1. CHRONIC PERIODONTITIS
By- DR. OINAM MONICA DEVI

2. Contents
• Definition
• Classification
• Clinical Features
• Clinical Diagnosis
• Gingivitis as a risk factor for chronic periodontitis
• Disease Distribution
• Disease Severity
• Symptoms
• Disease Progression
• Models to describe the rate of disease progression
• Prevalence
• Immunopathology
• References

3. • Chronic periodontitis has been defined as "an infectious disease resulting in
inflammation within the supporting tissues of the teeth, progressive
attachment loss, and bone loss."‘
• This definition outlines the major clinical and etiologic characteristics of
the disease:
(1) Microbial plaque formation
(2) Periodontal inflammation
(3) Loss of attachment and alveolar bone
Definition

4. Classification of periodontitis based on stages defined by severity Papapanou et al., 2018

5. Classification of periodontitis based on grades
Papapanou et al., 2018

6. General Characteristics
1. Supragingival and subgingival plaque and calculus
2. Gingival swelling, redness, and loss of gingival stippling
3. Altered gingival margins (rolled, flattened, cratered papillae, recessions)
4. Pocket formation
5. Bleeding on probing
6. Attachment loss
7. Bone loss (angular/vertical or horizontal)
8. Root furcation involvement
9. Increased tooth mobility
10. Change in tooth position
11. Tooth loss
Clinical Features

7. Clinical Diagnosis
Detection of chronic
inflammatory changes in
the marginal gingiva
Presence of periodontal
pockets
Loss of clinical
attachment
It is diagnosed radio graphically by: Localized or generalized loss of
alveolar supporting bone, horizontal or vertical
Differential diagnosis - Aggressive periodontitis
• Based on the age of the patient, rate of disease progression over time, familial nature
of aggressive disease, and relative absence of local factors

8. Gingivitis as a risk factor for chronic periodontitis
• Gingival inflammation is invariably a component of chronic periodontitis.
• Gingivitis precedes the onset of periodontitis, manifest after only days or
weeks of plaque accumulation.
• Destructive chronic periodontitis is a condition that in the majority of cases
requires far longer periods of plaque and calculus exposure to develop.

9. Disease Distribution
• Chronic periodontitis is considered a site-specific disease.
• The clinical signs - inflammation, pocket formation, attachment loss, and bone
loss are believed to be caused by the direct, site-specific effects of subgingival
plaque accumulation.
• Localized periodontitis: less than 30% of the sites demonstrate attachment loss
and bone loss
• Generalized periodontitis: less than 30% or more of the sites demonstrate
attachment loss and bone loss

10. Localized chronic periodontitis
A. Clinical view of anterior teeth
showing minimal plaque and
inflammation
B. Radiographs showing presence of
localized, vertical, angular bone loss on
the distal side of the maxillary left first
molar
C. Surgical exposure of the
vertical, angular defect
associated with the chronic
plaque accumulation and
Carranza,
11th ed

11. Generalized chronic periodontitis
A. Clinical view showing minimal
plaque and inflammation
B. Radiograph showing severe,
generalized, horizontal pattern of
bone loss
Carranza, 11th
ed

12. The pattern of bone loss
Vertical Horizontal
• When attachment and bone loss
proceeds at a on one tooth surface
• Vertical hone loss is usually
associated with angular bony defects
and intrabonv pocket formation.
• When attachment and bone loss
proceeds at a uniform rate
• Horizontal bone loss is usually
associated with suprabony
pockets

13. Disease Severity
• With increasing age, attachment loss and bone loss become more prevalent
and more severe.
• Slight (mild) periodontitis: No more than 1 to 2 mm of clinical attachment
loss
• Moderate periodontitis: 3 to 4 mm of clinical attachment loss
• Severe periodontitis: 5 mm or more of clinical attachment loss

14. American Academy of Periodontology Task Force Report on the Update
to the 1999 Classification of Periodontal Diseases and Conditions
• This update addresses specific areas of concern with the current classification: 1.
Attachment level, 2. Localized versus generalized periodontitis.
1. Use of attachment levels in diagnosis of periodontitis
• In clinical practice, measurement of CAL is challenging, and time consuming.
• Measuring the location of CEJ when the gingival margin is located coronal to the CEJ is
difficult and may involve some guesswork when the CEJ is not readily evident via
tactile sensation.
• The clinician may chart probing depths alone or probing depths with a single recession
measure at the mid-facial or mid-lingual and only when recession is actually present.
American Academy of Periodontology Task Force Report on the Update to the 1999 Classification of Periodontal Diseases and
Conditions. J Periodontol 2018; 86 (7), 835–38.

15. • Another common error occurs when gingival margin measures are charted as ‘‘0 mm’’
when in fact the gingival margin is not right at the level of the CEJ, resulting in
attachment levels that are incorrectly charted as being equal to probing depth.
• In general, a patient would have periodontitis when one or more sites had bleeding on
probing, radiographic bone loss, and increased probing depth or clinical attachment
loss.
American Academy of Periodontology Task Force Report on the Update to the 1999 Classification of Periodontal Diseases and Conditions.
J Periodontol 2018; 86 (7), 835–38.

16. Symptoms
Slowly progressive disease , does not cause the affected individual to feel
pain.
Gingival bleeding during oral hygiene procedures or eating
Black triangles between the teeth or tooth sensitivity in response to
temperature changes (i.e., cold and heat).
In patients with advanced attachment and bone loss, tooth mobility, tooth
movement, tooth loss may be reported.
Areas of localized dull pain that radiate to other areas of the mouth or head
Presence of areas of food impaction
Gingival tenderness or “itchiness”

17. Disease Progression
• Patients appear to have the same susceptibility to plaque induced chronic
periodontitis throughout their lives.
• The rate of disease progression is usually slow but may be modified by
systemic or environmental and behavioral factors.
• Onset of chronic periodontitis can occur at any time, and the first signs
may be detected during adolescence in the presence of chronic plaque and
calculus accumulation.
• Because of its slow rate of progression, however, chronic periodontitis
usually becomes clinically significant in the raid-30s or later.

18. • Chronic periodontitis does not progress at an equal rate in all affected sites
throughout the mouth.
• Some involved areas may remain static for long periods, whereas others may
progress more rapidly.
• More rapidly progressive lesions occur most frequently in interproximal areas'
and may also be associated with areas of greater plaque accumulation
and inaccessibility to plaque control measures.

19. The continuous model
• Disease progression is
slow and continuous
• Affected sites show a
constantly progressive rate
of destruction throughout
the duration of the disease
The ramdom model, or
episodic-burst model
• Periodontal disease
progresses by short
bursts of destruction
followed by periods of
no destruction
• Random pattern with
respect to the tooth sites
affected and the
chronology of the disease
process.
The asynchronus, multiple-
burst model of disease
• Periodontal destruction
occurs around affected
teeth during defined
periods of life
• Bursts of activity are
interspersed with periods
of inactivity or remission
• Chronology of these
bursts of disease is
asynchronous for
individual teeth or
groups of teeth.
Models to describe the rate of disease progression

20. Socransky et al. 1984
Various models of disease
progression
Socransky, S. S., Haffajee, A. D., Goodson, J. M., & Lindhe, J. (1984). New
concepts of destructive periodontal disease. J Clin Periodontol 1984; 11(1); 21–32

21. Prevalence
• Chronic periodontitis increases in prevalence and severity with age, generally
affecting both genders equally.
• Periodontitis is an age-associated, not an age-related, disease.
• It is not the age of the individual that causes the increase in disease prevalence,
but rather the length of time that the periodontal tissues are challenged by
chronic plaque accumulation.

23. RISK
FACTORS
FOR
DISEASE
1. Prior
History of
Periodontitis
2.
Microbiogolical
Aspects
3. Local Factors
4. Systemic
Factors
5.
Immunologic
Factors
6.
Environmental
& Behavioural
Factors
7. Genetic
Factors

24. Categories of Risk Elements for Periodontal Disease
Risk - Defined as is the probability that an individual will get a specific
disease in a given period.
RISK FACTORS:
Tobacco smoking
Diabetes
Pathogenic bacteria
Microbial tooth deposits
RISK DETERMINANTS:
Genetic factors
Age
Gender
Socioeconomic status
Stress
RISK INDICATORS:
HIV/Aids
Osteoporosis
Infrequent dental visits
RISK MARKERS/PREDICTORS:
Previous history of periodontal
disease
Bleeding on probing

25. Prior History of Periodontitis
• Disease predictor
• Puts patients at greater risk for developing further loss of attachment and
bone, given a challenge from bacterial plaque accumulation
• A chronic periodontitis patient who has been successfully treated will
develop continuing disease it plaque is allowed to accumulate
• Emphasizes the need for continuous monitoring and maintenance of
periodontitis patients to prevent recurrence of disease

26. B. Microbiological Factors
• Plaque accumulation primary initiating agent in the etiology of chronic
periodontitis.
• Attachment and bone loss are associated with an increase in the proportion of
gram-negative organisms in the sub-gingival plaque biofilm.
• Specific plaque hypothesis- with specific increases in organisms (pathogenic
and virulent) Bacteroides gingivalis, Bacteroides forsythus, and Treponema
denticola, “Red complex,”.
• Impart a local effect on the cells of the inflammatory response and the cells
and tissues of the host, resulting in a local, site-specific disease process.

27. • Role of immune response-may not depend on the presence of one specific
bacterium or bacterial complexes alone.
• The occurrence of periodontitis depends on the individual immune response
that modifies the onset and progression of the disease.
• Poly-microbial disease- It is the result of multi-species infection with a number
of different bacteria that influence the pro-inflammatory immune response of
the host and produces proteases that directly influence tissue stability and host
immune response

28. Role of Viruses - Slots in 2010, A high periodontal load of active Epstein–Barr
virus or cytomegalovirus is statistically associated with aggressive periodontitis,
and latent herpes virus infections are preferentially found in chronic
periodontitis and gingivitis sites.
• Diagnostic difficulties and natural fluctuation of periodontal herpes virus
Role of Archea - Pérez-Chaparro et al. in 2014, “association” studies. The
results suggested the association of 17 species or phylotypes have an
association with disease.
Virus Prevalence
Herpes simplex 37-100%
Epstein-Barr virus 3-89%
Cytomegalovirus 0.3-89%

29. C. Local Factors
Calculus
Sub gingival and/or
overhanging margins of
restorations
Carious lesions
that extend
subgingivally
Furcations
Crowded and
malaligned teeth
Root grooves
and concavities
Plaque retentive factors are important in the development and progression of
chronic periodontitis because they retain plaque microorganisms in close proximity
to the periodontal tissues, providing an ecologic niche for plaque growth and
maturation.

30. D. Systemic Factors
Syndromes- Haim-munk syndrome,
Ehler-Danlos Syndrome, Kindlers
syndrome and Cohen syndrome
Human immunodeficiency virus
acquired immunodeficiency
syndrome
Osteoporosis
A severely unbalanced diet
Stress
Dermatologic, hematologic
and neoplastic factor
interfere with periodontal
inflammatory responses.
Severe systemic disease such
as diabetes mellitus,
cardiovascular disease, stroke
and lung disease

31. E. Immunologic Factors
Patient may show alteration in their peripheral
monocytes, which are related to the reduced
reactivity of lymphocyte or an enhanced B-cell
response.
B-cells, macrophage, periodontal ligament
cells, gingival fibroblast, and epithelial cells
synthesize pro-inflammatory mediators (e.g.
Interleukin-1 beta, Interleukin-6, Interleukin-8,
prostaglandin E-2, tumor necrosis factor –
alpha) and modify innate and adaptive immune
response at periodontal site.
Onset progression and severity of disease depend on the individual hosts immune
response

32. F. Environmental and Behavioural Factors
Smoking
Smoking is a major risk factor
for development and
progression of generalized
chronic periodontitis.
Periodontitis is affected by
smoking in a dose dependent
manner.
The intake of more than 10 cigarettes per day
tremendously increases the risk of disease
progression as compared to nonsmoker and
former smoker.
As compared with non-smoker, the following features are found
in smokers-
• Increased probing pocket depth of more than 3 mm
• Increased attachment loss
• More recession
• Increased bone loss,
• Greater incidence of furcation involvements
• Increased tooth loss
• Fewer sign of gingivitis (Less bleeding on probing)

33. Stress
The mechanisms by which stress could affect periodontal disease progression and wound
healing have been divided into two main categories:
• (i) Health-impairing behaviors such as poor oral hygiene, increased tobacco and
alcohol consumption, and poor nutritional intake;
• (ii) Pathophysiological factors that lead to higher glucocorticoid and catecholamine
levels which indirectly affect hormonal, inflammatory and immunological profiles,
leading to an increased susceptibility to periodontal disease.
 Patients with CP often report the experience of family or
work related stress.
 Positive correlation between cortisol level and periodontal
indices, bone loss, and missing teeth has been recorded.
 Risk indicator

34. G. Genetic Factors
– Each factor in turn directly related to individual genetic condition.
– Genetic variation such as single nucleotide polymorphism (SNPs), and
genetic copy number variations may directly influence innate and
adaptive immune response as well as the structure of periodontal tissue.
– Studies of monozygotic twins suggest a genetic component to chronic
periodontitis, but the influences of bacterial transmission among family
members and environmental effects make it difficult to interpret a
complex interaction.

35. Factors Risk of tooth loss
IL-1 genotype 2.7 times
Heavy smokers 2.9 times
Heavy smokers + IL-1
genotype
7.7 times
– Interleukin 1-a and interleukin 1-ß polymorphism is associated with an increased
susceptibility to a more aggressive form of chronic periodontitis in subjects of
Northern European origin.
– McGuire & Nunn 1999, followed 42 patients with periodontitis for 14 years and showed
that the risk of tooth loss as a result of periodontal disease.
– Genome- wide association studies have revealed a significant association between
periodontitis and coronary heart disease.
– A complex genotype is likely to be identified for many different clinical forms of
periodontitis.

36. Pathogenesis of Periodontitis

37. Immunopathology
CHARACTERISTICS OF A PROGRESSIVE LESION-
• Apical migration of plaque on the root surface, accompanied by sub-gingival calculus
formation.
• Alveolar bone is destroyed within 2 mm of the plaque front,
• Attachment loss and bone resorption cyclical/ intermittent
• A predominance of plasma cells
• Lesion is further encapsulated by a fibrous band surrounding the infiltrated tissues;
however, local fibroblasts in the body of the lesion are reduced in number and altered in
appearance.
• Relatively few macrophages in the advanced lesion, and it is thought that B cells may be
the major source of interleukin-1 and other pro-inflammatory cytokines that produces
matrix metalloproteinases, especially by fibroblasts. Results in degradation of the
surrounding extracellular matrix.
CP is characterized by cycles of progression and stability

38. Stable T-cell lesion is mediated by Th1 cells, while the progressive B-cell, plasma
cell lesion is associated with Th2 cells. The majority of these T cells are also
CD45RO-positive memory cells. Stable, predominantly T-cell lesion and a
progressive B-cell lesion.
• Recently, Th-17 cells are identified as a separate phenotype
• The signature cytokine of these cells is IL-17A, also produce IL-21 and IL- 22
• IL- 17A is important for the recruitment of neutrophils as they up-regulate
CXCL8 expression.
• Th17 cells may be involved in Th1 modulation and enhanced inflammatory
mediators’ production by gingival fibroblasts in periodontal disease
• Th17 cells may be primary source of RANKL production in periodontal
disease.
KV Arun, JISP 2010

39. References
1. Newman, Takei, Klokkevold, Carranza. Carranza’s, clinical periodontology, 10th ed; 632-34.
2. Newman, Takei, Klokkevold, Carranza. Carranza’s, clinical periodontology, 13th ed; 1880-1916.
3. Papapanou, P. N., Sanz, M., Buduneli, N., Dietrich, T., Feres, M., Fine, D. H., … Tonetti, M. S.
Periodontitis: Consensus report of workgroup 2 of the 2017 World Workshop on the Classification
of Periodontal and Peri-Implant Diseases and Conditions. J Periodontol 2018;89: S173-82.
4. American Academy of Periodontology Task Force Report on the Update to the 1999 Classification
of Periodontal Diseases and Conditions. J Periodontol 2015; 86 (7), 835–38.
5. Socransky, S. S., Haffajee, A. D., Goodson, J. M., & Lindhe, J. (1984). New concepts of
destructive periodontal disease. J Clin Periodontol; 11 (1): 21–32.
6. Pérez-Chaparro, P. J., Gonçalves, C., Figueiredo, L. C., Faveri, M., Lobão, E., Tamashiro, N., …
Feres, M. Newly Identified Pathogens Associated with Periodontitis. J Dent Res 2014; 93 (9),
846–58.
7. McGuire, M. K., & Nunn, M. E. (1999). Prognosis Versus Actual Outcome. IV. The Effectiveness
of Clinical Parameters and IL-1 Genotype in Accurately Predicting Prognoses and Tooth Survival.
J Periodontol;70 (1) : 49–56.

40. THANK YOU