● 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.
● 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.
● Chronic periodontitis occurs most frequently in adults.
● It may also be diagnosed in children and adolescents
when associated with chronic plaque and calculus
● Therefore, it should be understood as age-associated, but
not age-dependent, complex chronic inflammation of the
-Early onset periodontitis
-Periodontitis associated with
-Periodontitis as manifestation of
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.”
● BASED ON DISEASE DISTRIBUTION:
1) Localized chronic periodontitis:
meaning that less than 30% of the teeth show
attachment and bone loss
1) Generalized chronic periodontitis:
meaning that 30% or more of the teeth show
attachment and bone loss
● BASED ON DISEASE SEVERITY:
1. Slight (mild) periodontitis:
Periodontal destruction no more than 1-2 mm of CAL.
1. Moderate periodontitis:
Periodontal destruction - 3-4 mm of CAL.
1. Severe periodontitis:
Periodontal destruction - more than 5mm of CAL.
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
14. 1. 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 ;
17. - Subgingival and/or overhanging
margins of restoration
- Deep carious lesions that extend
- 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
20. 4. Environmental and behavioural
● 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
● 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
● Reduced counts in neutrophils influence the degree of
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
3. Loss of
1. Microbial plaque
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.
●Bleeding gums during brushing or eating.
●Increasing spacing between teeth as a result of tooth
●Usually painless, but sometimes localized dull pain
radiating deep into the jaw
●Sensitivity to heat, cold or both due to exposed roots
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
● 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 :
1. Interproximal areas
2. Areas of greater plaque accumulation
3. 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 :
1. The Continuous Model (SOCRANSKY et al 1984)
2. The Random or Episodic-burst Model
3. The Asynchronous, Multiple-burst Model
• Describes slow and continuous
• Suggests that sites exhibit a constant
progression rate of attachment loss
throughout the duration of the disease
• Describes the episodic occurrence of
short progressive bursts of periodontal
destruction followed by periods of
• Sites, teeth, and the chronology of
bursts and stagnation are subject to
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
On basis of the site- specific nature and number of
teeth with clinical attachment loss :
periodontitis( ≥ 30% of
41. PATTERNS OF BONE LOSS
1. When attachment and
bone loss on one tooth
surface is greater than
that on adjacent
2. Associated with angular
bony defects and
1. When attachment and
bone loss proceeds at
uniform rate on the
majority of tooth
2. Associated with
Clinically diagnosed as:
● Detection of chronic inflammatory changes in the
● Presence of periodontal pockets
● Loss of clinical attachment
● Evidence of bone loss
A differential diagnosis is based on :
1. Age of patient
2. Rate of progression over time
3. Familial nature of aggressive disease
4. 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
Chronic periodontitis can be treated effectively by a
systematic periodontal therapy that includes:
1. Optimal long-term plaque control
2. Debridement of soft and hard deposits
3. Surgical pocket reduction (case-dependently either
resective osseous surgery or regenerative surgery)
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)
● 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.
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)