Juvenile periodontitis

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Almost covers all the information regarding localized & generalized aggressive/juvenile periodontitis

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Juvenile periodontitis

  1. 1. :Contents: Introduction Classification Localized Juvenile Periodontitis: Etiology Clinical Features Radiographic Features Generalized Juvenile Periodontitis Etiology Clinical Features Radiographic Features Microbiology Immunology Differential Diagnosis Treatment Conclusion References
  2. 2. PERIODONTIUM: The normal healthy periodontium consists of several tissues namely: 1. Gingiva , 2. Periodontal ligaments(PDL) , 3. Cementum , 4. Alveolar bone For the maintenance of the tooth in the oral cavity, the health of the periodontium as a whole is of paramount importance.
  3. 3. Cementum Gingiva
  4. 4. Early onset Periodontitis, Aggressive Periodontitis INTRODUCTION:  Juvenile Periodontitis is the most uncommon severe form of the Periodontal disease  Described by Wannenmacher(1938) as destruction of the supporting tissues of the teeth that becomes clinically significant during adolescence or early adulthood.
  5. 5. CLASSIFICATION: Ranney,1993,classified the disease in Localized & Generalized form 1.Localized aggressive periodontitis: - Characterized by bone loss around the first molars & incisors - Occurring in otherwise healthy individuals 2.Generalized aggressive periodontitis: - Characterized by a more widespread pattern of periodontal destruction - Associated with a variety of diseases of other systems
  6. 6. 1.LOCALIZED JUVENILE PERIODONTITIS  ETIOLOGY:- • Actinobacillus actinomycetemcomitans are the most commonly found bacteria at the diseased sites . • Other micro-organisms found are: P. gingivalis, E.corrodens, Capnocytophaga, Spirochetes ,Bacillus,etc. • Elevated levels of A.a. found in active sites (low in numbers at healthy sites)
  7. 7. •Produce leukotoxins, collagenase,bone resorbing factors & other immunosuppressive factors that help in invasion of host tissues,evasion of host defences leading to the destruction of periodontal tissue. •Incidence of A.a. found to be greater in younger persons compared to older clients •Younger patients experience more destruction in a shorter period of time
  8. 8. CLINICAL FEATURES:- Onset around the time of puberty .  Occur in an otherwise healthy individual, clinical inflammation may not be obvious.  Localized almost exclusively to the incisors & first molars, less than 30% of sites are involved.  Females are affected more than males  Blacks affected more than whites  Abnormality in the phagocyte function.  Self arresting disease progression.
  9. 9.  Earliest Sign Drifting of teeth in a patient having a good oral hygiene Affected teeth becomes mobile followed by pocket formation.  Progression of bone loss is 3-5 times faster than adult periodontitis.  Maxillary incisors migrate in distolabial direction  diastema.  Sensitive root surfaces  Deep,dull,radiating pain may occur with mastication (irritation of the supporting tissues)  Periodontal abscess formation
  10. 10. Diastema
  11. 11. Denuded root surface
  12. 12. Some reasons why disease activity affects certain teeth:  A.a. colonize first perm. teeth to erupt - Evade host defenses - Following initial attack, host responds - Antibodies produce which improve phagocytosis of bacteria - This may prevent colonization at other sites  A.a. may lose its ability to produce leukotoxin - This may slow or arrest the disease process
  13. 13.  Antagonistic bacteria - Anti-A.a. bacteria may colonize sites & prevent A.a. from colonizing other sites in mouth - Localizes the infection & tissue destruction  Denuded root surfaces - The root surfaces of patients with LJP are often denuded (absence of cementum) - Allows bacteria to penetrate the root and colonize the site
  14. 14. RADIOGRAPHIC FEATURES: 1.A localized vertical bone loss with widening of PDL space 2. Arc shaped bone destruction starting from the distal margin of the second premolar & extending to the mesial margin of the second molar
  15. 15. 2. GENERALIZED JUVENILE PERIODONTITIS ETIOLOGY: • Actinobacillus actinomycetemcomitans along with the diverse microbiota. • Defective neutrophil or monocyte function. • Poor serum antibody response to infecting agent is seen. • Subgingival tissues shows the presence of gram negative rods including P.Gingivalis & exhibit suppressed neutrophil chemotaxis.
  16. 16. CLINICAL FEATURES: Usually affect an individual under 30 years of age  Generalized involvement of permanent teeth, more than 30 percent.  Affects atleast 3 permanent teeth other than first molar & incisors  The destruction often appears episodically, with periods of advanced destruction followed by stages of quiescence of variable length.  Patients often have small amounts of bacterial plaque associated with the affected teeth.  Destructive phase: Tissue appears severely inflamed, ulcerated & fiery red Bleeding with or without stimulation Suppuration Attachment & bone loss usually occurs
  17. 17. Non-destructive phase: Tissues appear pink with some stippling Lack of inflammation Probing will reveal deep pockets Bone & attachment levels relatively stable Some patients with GAP may exhibit: Weight loss, Mental depression, General malaise. Systemic conditions may predispose patient to GAP, these include: Chronic neutrophil defects, leukocyte adherence deficiency,etc.
  18. 18. Destructive phase Non destructive phase
  19. 19. Pus formation
  20. 20. RADIOGRAPHIC FEATURES: 1.Severe bone loss associated with minimal no. of teeth to advanced bone loss affecting the majority of the teeth
  21. 21. MICROBIOLOGY: Actinobacillus actinomycetemcomitans appears to be primarily associated with the disease. - Gram negative anaerobes - Rod shaped organisms - Localized predominantly at the base of the defect The presence of a recently discovered genus termed Capnocytophaga, has been associated with the progression of periodontitis lesions.
  22. 22. IMMUNOLOGY: Defective function or production of circulating neutrophils & monocytes is often associated with an increased frequency & severity of bacterial infection. DIFFERENTIAL DIAGNOSIS: Conditions that could contribute to alveolar bone loss in the primary dentition & premature loss of primary teeth: 1. Hypophosphatasia 2. Papillon – Lefevre syndome 3. Cyclic Neutropenia
  23. 23. HYPOPHOSPHATASIA:
  24. 24. TREATMENT: 1.Early diagnosis aids in successful treatment. 2.Extraction of involved teeth (depends on severity of tissue loss) 3.Antibiotics can be provided against infective microorganisms: Tetracycline is consider the drug of choice (1g/day orally for 14 days ) Tetracycline+Metronidazole Doxycycline 4. Periodontal therapy:  Scaling & root planning Plaque control instruction Debridement with or without flap surgery Subgingival Irrigation with iodine & hydrogen peroxide Bone grafts, root resections, hemi sections
  25. 25. CONCLUSION: Periodontal Disease accounts for a majority of missing teeth in adults & results in tremendous economic & social burdens both to the individual & the society. Periodontal disease is so prevalent that only possible solution to the problem is its “prevention” by maintaining the good oral hygiene.
  26. 26. REFERENCES: 1.Essential of Pediatric Oral Pathology  By Mayur Chaudhary, Sweta Dixit Chaudhary 2.Textbook of Pedodontics  By Shobha Tandon 3.Textbook of Oral Pathology  By Shafer’s 4.Principle & practice of Pedodontics  By Aarthi Rao

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