failure rate 3.8% Short implants in type IV bone had a much higher failure rate (14.3%) than longer implants in type IV bone (1.6). Implants can be placed in type IV bone but they need to be at least 10 mm in length. Saadoun (IJPRD 92) Comparison of SteriOss titanium screws, HA cylinders, and HA screws. Posterior areas revealed a lower success rate than anterior areas in both the Max and MN MX success rates Anterior 95.1% Posterior 87.1% MN success rates Anterior 98.6% Posterior 93% IMPLANT FAILURE Morgan, James Pilliar (IJOMI 93): High lead stresses result of 3 conditions 1. Bone resorption coronally, developing higher bending stresses
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2. Bone loss extends to a level corresponding to the end of the abutment screw 3. Sharp corner at root of a thread creates an area of stress concentration Worthington (IJOMI 1988 26-9): Most implant problems are iatragenic and prevented by careful treatment planning. Faulty placement, faulty alignment, excessive countersinking, wobbling drill, echymosis, stripping bone threads and stitch abscess. Prosth problems: speech diff, prosth fracture, Au screw fracture, inadequate lip support and ingestion/inhalation. AILING IMPLANTS Meffert (Impl Dent 92 26-20): Active infection: Flap, debride, remove contaminated HA, TCN paste 2-3 min, Graft rinse. No active infection: flap, detoxify with 40% CA 30-6- sec, rinse, graft. IMPLANT TO BONE INTERFACE Hansson (JPD 83 26-2) LM and SEM study of interface between bone and Ti implants. Found ground substance consisting of proteoglycans 20 nm (200 A) wide between bone and implant Lindner (AOS 83 26-1) On light microscope level, the bone titanium interface is melded. On the TEM’s there is a 20-50 nm gap - proteoglycans. Strength of bond inversely proportional to proteoglycan layer. 100-500 nm collagen layer peripheral to proteoglycan layer. Piatelli, Trisi (JP 93) Bone Ha interface in human retrieved implant with stain morphology varied nonmineralized matrix interposed between HA and bone with only a small amount of calcified tissue directly on the HA surface. Ca content increased from bone to coating and then decreased at the interface Ca-P rich. Piatelli et al (IJOMI 93) Human histology HA (IMZ) LM 70% intimate contact, no inflammation. Laser Scanning Micro dark staining lines resembling reversal lines, WET-SEM amorphous granular substance at interface of HA appears osseointegrated. Gottlander (IJOMI 91) threaded HA implants vs. commercially pure titanium (CPTi) in rabbit tibia. 6 weeks and 1 year results. 6 weeks more direct bony contact with HA. 1 year more bone to implant contact with CPTi. Carlson (J Orthoped Res 94) Rough CPTi vs. smooth CPTi vs. HA coated implants inserted into human arthritic knees. Smooth implants were mostly encapsulated in fibrous tissue. Marrow space response to implants Rahal, Branemark, Osmond (IJOMI 93) Mice femurs, the implants that impinged on the medullary cavity became intimately surrounded by regenerating bone and with no attempt encapsulate implant. IMPLANT EPITHELIAL ATTACHMENT NO Berglund, Lindhe Periimplant mucosa cufflike adhesion, well keratinized with good plaque control implant tissues can be maintained Arnim and Hagerman (53) CT band encircling teeth maintain gingival tone, only in keratinized tissue YES
Gould (JPD 84 26-3) Noted hemidesmosomal attachment between epithelium and Ti coated epon implant. Bauman et al (IJOMI 93 24-3) Review article on Peri-implant sulcus, the attachment of implants was compared to the natural tooth. Findings in the literature support similarities in sulcular epithelium, junctional epithelium (basal lamina, hemidesmosomes, glycoprotein adhesion) but the difference is in the connective tissue fiber insertion (no Sharpey’s fibers) it hasn’t been proven in implants although the fibers have been sited in the area. Listgarten (91) Junctional epithelium is attached to implants via a basal lamina and hemidesmosomes McKinney et al (JP 85) Attachment complex on aluminum oxide (sapphire implants). saw internal basal lamina, including sublamina lucida and hemidesmosomes Carmichael, McCulloch (JDR 91) Immunohistological marker (keratin I) and desmoplakins (desmosomes) found a different cell population and a JE subpopulation attached to implants Schroeder (81) reported functional hemidesmosomes and basal lamina on Ti sprayed implants in monkeys.
PERIODONTAL LIGAMENT FORMATION AROUND IMPLANTS Buser (IJOMI 90 26-5) Placed implants next to retained apical root fragments, got cementum and PDL to form on implant. Histo can’t tell if cementum. Warrer, Karring Gotfredson (JP 93) Ti implants placed in mandibular bone in areas contacting retained root had healed with intimate bone -implant contact. In 8/14 a newly formed cementum layer
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consisting of dentin or original cementum as well as the entire implant surface. In 4/14 a dome shaped soft tissue area was between the root and the implant surface within this space were indistinct fibers with varying orientation IMPLANT IMAGING Poon et al (92) X-sectional tomography is simple precise reproducible and economical Ekestubbe (COIR 93) Spiral tomography offers images with slightly better reliability as compared to images obtained with linear tomography. Lindhe (JOMI 89) Canal could not be identified in 17% of tomos and 35% panos. Sonick (94) PA vs. Pano vs. CT. Distortion CT 1.8%, PA 14% Pano 23.5% Todd and Gher (JP 93 24-7) Linear vs. CT 8.7 mm difference between linear and CT IAC location. CT was superior to linear tomos. The IAC was hard to identify in the linear tomos (only seen in 6/22) MICROBIOLOGY OF IMPLANTS General Studies Bacteria of periimplantitis and adult periodontitis similar Mombelli (87) Microbiology of failing implants Gr.- anaerobes, BPBs, Fusos Staph and Candida. No Aa found Quirynen (JCP 95) Rough surfaces, crowns, implant abutments and denture bases, accumulate and retain more plaque (thickness, area colony forming units) Ong (92) Branemarks, cultured for Aa, Pg, Pi periimplant sites clinically healthy, 7 of 32 sites with Pi Aa and Pg minimal. Meffert (PP&Esth Dent 1993): Implants place in the partially edentulous mouth are at greater risk since the bacteria are more pathogenic. Periodontitis and periimplantitis are one and the same caused by the same bacteria. Micro of Implants in Edentulous vs. Partially Edentulous Quirynen (90) Plaque adheres better to titanium than enamel. Rough abutments 25X more bacteria. Fewer cocci and more spirochetes around implants in partially edentulous than fully edentulous patients. Used when citing “microflora is different around implants placed in a partially edentulous mouth vs. those placed in fully edentulous patients” Apse (89) Found few microbiological differences between teeth and implants. However did see a lot fewer pathogens in fully edentulous cases. Suggests that natural teeth microflora may seed implants. Rosenberg (91) Different flora associated with infected implant and those failing due to TFO more partially edentulous failures than edentulous. More anterior implants lost due to trauma and posterior implants due to infection Micro of Teeth vs. Implants Bauman Bacteria of implants and teeth the same van Steenberghe (JP 93) A greater accumulation of plaque was noted on abutments than natural teeth Leonhardt (COIR 93) Followed 19 patients out to 36 months. Proportion of bacteria is the same for teeth and implants within 1 month. By 3 years, putative pathogens have reached the same levels around implants as are seen around natural teeth. Mombelli (JCP 95 26-14) Evaluated pathogens at residual pockets of periodontally treated patients and implants in these patients that were exposed to the oral environment for 3 and 6 months. Individual bacteria and their proportions were similar between the 2 groups at both 3 and 6 months. At 3 months pathogen levels around the implants already mimicked those levels seed in residual pockets at baseline. Cross-Infection From Teeth to Implants Gouvoussis, Sindhusake, Yeung (IJOMI 97): Supports transmission of perio pathogens from periodontitis sites to implant sites. When teeth had Aa or E corrodens, 100% of implants Aa and E corrodens. This was 83% and *5% for Pi and F nucleatum.
IMPLANT SYSTEMS HA IMPLANTS SUPPORT Gottlander (IJOMI 91 25-31) More bony contact with HA coated implant than Ti. After one year the Ti implant had more bony contact
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Saadoun (IJPRD 92) Different lengths of Ti screw vs. HA cylinder vs. HA screw implants placed in maxilla and mandible, anterior and posterior Overall success rate 92.64% Ti screw 85% HA screw 97.14% HA cylinder 98.5 Differences become even greater when looking at shorter implants 8 mm Ti screw 30% success rate 9 mm HA screw 88.9% 8 mm HA cylinder 100% Suggests use of HA implants when shorter implants are indicated Koster Better adhesion of epithelial cells to HA Bowers More epithelial adhesion to a rough frosted collar Harrell Bone will bridge to HA 0.5 mm Block (87) More HA to bone interface than non-HA coated implants at ultrastructural level, HA-bone contact 66%, Ti 50% contact. Bone maturation was faster around HA implants. Lack of osseointegration at Phase 2 0.2% Cook (87) HA has 5-8 X interfacial shear strength of grit blasted Ti at 10-32 weeks Kent (88) Clinical biointegration as early as 8 weeks. Bottom Line on HA. HA implants tend to integrate faster (as early as one month) which may be helpful in an area of soft bone. Against HA Johnson (92) Screw shaped fixtures may provide greater resistance to relative motion than press fit implants Adell (86) 734 MX Branemarks 5-12 year success was MX 81% MN 91% success. mean crestal bone loss was 1.5 for the first year and 0.1 mm thereafter. Bahat (IJOMI 93) 5.5 years 213 consecutive Branemark posterior maxilla. Overall failure rate 4.8% Type IV bone 5.5 % 7 mm implant in Type IV bone 14.3% compared to 1.6% with 10-20 mm implants. BL: Long implants in adequate bone can be successful in post maxilla. IMZ
Babbush (IJOMI 93) 5 year success rate 95%, 8.0 mm and 3.3 mm diameter have less success also those placed in maxilla. Intramobile element popularized to simulate the PDL so implants could be attached to natural teeth. It was later found that there is enough give tin the screw assembly that the mobile element wasn’t needed.
ITI One stage implant design. No second stage surgery. Salonen et al (IJOMI 93) Analyze implant failure of TPS ITI, Bonefit, Biolox. The ITI had the highest failure rate both fixture and prosthetically. Buser (IJOMI 91 24-33) 3 year success rate 96.2% Behneke et al (ITI World Symposium 95) ITI implants placed in edentulous and partially edentulous patients. 774 implants (288 implants in function between 3 and 6 years). Overall failure rate 1.9% 1 Year success rate 98.1% 3 year success rate 97.3% 5 year success rate 97.3% Mean bone loss between insertion and restoration 0.8 mm Mean bone loss between restoration and 4th annual exam 0.1 mm annual bone loss Behnek, Behneke, d’Hoedt (IJOMI 97): ITI implants had 98.1% success after 3 years. GCF correlates with bone loss, more horizontal bone loss than vertical loss. OTHER IMPLANT TYPES Subperiosteal implants metal framework of Vitallium, introduced in the 1940’s, poor success rates. Blade implants Implants surrounded by fibrous connective tissue. Smithloff and Fritz (87) 15 year evaluation of Linkow-type blades, 50% success rate, 26 of 49 left, 13 of remaining were ailing Vitreous Carbon Stainless steel core covered in 99.9% carbon, 65% success at five years. Single crystal sapphire implant Tubingen aluminum ceramic implant
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Tri-calcium Phosphate implant Titanium Plasma Sprayed Transosteal Mandibular staple
IMPLANT PLACEMENT CONCERNS ANATOMIC CONCERNS Mandibular Nerve Anderson (JOI 91 25-1) Three types of IAN one as a single trunk and two with extensive branching. Misch Text (93) Safety zone viewing the canal radiographically with Panorex, staying above canal 100% to mesial to first molar, 97% distal to first molar, 43% mesial second molar, 5.5% distal to second molar. Rosenquist (IJOMI 92 25-22) Ring of bone surrounding mental nerve removed, cortical plate removed, alveolar nerve lifted from canal, implants placed, nerve allowed to lie passively against implants. All sites had normal sensory function at one year. Friberg Lekholm (IJPRD 92 25-23) Inferior alveolar nerve transposition, technique - remove buccal plate of bone, carefully dissect. initial paresthesia definite with possible permanent damage, other complications infection, osteomyelitis. MENTAL NERVE AND ITS ANTERIOR LOOP Arzouman (93): 25 skulls anterior loop measured directly with flexible tubing and also via a pano. 90+ % of the skulls revealed loops of >2mm when measured directly. Loops >2mm were seen in 66% of the cases according to the panos. The avg. loop length was 6.95mm by direct measurement and 3.33m by pano. Pano radiographs may not indicate the true incidence or extent of anterior loops. Bavitz (IJOMI 93 25-3): 24 cadavers. Loops measured anatomically and radiographically. Anatomic Radiographic measurement measurement Dentate avg. 0.2 mm avg. 2.5 mm range 0-1 mm range 0-7.5 mm Edentulous avg. 0.0 mm avg. 0.6 mm range 0-2 mm Implants can be placed as close as 1 mm anterior to the radiographic mental foramen Solar (94): 37 human man specimens. 15/37 had no ant looping. 22/37 had looping ranging from 0.5 to 5mm with the average being 1.2mm. Looping was not dependent on the residual ridge type. (BOARD QUESTION) Misch Text (93) Presence of anterior loop 12% (5 mm average forward), absence 88% Arsouman (IJOMI 93) Average length of the anterior loop based on direct measurements was 6.95 mm, radiographic assessment 3.18 mm pano and The loop of the inferior alveolar nerve at the mental canal is superior to the orifice of the mental foramen. (BOARD QUESTION) Vasculature Bavitz (OOO 94 1-23) There can be an extra artery in the floor of the mouth. Watch out if you perforate the lingual cortex when preparing an implant site. Ten Bruggenkate (IJOMI 93 25-4) Hemorrhaging in floor of mouth after perforation of lingual cortex. 1 case described with late bleeding, the other with immediate bleeding. Careful!!!! Sinus Lifts Smiler (DCNA 92 25-29) Review article on sinus lifts. Indications: crestal bone less than 3-4 mm (which is needed for initial stabilization of the implant) Likes using HA Wood (88) Grafting of maxillary sinus with intraorally harvested autogenous bone prior to implant placement. Small Zinner (IJOMI 93) Simultaneous implant with surgical lift, grafting with nonresorbable, porous HA and DFDBA Whittaker (JOI 89 25-28) Histo of sinuses grafted with resorbable HA and DFDBA. Found implants to be osseointegrated, HA osteoconductive, DFDBA osteoinductive.
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Maxillary Tuberosity Bahat (IJOMI 92) 72 implants in tuberosity, 93% success rate. Khayat (PPAD 25-24) Indications for tuberosity implants. Low sinus floor, cannot place implants in molar regions, high smile line, pt desires restoration of all teeth. Contraindications: inadequate bone in tuberosity, implants can be placed in molar regions, inadequate access. Pterygomaxillary-Pyramidal Region Valeron, Velazquez (IJOMI 97): Tech article 93.5% success after 3 years. Indications resorbed maxillary tuberosity, can avoid sinus lift. MEDICAL CONCERNS Smith Berger and Dodson (IJOMI 92 26-11) The number of medical problems and the ASA status were not statistically associated with an increased risk of implant failure. Irradiated Bone Albrektsson (JP 88 25-20) Good success rates in irradiated bone. Ueda et al (IJOMI 93 26-13) Recommend implant surgery be performed at least 1 year after radiation therapy, use of hyperbaric oxygen increased survival rate to 92.3% while Parel cited a survival rate of 64.7% with tx after radiation. Johnsson et al (IJOMI 93) Rabbits irradiated 15 Gy, then implant placement, 8 weeks removed hyperbaric oxygenation increased the amount of torque required for removal 44% over non-HBO sites. Granstrom, Albrektsson (IJOMI 93) If irradiation is to be performed in areas where titanium implants have been placed, it is recommended that all prostheses, frameworks, and abutments be removed before irradiation, the fixtures should be allowed to remain intact but should be covered with skin or mucosa. Franzen (IJOMI 95) 5 patients treated with radiation and surgery for oral malignant tumors. 20 Branemark implants placed in irradiated bone of the mandible. 1/20 implants did not integrate. The other 19 were stable after 3-6 years. Osteoporosis Lindsey Osteoporotic changes in the jaws are similar to other bones in the body. The structure of the bone is normal, however the cortical plates are thinner , trabecular bone pattern more discrete, and advanced demineralization occurs. Dao, Anderson, Zarb (IJOMI 93) Osteoporosis as diagnosed at one particular site of the skeleton is not necessarily seen at another distant site. 25% of women over 45 years suffer from it. Results of this study which was on several older individual didn’t show any difference in success/failure although they did not identify the osteoporosis patients. Von Wowern (IJOMI 90 24-14) Bone mineral content in mandible was measured after implant therapy. Implants increased loading counteracted BMC loss. Diabetes Shernoff (DI 94) 178 implants in 89 type I diabetics, 4 failures at uncovering (2.2%) at one year 7.3% failed. Suggests that root form implants can be successful in these patients. Smoking Bain and Moy (IJOMI 93 24-17) 1. Total implant failures were 130 out of 2,194 (5.92%) 2. Smoker failure rate 11.28%. 3. Non smoker failure rate 4.76%. 4. Highest failure was in the posterior maxilla (12.3%) lowest in mandibular anterior 1.1% 5. Smokers had higher failure rates in all areas except the posterior mandible 6. Shorter implants ( rhBMP-2/ mem (3.7 mm) > rhBMP-2/mem (2.4 mm) > rhBMP-2/ mem (2.2 mm). Schwartz-Arad, Chaushu (JP 97): 95% success rate in immediate implants placed with autog grafts, without membranes, obtaining primary closure and using temporary immediate dentures. MEMBRANE EXPOSURE IN GBR Simion et al (IJPRD 94) e-PTFE GTAM implants inserted into extraction sites. Membranes not exposed did not sow evidence of bacteria and demonstrated 96.6% regeneration. Membranes that became exposed were removed 30-45 days later and showed many bacteria and regeneration of 41.6%. Bacteria were
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evaluated with TEM, exposed membranes were not maintained with CHX. Early membrane exposure may result in complications that interfere with the effects of bone regeneration. GRAFTS WITH IMPLANTS Nystrom, Albrekson (IJOMI 93) Histo of hip graft 4 months after placement with 6 Branemark implants which secured graft. Results: fusion between transplanted bone and alveolar process without demarcation line, no sequestration noted, new bone formation but gap not bridged. IMPLANT MUCOGINGIVAL CONCERNS Adell - attached keratinized tissue is present at 65% of implants. Keratinized tissue necessary around implants? Kirsch (89) failure rate of 2.2%. Attributed the main cause of implant failure to insufficient width of attached gingiva of insufficient mucogingival attachment. Keratinized tissues more resistant to Periimplantitis. Warrer et al (ITI World Symposium 95) 30 implants placed in edentulous areas of 5 monkeys with KT either present or absent. 3 month healing period with optimal plaque control, then disease induced by ligatures. Ligated implants without KT demonstrated significantly more recession and slightly more attachment loss than implants with KT. (BOARD QUESTION) CRESTAL BONE CHANGES Herman, Cochran Nummikoski Buser (JP 97): Location of rough/smooth interface and location of microgaps may influence bony remodeling after implant placement. Rough surface - better around bone. Smooth Surface - better around tissue. Microgap responsible for initial bone loss: 1) bacterial colonization of microgap leading to epithelial proliferation, 2) micromovements may cause epithelium forming around non-moving implant, 3) interruption of blood supply when abutments placed. Keratinized tissue is generally easier for patients to keep clean, it is also more esthetic. KT not necessary around implants Wennstrom (COIR 94) Eval of 39 patients 171 implants with either a full arch FPD in function > 10 years or a partial FPD in function > 5 years. 24% of the implants lacked KT with an additional13% containing