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Localized Aggressive Periodontitis (LAP): By: Rebecca Goldberg, Pediatric Dentistry What is Localized Aggressive Periodontitis According to Dr. Joseph Califano, 2003, Position Paper: “Periodontal Diseases of Children and Adolescents Rapid and severe loss of alveolar bone around more than one permanent tooth, usually the first molars and incisors Characterized by interproximal attachment loss on at least 2 permanent first molars and incisors, with attachment loss on no more than 2 teeth other than first molars and incisors Frequently disease is localized to permanent molars and incisors, however some retrospective data on LAP patients suggest that findings of bone loss around primary teeth can be early finding in disease Occurs in otherwise healthy children and adolescents without clinical evidence of systemic disease Patients have little or no tissue inflammation and very little supragingival dental plaque or calculus Rates of Bone Loss Progression Adult Periodontitis: 0.072-0.736mm per year LocalizedAggressive Periodontitis: 1.08-1.80mm per year *Approximately 5x’s more bone loss per year in LAP 3 Localized Aggressive Periodontitis * Term used to be Localized Juvenile Periodontitis (LJP) Epidemiology According to Dr. Terry D. Rees, 2004, American Academy of Pediatric Dentistry: Periodontal Diseases of Children” Overall prevalence range in United States is 0.2% to 15% Most estimates suggest a low prevalence of 0.2% African Americans estimated prevalence greater than 2.5% Hispanics estimated prevalence at 1.0% Caucasian estimated prevalence at 0.1% Incidence increases in adolescents aged 12-17 when compared to children 5-11 years old Due to influence of race on prevalence of LAP, the risk of this disease implies genetic component Genetic Defects in LAP Patients According to Dr. Harvey Schenkein, 1998, American Academy of Periodontology: The Pathogenesis of Periodontal Diseases Neutrophil chemotactic defects Neutrophil Chemotactic Defects According to Thomas E. Van Dyke, 1985, “Role of Neutrophil in Oral Disease: Receptor Deficiency in Leukocytes from Patients with Juvenile Periodontitis” Thefunction of the neutrophil is thought to be clearance of infecting organisms and other noxious substances Theabnormality of chemotaxis in LAP is characterized by a decrease in the rate of cell migrations in response to a chemotactic gradient StudyPurpose: Investigate the total binding of labeled C5a to LAP neutrophils compared to neutrophils of non-LAP patients Neutrophil Chemotactic Defects According to Thomas E. Van Dyke, 1985, “Role of Neutrophil in Oral Disease: Receptor Deficiency in Leukocytes from Patients with Juvenile Periodontitis” C5a was isolated from human plasma These cells were placed in polyethylene tubes containing 125I-labeled C5a (LAP) After incubation at 4˚C the cells were tagged with radioactivity Results: There was a significant reduction of 125I-labeled C5a specifically bound to LAP neutrophils as compared to those bound by unlabeled “control” neutrophils Results: The number of LAP binding sites for LAP neutrophils was 133,000 and 218,000 sites for control neutrophils (~50% difference) Complement Pathways Alternative Pathway (Innate Immunity): C3b is receptor on PMN’s and acts as docking agent for bacteria C3b-Bb (C3 Convertase) breaks up C3 into more C3b C3b binds to C3 Convertase to form C5 Convertase C5 Convertase forms C5b (attaches to LPS to initiate MAC) and C5a (chemoattracts PMN’s) Classical Pathway (Adaptive Immunity-Humoral): Antibodies bound to bacterial agent activates C1 C1 activates C2 and C4 C2 forms C2a and C2b C4 forms C4a and C4b Together these form C3 Convertase to break up more C3 into more C3b C3b binds to C3 Convertase to form C5 Convertase C5 Convertase forms C5b (attaches to LPS) and C5a (chemoattracts PMN’s) Complement Pathways What Causes LAP According to Graaff, Winkelhoff, Goene, 2000, “The Role of Actinobacillus Actinomycetemcomitans in Localized Aggressive Periodontitis” Actinobacillus actinomycetemcomitans (A.a.) Characteristics: -Gram negative rod -Non-spore forming -Nonmotile -Facultatively anaerobic -Isolated mainly from subgingival plaque but may be found in supragingival plaque & on mucosal surfaces -Normally found in oral flora of 36% of population -Found to occur in actively diseased sites at levels 100 fold greater than those of the non-actively diseased sites * Now known as “Aggregatibacter actinomycetemcomitans Aggregatibacter actinomycetemcomitans Aggregatibacter actinomycetemcomitans According to Graaff, Winkelhoff, Goene, 2000, “The Role of Actinobacillus Actinomycetemcomitans in Localized Aggressive Periodontitis” growth of S. sanguis and A. viscous and other Inhibits supragingival plaque forming organisms through bacteriocin (actinobacillin) Produces virulence factors to promote its colonization and survival • Leukotoxin is the prime virulence factor (other virulence factors: collagenase, bone resorption inducing factor, catalase positive) Fivedistinct serotypes of A.a. • Serotype B (Y4) most commonly associated with LAP What Does Leukotoxin Do? KillsPMN’s and monocytes Inhibits PMN’s functions Resistant to complement mediated killing How Does Leukotoxin Affect Our Cells According to Edward Lally, 1997- A.a.’s leukotoxin (RTX) kills human immune cells by binding to neutrophils and causing cytolysis(cell death) According to Yamaguchi, 2001- A.a.’s leukotoxin induces apoptosis through a mitochondrial pathway that involves decreased levels of ADP in the mitochondrial matrix and arrest of oxidative phosphorylation 15 Leukotoxin (LTX) According to Bruce Shenker, 1988, “Infection and Immunity: Immunosuppressive Properties of A.a. Leukotoxin” Study Purpose: To examine A.a.’s leukotoxin (LTX) and its ability to alter human lymphocyte function HPBLs (Human Peripheral Blood Lymphocytes) from blood of healthy donors was centrifuged for 15 minutes at 15˚C 4 x 107 HPBLs were isolated and then washed 2X with HBSS (Hank’s Balanced Salt Soltn) These HPBLs were incubated at 37˚C for 90 minutes with either (1) LTX, (2) Medium, and (3) Pre-treated LTX with neutralizing monoclonal antibody The non-viable cells were identified using trypan blue stain uptake Leukotoxin (LTX) According to Bruce Shenker, 1988, “Infection and Immunity: Immunosuppressive Properties of A.a. Leukotoxin” Results of Groups 1, 2, 3: (1) It was determined that 80-85% of the total monocytes exposed to LTX died (2) It was determined that there was no change in cell viability in cultures exposed to medium (control) (3) It was determined that there was no change in cell viability in cultures exposed to pre-treated LTX with monocolonal antibody -The monoclonal antibody neutralizes the lethal effects of LTX on monocytes Note: Although this study determined that pre-treated LTX with monoclonol antibody neutralizes A.a.’s leukotoxin virulence factor, it does not have an affect on the T-cell immunosuppressor activation ability of A.a. How Do You Treat Patient With LAP? According to Dr. Terry D. Rees, 2004, American Academy of Pediatric Dentistry: Periodontal Diseases of Children” It is common practice that patients with periodontitis are given oral hygiene instruction and treated mechanically with debridement of dental plaque in subgingival and supragingival areas • However, the arrest of LAP in this manner was found to be not possible due to the inability to eliminate A.a. • A theory as to why: Because A.a. invades periodontal tissues and epithelium which makes the bacteria less accessible for mechanical removal (SRP) There is some disagreement among studies on treatment of LAP-but most recommend a combination of surgical or non- surgical root debridement in conjunction with antibiotic therapy How Do You Treat Patient With LAP? According to Graaff, Winkelhoff, Goene, 2000, “The Role of Actinobacillus Actinomycetemcomitans in Localized Aggressive Periodontitis” Study: 30 LAP patients were selected and randomly divided into 3 different groups (1) Consisted of 7 LAP patients receiving IT (initial treatment: oral hygiene instruction and mechanical debridement of supragingival and subgingival plaque) (2) Consisted of 12 LAP patients receiving IT and tetracycline as adjuct antimicrobial therapy for 7 days (3) Consisted of 11 LAP patients who received IT, and adjuct antimicrobial therapy of a combination of metronidazole (250mg 3X daily) and amoxicillin (375mg 3X daily) for 7 days How Do You Treat Patient With LAP? According to Graaff, Winkelhoff, Goene, 2000, “The Role of Actinobacillus actinomycetemcomitans in Localized Aggressive Periodontitis” Group (1): All 7 remained colonized with A.a. and further progression of disease was observed Group (2): After four months, only 5 patients became free of A.a. These patients clinically gained periodontal attachment and the disease was arrested The other 7 patients remained colonized with A.a. and no arrest of disease was observed Group (3): Clinical and microbiological evaluation was carried out for 2, 4, and 10 months after therapy After this therapy, no A.a. could be detected in all 11 patients How Do You Treat Patient With LAP? According to Graaff, Winkelhoff, Goene, 2000, “The Role of Actinobacillus actinomycetemcomitans in Localized Aggressive Periodontitis” Results: The finding that A.a. was still undetectable after 10 months of therapy suggests that this treatment is effective Theclinical condition after treatment of Group (3) determined that the probing pocket depth of the sampled sites reduced with significantly less bleeding *These findings show that the success of treating LAP is associated with the eradication of A.a. LAP Clinical Case Tapper Dental Clinic (2007-Present) 7 year old, Caucasian male presents with only medical history of ADHD and chief complaint “teeth are mobile” Treatment Protocol: (1) Biopsy plaque and saliva (2) Initial SRP & Prophy (3) CHX Periochip in pocket sites (4) 10 day course of Ampicillin (5) Follow-up with Arestin (minocycline HCL) in pocket areas *From 9-07 to 10-08 patient returned to clinic continuously for SRP and Arestin Injection treatments 22 Initial Pocket Depths (2007) Upper 333 222 343 333 323 324 323 722 333 213 313 223 3 A B C 7 8 9 10 11 I J 14 412 212 212 212 224 813 324 313 312 212 212 212 Lower 322 222 212 333 212 212 212 212 222 212 212 213 30 T S R 26 25 24 23 M L K 19 322 212 212 212 332 212 212 212 322 122 122 223 23 Final Pocket Depths (2008) Upper 233 212 333 323 323 323 422 333 213 313 223 3 4 C 7 8 9 10 H I J 14 312 212 212 223 413 324 313 312 212 212 212 Lower 322 222 PE 333 212 212 212 212 322 212 212 213 30 T 28 R 26 25 24 23 M L K 19 322 212 PE 212 332 212 212 212 222 122 122 223 24 March 2011 11 year old patient presents with teeth 3, 4, 5, 6, 7, 8, 9, 10, 12, 13, 14, 19, K, 21, 22, 23, 24, 25, 26, 27, 28, T, 30 All probing depths are 3mm and under 25 Localized Aggressive Periodontitis Questions…..
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