This document provides an overview of chronic periodontitis. It discusses the introduction, history, prevalence, etiology, pathogenesis, clinical features, models of disease progression, microbiological and immunological considerations, and risk factors of chronic periodontitis. Chronic periodontitis is a complex polymicrobial infection that results from an imbalance between pathogenic bacteria in plaque and the host immune response. It begins as plaque-induced gingivitis and progresses to the destruction of connective tissue and alveolar bone through periods of activity and remission, leading to pocket formation and potential tooth loss over time if left untreated. Systemic and environmental risk factors like smoking can increase the risk and rate of disease progression.

1. Chronic Periodontitis

2. Contents
 Introduction
 History
 Prevalence
 Etiology
 Pathogenesis
 Clinical features
 Models of disease progression
 Microbiologic and immunologic considerations
 Risk factors
 Conclusion
 References

3. Introduction
An infectious disease resulting in inflammation within
the supporting tissues of the teeth, progressive
attachment loss and bone loss
- Flemmig, 1999

4. ….introduction
 Complex infection occurring in susceptible hosts
 Starts as plaque induced gingivitis

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. …history
 Slowly progressing periodontitis
 Adult periodontitis …..World workshop in Periodontics, 1989
Adult Periodontitis Chronic Periodontitis

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.  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. …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. 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. …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. …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.  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.  Methanobrevibacter oralis
 Patients harbouring Archaea: 19–73%
(Vianna et al, 2008; Lepp et al, 2004)
…etiology

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.  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. Pathogenesis
 Gingivitis → Chronic Periodontitis
Initial
Early
Established
Advanced

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.  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.  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.  Advanced lesion
Alveolar bone loss, pocket formation and further
apical migration of junctional epithelium
…pathogenesis

22. …pathogenesis
Page and Kornman, 1997

23.  General characteristics
Clinical features
Plaque
accumulation
Gingival
inflammation
Loss of
attachment
Pocket formation
Alveolar bone loss
Occasional suppuration

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. …clinical features
 Disease distribution
o Site specific disease
o Localised / Generalised
o Vertical / Horizontal

26.  Disease severity
o ↑ with age
o Mild / Moderate / Severe
…clinical features

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.  Socransky et al 1984
1. Continuous model
Models of disease progression

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. 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. 3. Asynchronous multiple burst
o Destruction within a short period with prolonged periods
of remission
…models of disease progression

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. …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. …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. 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.  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.  Active periodontal destruction
o Activation of alternate complement pathway
…microbiologic and immunologic considerations

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. 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. …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.  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.  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. Conclusion

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. Thank you!!