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chronic periodontitis

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chronic periodontitis

  1. 1. Chronic Periodontitis
  2. 2. Contents  Introduction  History  Prevalence  Etiology  Pathogenesis  Clinical features  Models of disease progression  Microbiologic and immunologic considerations  Risk factors  Conclusion  References
  3. 3. Introduction An infectious disease resulting in inflammation within the supporting tissues of the teeth, progressive attachment loss and bone loss - Flemmig, 1999
  4. 4. ….introduction  Complex infection occurring in susceptible hosts  Starts as plaque induced gingivitis
  5. 5. History  19th century o Riggs’ disease …………………... early 19th century o Calcic inflammation of peridental membrane…….......... GV Black, 1886 o Simplex periodontitis …………..Orban, 1942 o Adult type Periodontitis………..Page and Schroeder, 1982
  6. 6. …history  Slowly progressing periodontitis  Adult periodontitis …..World workshop in Periodontics, 1989 Adult Periodontitis Chronic Periodontitis
  7. 7. Prevalence  Most prevalent  Severity and prevalence - ↑ with age  < 10% - Teenagers ~ 90% - mid thirties ~ 100% - > 40 years (Marshall- Day et al, 1955)  Age associated, not age related
  8. 8.  Age of onset and rate of progression o Vary in individuals o Influenced by genetics and environmental risk factors  Twin study o Michalowicz et al, 2000 1. 38% - 82% of population variance attributed to genetics 2. 50% heritability …prevalence
  9. 9. …prevalence  Extent o Low – 1-10 sites o Medium – 11-20 sites o High - > 20 sites  Severity o Mild – 1-2 mm CAL o Moderate – 3-4 mm CAL o Severe - ≥ 5 mm CAL
  10. 10. Etiology 1. Bacteria  500 bacterial species in the oral cavity  Each periodontal pocket – 30-100 types of microflora  Healthy sites (PPD < 3 mm) – 103 microorganisms  Deep pockets (PPD > 6 mm) – 108 microorganisms (Haffajee and Socransky, 1994)  Anaerobic (90%), gram-negative (75%) bacterial species (Doyle et al, 1990)
  11. 11. …etiology  1996 World Workshop of Periodontics Strong evidence A. actinomycetemcomitans, P. gingivalis, T. forsythus Moderate evidence P. intermedia, C. rectus, E. nodatum, Treponema sp Intial evidence S. intermedius, P. micros, F. nucleatum, E. corrodens
  12. 12. …etiology  Current status o Periodontitis – polymicrobial o 16sRNA analysis and other molecular diagnostic techniques – wider range of microbial diversity o Not all strains or clones of a pathogen are equally pathogenic
  13. 13.  Archaea - prokaryotes that physically resemble bacteria but have different nucleotide sequences in their 16S rRNA genes  Appear in progressively greater numbers subgingivally  Never found subgingivally in periodontally healthy individuals (Lepp et al, 2004) …etiology
  14. 14.  Methanobrevibacter oralis  Patients harbouring Archaea: 19–73% (Vianna et al, 2008; Lepp et al, 2004) …etiology
  15. 15. 2. Virus  Diagnostic difficulties and natural fluctuation of periodontal herpes virus  Can multiply in gingival tissues  Higher counts in gingival tissue than subgingival sites (Kubar et al, 2004) …etiology Virus Prevalence Herpes simplex 37-100% Epstein-Barr virus 3-89% Cytomegalovirus 0.3-89%
  16. 16.  Herpes virus – lower frequency at periodontally healthy sites  Antibodies against Epstein-Barr virus in 32% and cytomegalovirus in 71% of GCF samples from 34 sites (Hochman et al, 1998)  Other viruses – Papilloma virus, HIV, Human T-lymphotropic virus, Hepatitis B virus, Hepatitis C virus, Torquetenovirus (Slots, 2010) …etiology
  17. 17. Pathogenesis  Gingivitis → Chronic Periodontitis Initial Early Established Advanced
  18. 18.  Initial lesion - 4 days after plaque accumulation Bacterial enzymes and metabolic end products Complement activation C3a and C5a stimulate mast cells Increased vascular permeability ↑ in GCF, accumulation of neutrophils, connective tissue disruption, release of TNF -α …pathogenesis
  19. 19.  Early lesion - 4–7 days after uninterrupted plaque accumulation o A change in the balance of inflammatory cells o Increasing numbers of lymphocytes and macrophages o Engagement of capillary vasculature and development of a perivascular inflammatory infiltrate …pathogenesis
  20. 20.  Established lesion Invasion in junctional epithelium and connective tissue Collagen destruction Lysosomes in junctional epithelium Plasma cell An inverse relationship exists between the number of intact collagen bundles and the number of inflammatory cells …pathogenesis
  21. 21.  Advanced lesion Alveolar bone loss, pocket formation and further apical migration of junctional epithelium …pathogenesis
  22. 22. …pathogenesis Page and Kornman, 1997
  23. 23.  General characteristics Clinical features Plaque accumulation Gingival inflammation Loss of attachment Pocket formation Alveolar bone loss Occasional suppuration
  24. 24.  Symptoms o Bleeding on brushing o Loose teeth o Spaces between teeth o Dull gnawing pain o Sensitivity to hot or cold o Food impaction o Gingival tenderness or itchiness …clinical features
  25. 25. …clinical features  Disease distribution o Site specific disease o Localised / Generalised o Vertical / Horizontal
  26. 26.  Disease severity o ↑ with age o Mild / Moderate / Severe …clinical features
  27. 27.  Disease progression o Slow progression – 0.2mm / year (facially) - 0.3 mm / year (proximally) o 8% - severe periodontitis 81% - moderate periodontitis 11% - gingivitis (Loe et al, 1986) o Modified by environmental and behavioral factors o Progression is not at equal rate (Lindhe et al 1989) …clinical features
  28. 28.  Socransky et al 1984 1. Continuous model Models of disease progression
  29. 29.  Evidence for disapproval 1. Attachment loss rates - too fast or too slow to be consistent with observed loss of attachment 2. Large number of sites (with or without prior attachment loss) do not show changes (Goodson et al, 1982; Haffajee et al, 1983) 3. Animal studies – disease does not progress in all lesions (Lindhe et al, 1975) 4. Sites with rapid destruction were brought in control by unknown mechanisms (Schroeder and Lindhe, 1975; Slots and Hausmann, 1979) …models of disease progression
  30. 30. 2. Random burst model …models of disease progression Prior history of disease would not necessarily make a site more likely for destruction nor would it exclude further destruction
  31. 31. 3. Asynchronous multiple burst o Destruction within a short period with prolonged periods of remission …models of disease progression
  32. 32. …models of disease progression Model Mechanism Epidemiologic model (Cohen et al, 1988) Consistent with continuous disease aging process that depends only on the duration of the process Brownian motion or stochastic model (Manji et al, 1989) Random periods of sharp bursts and/ or remission can occur, but the underlying disease activity remains constant Random walking model (Manji et al, 1989) Similar to Brownian motion when observed at regular intervals Fractural model (Landini et al, 1989) Multifactorial model; simulates disease advancing with age in bursts and remission
  33. 33. …models of disease progression  Periods of exacerbation – periods of activity Periods of remission – periods of inactivity  Periods of activity- attachment and bone loss, deepening of periodontal pocket, gingival bleeding, greater amounts of gingival exudate  Periods of inactivity - ↓ inflammatory response, little or no bone or attachment loss
  34. 34. …models of disease progression  Reasons for onset of destructive activity o Subgingival ulceration and acute inflammatory reaction → rapid bone loss (Schroeder et al, 1980) o T lymphocyte lesion → B lymphocyte lesion (Seymour et al, 1979) o ↑ in motile, gram – ve bacteria (Newman et al, 1979)
  35. 35. Microbiologic and Immunologic considerations  Periodontal diseased sites o ↑ levels of microorganisms (Ebersole et al 1985, 1987) o Ongoing destruction - ↑ red complex o ↑ serum and GCF antibodies to pathogens o Synergistic action (eg – F.n and P.g) enhances virulence (Feuille et al 1996)
  36. 36.  Periodontal therapy o ↓ in P.g, T.f, T.d (Loesche et al 1985, Haffajee et al 1997) o Poorly responding sites - ↑ F.n, P.m (Haffajee et al, 1985) o Initial increase in serum antibody levels, return to pretreatment levels by 8-12 months post treatment (Ebersole et al, 1985) …microbiologic and immunologic considerations
  37. 37.  Active periodontal destruction o Activation of alternate complement pathway …microbiologic and immunologic considerations
  38. 38. o ↑ MMP - 8 (Ingman et al, 1998) o Phagocytosis of T.d, F.n - high levels of elastase and MMP-8 from neutrophils (Ding et al, 1997) …microbiologic and immunologic considerations
  39. 39. Risk factors  Prior history of periodontitis o Not a true risk factor, but a predictor o Greater risk of further loss of attachment and bone loss (Papapanou PN, 1998) o Importance of maintenance therapy
  40. 40. …risk factors  Local factors o Plaque - etiology o Plaque retentive factors  Systemic factors o Rate of progression ↑ o Synergistic effect of plaque accumulation + systemic infection
  41. 41.  Environmental and behavioral factors 1. Smoking o Risk attributable to tobacco – 2.5-7.0 (Kinane and Chestnutt, 2000) o ↑ severity, extent and rate of disease o Smokers – more attachment loss, bone loss, furcation involvement, deeper pockets. (Bergstrom, 1983; Haffajee and Socransky, 2001; Mullally and Linden, 1996) 2. Emotional stress o May influence extent and severity of disease (Genco et al, 1998) …risk factors
  42. 42.  Genetic factors o Polymorphisms in IL-1α and IL-1β gene - ↑ susceptibility to aggressive form of chronic periodontitis (Kornman, 1998) o Presence of composite IL-1 genotype - ↑ risk of moderate to severe periodontitis (McGuire et al, 1999) Factors Risk of tooth loss IL-1 genotype 2.7 times Heavy smokers 2.9 times Heavy smokers + IL-1 genotype 7.7 times …risk factors
  43. 43. Conclusion
  44. 44. References  Newman, Takei, Klokkevold, Carranza. Carranza’s Clinical Periodontology. 10th edition. W. B. Saunders Company.  Lindhe J, Lang NP, Karring T. Clinical Periodontology and Implant Dentistry. 5th edition. Blackwell Munksgaard.  Socransky S, Hafajjee A, Goodson JM, Lindhe J. New concepts of destructive periodontal disease. J Clin Periodontol 1984; 11: 21-32.  Greenstein G, Lamster I. Changing periodontal paradigms: Therapeutic implications. Int J Periodontics Restorative Dent 2000; 20: 337-357.  Listgarten MA. Pathogenesis of Periodontitis. J Clin Periodontol 1986; 13: 418-425  Armitage GC, Cullinan MP, Saymour GJ. Comparative biology of Chronic and Aggressive periodontitis. Periodontology 2000 2010; Volume 53. Wiley Blackwell
  45. 45. Thank you!!

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