Chronic periodontitis

Periodontitis

1. http://www.free-powerpoint-templates-design.com CHRONIC PERIODONTITIS

2. INDEX Introduction History Definition Classification Prevalence Risk factors Major clinical and etiological features Clinical features

3. 09. Disease progression 09. Disease distribution 10. Disease severity 11. Diagnosis 12. Radiographic features 13. Management 14. Prognosis 15. Conclusion 16. Reference

4. INTRODUCTION Chronic periodontitis, formerly known as “ adult periodontitis ” or “ chronic adult periodontitis ”, is the most prevalent form of periodontitis. It is generally considered as a slow progressing disease.

5. INTRODUCTION Chronic periodontitis is considered to start as plaque- induced gingivitis, a reversible condition that, left untreated, may develop into chronic periodontitis. Chronic periodontitis lesions include loss of attachment and bone and are regarded as irreversible .

6. INTRODUCTION Chronic periodontitis occurs most frequently in adults. It may also be diagnosed in children and adolescents when associated with chronic plaque and calculus accumulation. Therefore, it should be understood as age-associated, but not age-dependent, complex chronic inflammation of the periodontal tissues.

7. HISTORY 1977 - Chronic marginal periodontitis -Juvenile periodontitis By AAP 1986 - Juvenile periodontitis ~Prepubertal ~Localized juvenile ~Generalized juvenile - Adult periodontitis - Necrotising ulcerative gingivo-periodontitis - Refractory periodontitis By AAP

8. 1989 - Early onset periodontitis Prepubertal ~Generalized ~Localized Juvenile ~Generalized ~Localized - Adult periodontitis - Necrotising ulcerative - Refractory periodontitis -Periodontitis associated with systemic disease By AAP 1999 -Chronic periodontitis ~Generalized ~Localized -Aggressive periodontitis ~Generalized ~Localized -Periodontitis as manifestation of systemic disease By AAP

9. DEFINITION By Carranza 10th ed; Chronic periodontitis is defined as “ an infectious disease resulting in inflammation within the supporting tissues of the teeth, progressive attachment loss, and bone loss.”

10. CLASSIFICATION BASED ON DISEASE DISTRIBUTION: Localized chronic periodontitis : meaning that less than 30% of the teeth show attachment and bone loss Generalized chronic periodontitis : meaning that 30% or more of the teeth show attachment and bone loss

11. CLASSIFICATION BASED ON DISEASE SEVERITY: Slight (mild) periodontitis: Periodontal destruction no more than 1-2 mm of CAL. Moderate periodontitis: Periodontal destruction - 3-4 mm of CAL. Severe periodontitis: Periodontal destruction - more than 5mm of CAL.

12. PREVALENCE Effects both gender equally Prevalence increases with age (From 11% to 30% of patients develop severe periodontitis at the age of 40 years or older.) The worldwide prevalence for severe chronic periodontitis is estimated at 10.5% to 12% of the world's population

13. RISK FACTORS 01 02 03 04 05 06 Prior history of periodontitis Local factors Systemic factors Environmental and Behavioural factors Immunologic factors Genetic factors

14. Prior history of periodontitis: Previous history of periodontitis enhances risk of further loss of tooth attachment and bone destruction due to bacterial plaque accumulation Though it is not a true risk factor for disease development but acts as a disease predictor .

15. 2. Local factors: These include plaque and plaque retentive factors. Plaque attached to the tooth and gingival surfaces at the dentogingival junction is considered to be the primary etiologic factor in chronic periodontitis. Porphyromonas gingivalis, Tannerella forsythia and Treponema denticola (red complex microorganism )are frequently associated with chronic periodontitis.

16. 2. Local factors: Plaque retentive factors are those that facilitate plaque accumulation or prevent the removal of plaque by routine oral hygiene procedures. They allow plaque microorganisms to be in close proximity to periodontal tissues. Some of these factors include ; Calculus

17. Subgingival and/or overhanging margins of restoration Deep carious lesions that extend subgingivally Crowded or malaligned teeth Root surface irregularities

18. 3. Systemic factors: The rate of progression of plaque-induced chronic periodontitis is generally considered to be slow. However, when chronic periodontitis occurs in a patient who also suffers from a systemic disease that influences the host response, the rate of periodontal destruction may be significantly increased.

19. 3. Systemic factors: Diabetes mostly type II , a non-insulin dependent diabetes mellitus can increase the severity and extent of periodontal disease.

20. 4. Environmental and behavioural factors : It is not only the risk of developing the disease that is enhanced by smoking , but also the response to periodontal therapy is impaired in smokers. Also, clinical features of both gingivitis and chronic periodontitis such as gingival redness and bleeding on probing get obscured due to dampening of inflammation.

21. 4. Environmental and behavioural factors: Stress and other psychosomatic conditions induce direct anti-inflammatory, anti-immune effects and behavior- mediated effects on the body’s defenses.

22. 5. Immunologic factors: Chronic periodontitis is a disease induced by bacteria organized in the dental biofilm. Onset, progression, and severity of the disease depend, however, on the individual host immune response. Patients may show alterations of peripheral monocytes, which relate to reduced reactivity of lymphocytes or enhanced B-cell response.

23. 5. Immunologic factors: Periodontal ligament cells, gingival fibroblasts, and epithelial cells synthesize proinflammatory mediators —such as IL-1α, IL-1β , IL-6, IL-8, PGE2, TNF- α - and many others— modify innate and adaptive immune responses at periodontal sites.

24. 5. Immunologic factors: Increased activity of MMPs and RANKL promotes bone degradation. Reduced counts in neutrophils influence the degree of periodontal inflammation.

25. 6. Genetic factor: Genetic basis for periodontal disease in recent studies that have demonstrated periodontal destruction among the family members and different generations within a family. Recent data indicate that a genetic variation or polymorphism in the genes encoding IL-1α and IL-1β is associated with increased susceptibility to more aggressive form of chronic periodontitis.

26. MAJOR CLINICAL AND ETIOLOGIC FEATURES 2. Periodontal inflammation 3. Loss of attachment and alveolar bone Microbial plaque formation

27. CLINICAL FEATURES Supra and subgingival plaque accumulation Gingival inflammation Pocket formation Loss of periodontal attachment Occasional suppuration Poor oral hygiene- gingiva typically may be slightly to moderately swollen

28. Color - pale red to magenta Consistency - soft or firm Surface topography - loss of stippling Blunted to rolled gingival margin Flattened or cratered papillae Furcation involvement Tooth mobility Pocket depths are variable and both suprabony and infrabony pockets can be found.

29. CLINICAL FEATURES Attachment loss with or without deep periodontal pocket Pocket depth are variable and both horizontal and vertical bone loss can occur

30. CLINICAL FEATURES Furcation involvement (in molars) and tooth loss are common in advanced cases of chronic periodontitis

31. SYMPTOMS Bleeding gums during brushing or eating. Increasing spacing between teeth as a result of tooth movement. Loose teeth Usually painless, but sometimes localized dull pain radiating deep into the jaw Sensitivity to heat, cold or both due to exposed roots Food impaction

32. SYMPTOMS Halitosis Gingival tenderness or itching

33. DISEASE PROGRESSION The progression rate of chronic periodontitis is slow . Onset and the rate of disease progression, however, may be influenced by a number of modifiable (e.g., smoking, diet) and nonmodifiable (e.g., genetic disorders) factors. The progression pattern does not show equal degrees of attachment loss on each affected site over time.

34. DISEASE PROGRESSION More rapidly progressive lesions occur at : Interproximal areas Areas of greater plaque accumulation Inaccessibility to plaque control measures (eg furcation areas, overhanging margins, sites of malposed teeth , or areas of food impaction)

35. DISEASE PROGRESSION The different models have been proposed to describe the rate of disease progression and determine the degree of attachment loss over time : The Continuous Model (SOCRANSKY et al 1984) The Random or Episodic-burst Model The Asynchronous, Multiple-burst Model

36. THE CONTINUOUS MODEL • Describes slow and continuous disease progression • Suggests that sites exhibit a constant progression rate of attachment loss throughout the duration of the disease

37. THE RANDOM OR EPISODIC BURST MODEL: • Describes the episodic occurrence of short progressive bursts of periodontal destruction followed by periods of stagnation • Sites, teeth, and the chronology of bursts and stagnation are subject to random effects

38. THE ASYNCHRONOUS,MULTIPLE BURST MODEL: • Describes the occurrence of periodontal destruction (bursts) during defined periods, which are asynchronously interrupted by periods of stagnation or remission for individual sites and teeth

39. DISEASE DISTRIBUTION Chronic periodontitis is a site- specific disease. Periodontal pocket formation, attachment, and bone loss may develop on one or more sites of a tooth, while other sites remain at a physiologic attachment level.( i.e. it may occur on one surface and other may be free of symptom )

40. Localized chronic periodontitis ( < 30% of sites affected) DISEASE DISTRIBUTION On basis of the site- specific nature and number of teeth with clinical attachment loss : Generalized chronic periodontitis ( ≥ 30% of sites affected)

41. PATTERNS OF BONE LOSS When attachment and bone loss on one tooth surface is greater than that on adjacent surface. Associated with angular bony defects and infrabony pocket formation. When attachment and bone loss proceeds at uniform rate on the majority of tooth surfaces. Associated with suprabony pockets. VERTICAL HORIZONTAL

42. PATTERNS OF BONE LOSS 1 2 3

43. DISEASE SEVERITY MILD PERIODONTITIS ≥ to 5 mm CAL 3-4 mm CAL 1-2 mm CAL SEVERE PERIODONTITIS MODERATE PERIODONTITIS

44. DIAGNOSIS CLINICAL RADIO GRAPHIC

45. DIAGNOSIS Clinically diagnosed as: Detection of chronic inflammatory changes in the marginal gingiva Presence of periodontal pockets Loss of clinical attachment Radiographically as: Evidence of bone loss

46. DIAGNOSIS A differential diagnosis is based on : Age of patient Rate of progression over time Familial nature of aggressive disease Relative absence of local factors in aggressive disease

47. RADIOGRAPHIC FEATURES Widening of PDL space Loss of corticated interdental crestal margin Localised or generalized loss of alveolar crest due to beginning of bone resorption Blunting of alveolar crest due to beginning of bone resorption Bone loss may be either horizontal or vertical

48. RADIOGRAPHIC FEATURES

49. MANAGEMENT Chronic periodontitis can be treated effectively by a systematic periodontal therapy that includes: Optimal long-term plaque control Debridement of soft and hard deposits Surgical pocket reduction (case-dependently either resective osseous surgery or regenerative surgery)

50. MANAGEMENT

51. MANAGEMENT Depending on the individual periodontal risk, each patient should be remotivated, reinstructed, and retreated (if necessary) during a systematic supportive periodontal therapy regimen (revisits every 3, 6, or 12 months)

52. CONCLUSION Chronic periodontitis is an infectious inflammatory disease of the tooth supporting apparatus with progressive attachment loss and loss of alveolar bone. The effective management of periodontal disease in clinical practice presents with many challenges and cannot be completely cured, hence, must be controlled in order to stabilise the progression of this destructive process in long-term.

53. REFERENCES Carranza’s Clinical Periodontology (10th ed) Newman and Carranza’s Clinical Periodontology (13th ed) Periobasics : A textbook of periodontology and implantology (2nd ed) Clinical Periodontology and Implant Dentistry (Jan Lindhe - 5th ed)

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