Periodontal disease comprises of a group of inflammatory conditions of the supportive tissues of the teeth that are caused by bacteria.

1. SEMINAR ON
CHRONIC
PERIODONTITIS
Presented by: Shivani Yadav
BDS 4th Year
(12083)

2. CONTENT
 Periodontal disease
 Classification
 Introduction
 Definition
 Major clinical and etiologic factor
 Prevalence
 Clinical features
 Symptoms
 Types
 Disease severity
 Disease progression
 Clinical diagnosis
 Radiographic features
 Risk factors for disease
 Treatment
 Prognosis

3. Periodontal disease
Definition:
Periodontal disease comprises of a group of
inflammatory condtions of the supportive tissues
of the teeth that are caused by bacteria.
 -Carranza

4. The Periodontal Disease Classification System of the
American Academy of Periodontology (AAP), 1999
I. Gingival Diseases
A. Dental plaque-induced gingival diseases
B. Non-plaque-induced gingival lesions
II. Chronic Periodontitis (slight: 1-2 mm CAL; moderate: 3-4 mm CAL;
severe: > 5 mm CAL)
A. Localized ( < 30% of sites are involved)
B. Generalized (> 30% of sites are involved)
III. Aggressive Periodontitis
A. Localized ( < 30% of sites are involved)
B. Generalized (> 30% of sites are involved)
IV. Periodontitis as a Manifestation of Systemic Diseases
A. Associated with hematological disorders
B. Associated with genetic disorders
C. Not otherwise specified

5. .
V. Necrotizing Periodontal Diseases
A. Necrotizing ulcerative gingivitis
B. Necrotizing ulcerative periodontitis
VI. Abscesses of the Periodontium
A. Gingival abscess
B. Periodontal abscess
C. Pericoronal abscess
VII. Periodontitis Associated With Endodontic Lesions
A. Combined periodontic-endodontic lesions
VIII. Developmental or Acquired Deformities and
Conditions
A. Localized tooth-related factors that modify or
predispose to plaque-induced gingival
diseases/periodontitis
B. Mucogingival deformities and conditions around
teeth
C .Mucogingival deformities and conditions on
edentulous ridges
D. Occlusal trauma

6. INTRODUCTION
 Chronic periodontitis, formerly known as adult
periodontitis or chronic adult periodontitis, is the
most prevalent form of periodontitis.
 It is generally considered to be a slowly
progressing disease.
 Although chronic periodontitis is most frequently
observed in adults, it can occur in children and
adolescents in response to chronic plaque and
calculus accumulation.

7. DEFINITION
 Chronic periodontitis has been defined
as “an infectious disease resulting in
inflammation with in supporting tissues
of the teeth, progressive attachment loss
and bone loss”.

8. Major clinical and etiologic
characteristics of the disease:
1. Microbial plaque formation.
2. Periodontal inflammation, and
3. Loss of attachment and alveolar bone.

10. PREVALENCE
 Effects both sexes equally.
 Increases with age.
 Age associated disease not age related and
occurs depending on disease duration.

11. CLINICAL FEATURES
 Most prevalent in adults but can occur
in children and adolescents.(age‐35+yrs)
 Supragingival and subgingival plaque
accumulation (frequently associated with
calculus)
 Gingival inflammation
 Pocket formation
 Loss of periodontal attachment
 Occasional suppuration
 Poor oral hygiene – gingiva is typically
may be slightly to moderately swollen

12. .
 Color- pale red to magenta
 Consistency – soft or firm
 Surface topography – loss of
stippling
 Blunted or rolled gingival margin
 Flattened or cratered papillae.
 Tooth mobility.
 Furcation involvement.
 Spontaneous gingival bleeding.
 Pocket depths are variable and
both suprabony and intrabony
pockets can be found.

13. Attachment loss with and without deep
periodontal pocket.
Pocket depths are variable, and both horizontal
and vertical bone loss can be found.

14. Furcation involvement in the molars
are common in advance cases of
chronic periodontitis.
Tooth mobility often appears in
advanced cases when bone loss has
been considerable.

15. 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
Halitosis
Gingival tenderness or itching

16. TYPES
DISEASE DISTRIBUTION
 Chronic periodontitis is considered to be as “site
specific disease”
 Inflammation, pockets, attachment loss and bone
loss are due to direct site-specific effects of sub-
gingival plaque accumulation as a result of this
local effect, attachment loss and pockets may
occur.
 It may occur on one surface of the tooth while the
other surface remain normal.

17. In addition to being site specific, chronic
periodontitis may be described as:
 Localized:
 Periodontitis is considered localized when <30% of the
sites assessed in oral cavity demonstrate attachment loss
and bone loss.
 Generalized:
 Periodontitis is considered generalized when >30% of
the sites assessed demonstrate attachment loss and bone
loss.
 The pattern of bone loss in chronic periodontitis can be
vertical or horizontal.

18. .
Localized-
less than 30%sites
are involved
Generalized-
When 30% or more sites
shows CAL & bone loss

19. • Localized ≤ 30% of the sites are affected

20. •Generalized > 30% of the sites are affected

21. MILD PERIODONTITIS
1 to 2 mm CAL
MODERATE PERIODONTITIS
3 to 4 mm CAL
SEVERE PERIODONTITIS
≥ 5 mm CAL
DISEASE SEVERITY
Severity can be categorized on the basis of the amount of Clinical
attachment loss (CAL) as follows:

22. EARLY PERIODONTITIS

23. MODERATE
PERIODONTITIS

24. SEVERE
PERIODONTITIS

25. DISEASE PROGRESSION
 The rate of disease progression is usually slow but
may be modified by systemic and/or environmental
and behavioral factors.
 Chronic periodontitis does not progress at an equal
rate in all affected sites throughout the mouth.
 More rapidly progressive lesions occur:
1. Interproximal areas
2. Areas of greater plaque accumulation
3. Inaccessibility to plaque control measures
(e.g., furcation areas, overhanging margins, sites of
malposed teeth, or areas of food impaction)

27. Clinical Diagnosis
 Inflammation of the marginal gingiva
extent to the attached gingiva.
 Clinical attachment loss.
 Radiographs(in case of bone loss).

28. Widening of PDL space
Loss of corticated interdental crestal margin
Localised or generalized loss of alveolar supporting bone.
Blunting of the alveolar crest due to beginning of bone resorption
RADIOGRAPHIC
FEATURES

29. RADIOGRAPHIC
FEATURES
 Pattern of bone loss may
be :
 Vertical,
 Horizontal,
 Vertical bone loss is
usually associated with
intra bony pocket
formation.
 Horizontal bone loss is
usually associated with
supra bony pockets.

30. RISK FACTORS FOR DISEASE
•Prior History of Periodontitis
•Local Factors
•Systemic Factors
•Environmental and Behavioral Factors
•Genetic Factors
Risk factor - is a characteristic, an aspect of behavior, or an environmental
exposure that is associated with destructive periodontitis

31. Prior History Of Periodontitis
 Although not a true risk factor for disease but rather a
disease predictor, a prior history of periodontitis puts
patients at greater risk for developing further loss of
attachment and bone, given a challenge from bacterial
plaque accumulation.
 Patient present with persistent gingivitis or
periodontitis with pocketing, attachment loss, and
bone loss ,may continue to lose periodontal support if
not successfully treated.

32. LOCAL FACTORS
 Plaque and plaque retentive factors.
 Microbiological Factors
Causative organisms of chronic periodontitis are:
• Porphyromonas gingivalis (P. gingivalis)
• Prevotella intermedia (P. intermedia)
• Treponema denticola
• Capnocytophaga
• A.actinomycetemcomitans (A.a)
• Eikenella corrodens (E. corrodens)
• Campylobacter rectus (C. rectus)
 Viruses including cytomegalo , Epstein Barr, Papilloma and
herpes simplex have been proposed to play a role in the
etiology of periodontal diseases, possibly by changing the host
response to the local subgingival microbiota.

33. LOCAL FACTORS
Plaque Accumulation
Oral Hygiene
Tooth Malposition
Restoration
Preserve & Quantity of certain bacteria
Host defences
Subgingival Restoration
Environment
Calculus, smoking
Connective Tissue destruction
Genetic influence
Inflammation
Periodontopathic bacteria
Smoking, Calculus
Loss of Attachment
M
O
D
I
F
Y
I
N
G
F
A
C
T
O
R
S

34. Plaque retentive factors:
Calculus
Overhanging
restorations

35. Trauma from occlusion
Micro-organisms

36. SYSTEMIC FACTORS
Non Genetic
-Smoking is a major risk factor
- Diabetes
-Conditions associated with compromised immune
responses (e.g. HIV)
- Nutritional defects
-Osteoporosis
-Medications that cause drug induced gingival
overgrowth (e.g. some calcium channel blockers,
phenytoin, cyclosporine)
Genetic factors (as yet poorly defined)

37. SMOKING
• Undoubtedly one of the main and most prevalent,
risk factors for chronic periodontitis, risk
calculations suggesting 40% of the cases of chronic
periodontitis may be attributable to smoking.
• It has been estimated that there are 1.1 billlion are
smokers worldwide and 182 million (16.6%) of them
live in India.

38. DIABETES
Hyperglyc
emia +
collagen
AGEs
Increases
cross
linking
between
collagen
molecules
Reduced
solubility
and
turnover
of
collagen
Failure in
periodontal
repair and
regeneration

39. .

40. STRESS

41. AGE
 Both the prevalence and severity of
periodontal disease increases with age.
 Intake of medications,
 Decreased immune function, and
 Altered nutritional status interaction

42. NUTRITION
Vitamin C or ascorbic acid is essential for the
formation of collagen and intercellular material,
bone and teeth.
↓ phagocytic function of neutrophils and
macrophages
↓ antibody response
↓ cytotoxic T-cell activity

43. OSTEOPOROSIS
 It is a disease characterized by low bone mass and deterioration of bone
structure that causes bone fragility and increases the risk of fracture.
 Both osteoporosis and periodontal diseases are bone resorptive diseases
 Osteoporosis could be a risk factor for the progression of chronic
periodontal disease.
 A direct association between skeletal and periodontal disease as
measured by loss of interproximal alveolar bone in postmenopausal
women has been reported.

44. HIV
 AIDS epidemics in US suggests HIV positive
patients especially those with AIDS and low
count of T Lymphocytes(CD4 <200 cells/ml)
were at increased risk of chronic periodontitis.

45. TREATMENT
1. NON SURGICAL THERAPY
 Initial therapy ( scaling and root planing)
 Antimicrobial therapy – as an adjunct to routine
periodontal therapy.
 Improvement in oral hygiene.
 Instruction, reinforcement, evaluation of plaque
control records.
 Removal of all the factors contributing to plaque
accumulation, e.g. correction of ill-fitting
appliances, overcontoured crowns, overhanging
restorations, etc.

46. 2. SURGICAL THERAPY
A variety of surgical treatment modalities may be
appropriate in managing the patient.
1. Pocket elimination procedures.
2. Regenerative therapy:
A. Bone replacement grafts;
B. Guided tissue regeneration;
C. Combined regenerative techniques.
3. Resective therapy:
A. Flaps with or without osseous surgery;
B. Gingivectomy.

47. PROGNOSIS
 Slight to moderate periodontitis, the prognosis is
usually good provided , the inflammation can be
controlled through good oral hygiene and the
removal of local plaque retentive factors.
 In patients with more severe disease, as
evidenced by furcation involvements and
increasing mobility, or in patients who are
noncompliant with oral hygiene practices, the
prognosis may be downgraded from fair to poor.