Chronic periodontitis is a slowly progressing infectious disease resulting in inflammation of the supporting tissues of the teeth and progressive bone and attachment loss. It is caused by bacterial plaque accumulation at the gumline. Key characteristics include site-specific or generalized bone and attachment loss, commensurate with plaque levels and modified by systemic and environmental risk factors like smoking and diabetes. The disease progresses in an episodic, intermittent manner with periods of rapid tissue destruction. Risk factors include prior history of periodontitis, specific pathogenic bacteria like P. gingivalis, local factors like calculus, and environmental factors like smoking which impair the host response.

1. CHRONIC
PERIODONTITISBY: Dr Shreeja Nair
PG R1
Dept of Periodontia
GDCH Ahmedabad
GUIDED BY
DR NEETA V BHAVSAR
PROFESSOR AND HOD
PERIODONTIA DEPT

2. Contents
• Introduction
• Definition
• Overall Characteristics
• Clinical Features
• Disease Distribution
• Disease Severity
• Clinical Course Of Chronic Periodontitis
• Progression Of Chronic Periodontitis
• Prevalence
• Pathogenesis
• Risk factors for Chronic Periodontitis
• Treatment
• Bibliography

3. INTRODUCTION
• Chronic Periodontitis is considered to be a complex slowly progressing
disease. However, in the presence of systemic, environmental factors that
may modify the host response to plaque accumulation, such as diabetes,
smoking or stress, disease progression may become more aggressive.
• Chronic periodontitis most frequently observed in the adults, may occur in
children and adolescents in response to chronic plaque and calculus
accumulation. Hence the name change to a more universal description of
“chronic” periodontitis that can occur at any age.

4. DEFINITION
• 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.”
• (Flemming T.F 1999).
• This definition outlines the major clinical and etiologic
characteristics of the disease:(1) microbial biofilm formation
(dental plaque); (2) periodontal inflammation (e.g., gingival
swelling, bleeding on probing); and (3) attachment as well as
alveolar bone loss.

5. Overall Characteristics
• Prevalent in adults but may occur in children.
• Amount of destruction of the periodontal tissues is
commensurate with the oral hygiene and plaque levels,
local predisposing factors, smoking, stress, and systemic
risk factors.
• Host factors determine the severity and rate of
progression of the disease.
• The rate of progression of chronic periodontitis is, slow
to moderate; sometimes with periods of rapid tissue
destruction.

6. Clinical features
Colour and texture alterations of Marginal gingiva
clinical attachment loss (CAL)
alveolar bone loss (BL)
Periodontal pockets
bleeding of the gingiva
enlargement or recession of the gingiva
Furcation involvement
Increased mobility, drifting, and/or tooth exfoliation may
occur

7. Disease Distribution
Chronic periodontitis is site specific and it
can be classified as:
• When less than 30% sites assessed
have attachment loss & bone loss.
I) Localized
periodontitis
• Greater than 30% sites.
II) Generalized
periodontitis

8. Disease Severity
Based on the severity of destruction
• when 1 to 2 mm of clinical
attachment loss has occurred.
I) Slight(mild)
periodontitis :
• 3 to 4 mm.
II) Moderate
periodontitis:
• more than 5 mm
III) Severe
periodontitis :

9. Based on extent
• 1 to 10 sitesLow -
• 11 to 20 sitesMedium -
• over 20 sitesHigh -
Fleming T. F. 1999

10. Clinical Course Of Chronic
Periodontitis
I. Role Of Gingivitis
II. Incidence, Characteristics And Time Of
Occurrence Of The Initial Periodontal Lesion
III. Patterns, Variations Of Attachment Loss

11. I. Role Of Gingivitis
• Epidemiological studies - gingival inflammation is invariably a
component of chronic periodontitis, and that gingivitis precedes
the onset of periodontitis.
• Two conditions - separate disease entities,
• bacterial plaque challenge induces overt gingivitis
• but the degree of host response (susceptibility) will determine
whether or not chronic periodontitis will develop.
• Findings from epidemiologic studies and prospective clinical trials
have indicated that the presence of gingivitis may be regarded as a
risk factor for chronic periodontitis.

12. II. Incidence,CharacteristicsAnd Time Of
OccurrenceOf The Initial PeriodontalLesion
The prevailing clinical concept of the pathogenesis of the early lesion
in chronic periodontitis included :
1. The formation and maturation of the supra-gingival plaque and the
development of gingivitis,
2. The extension of the bacterial plaque and the chronic inflammatory
process into the subgingival area and the initial destruction of the
connective tissue attachment of the teeth
3. The apical extension of the junctional epithelium and the formation
of the periodontal pocket and loss of alveolar bone.

13. III. Patterns and Variations Of
Attachment Loss
• Initial attachment loss in combination with pocket formation may
be seen primarily in interproximal areas, often in combination with
pocket formation and gingival recession.
• Pocket formation increases slowly by deepening of the initial
lesions and the addition of new sites.
• Gingival recession in combination with pockets may, as indicated
before, be caused by factors inherent in the pathogenesis of
periodontal destruction, other than iatrogenic insults.

14. Disease Progression
• The rate of disease progression is usually slow but may be modified by
systemic or environmental and behavioural factors.
• 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
(e.g., furcation areas, overhanging margins, sites of malposed teeth,
areas of food impaction).

15. Proposedmodelstodescribetherateofdiseaseprogression.
Progression is measured by determining the amount of attachment loss
during a given period, as follows:
• The continuous model suggests that disease progression is slow and
continuous, with affected sites showing a constantly progressive rate of
destruction throughout the duration of the disease.
• The random model, or episodic-burst model, Socransky et al, 1984,
proposes that periodontal disease progresses by short bursts of
destruction followed by periods of no destruction. This pattern of
disease is random with respect to the tooth sites affected and the
chronology of the disease process.
• The asynchronous, multiple-burst model of disease progression In
1989, Manji and Nagelkerke, suggests that periodontal destruction
occurs around affected teeth during defined periods of life, and that
these bursts of activity are interspersed with periods of inactivity or
remission. The chronology of these bursts of disease is asynchronous for
individual teeth or groups of teeth.

16. Periods of Destruction
• Periodontal destruction occurs in an episodic, intermittent manner,
with periods of inactivity or quiescence.
• Periods of destructive activity are associated with subgingival
ulceration and an acute inflammatory reaction, resulting in rapid loss
of alveolar bone; it was hypothesisied that this coincide with the
conversion of a predominantly T-lymphocyte lesion to one with a
predominantly B-lymphocyte–plasma cell infiltrate.
• Periods of exacerbation are associated with an increase of the loose,
unattached, motile, gramnegative, anaerobic pocket flora, and
• periods of remission coincide with the formation of a dense,
unattached, nonmotile, gram-positive flora with a tendency to
mineralize.
• Tissue invasion by one or several bacterial species is followed by an
advanced local host defense that controls the attack.

17. Prevalence
• Chronic periodontitis increases in prevalence and severity with age.
• Affects both the gender equally.
• The worldwide prevalence for severe chronic periodontitis is
estimated at 10.5% to 12% of the world's population. (Global
burden of severe periodontitis in 1990-2010: A systematic review
and meta-regression. J Dent Res. 2014;93:1045–1053.)
• Shah observed that for periodontal diseases, the prevalence at
present is 45% for age group 15+. Due to rampant use of pan
masala and guthka by the persons of all age groups, the proportion
of population with the disease could be 80-90%. (prevalance of
periodontitis in the Indian population : a literature review; jp shah
2011)

18. PATHOGENESIS
Gram negative organism dominate:
P. gingivalis, P. intermedia, A. actinomycetemcomitans
Nonmotile rods:
Facultative:
Actinobacillus a. , E. corrodens
Anaerobic:
P. gingivalis, P. intermedia, T. forsythia, F. nucleatum
Motile rods:
Facultative:
Campylobactor rectus
Spirochetes:
Anaerobic, motile:
Treponema denticola
MICROBES

19. Socransky (1979)
• suggested five types of criteria that support an etiological role for
microorganisms in periodontal infections:
(i) association with disease,
(ii) elimination or suppression of the organism,
(iii) host response,
(iv) animal pathogenicity, and
(v) mechanisms of pathogenicity.

20. Bone Destruction Caused by the
Extension of Gingival Inflammation
• The most common cause of bone destruction in periodontitis
is the extension of inflammation from the marginal gingiva
into the supporting periodontal tissues.
• As stated previously, the transition from gingivitis to
periodontitis is associated with changes in the composition of
the bacterial biofilm. In advanced stages of disease, the
number of motile organisms and spirochetes increases,
whereas the number of coccoid rods and straight rods
decreases.
• The cellular composition of the infiltrated connective tissue
also changes with increasing severity of the lesion.

22. • Interproximally, inflammation spreads to the loose
connective tissue around the blood vessels, through the
fibers, and then into the bone through vessel channels
that perforate the crest of the interdental septum at the
center of the crest, toward the side of the crest, or at the
angle of the septum.
• The inflammation spreads from the gingiva directly into
the periodontal ligament and from there into the
interdental septum.
• Facially and lingually, inflammation from the gingiva
spreads along the outer periosteal surface of the bone
and penetrates into the marrow spaces through vessel
channels in the outer cortex.

23. Periodontal Pocket Formation
• The transformation of a gingival sulcus into a
periodontal pocket creates an area in which
plaque removal becomes impossible.
• Pocket formation starts as an inflammatory
change in the connective tissue wall of the
gingival sulcus.
• The cellular and fluid inflammatory exudate
causes degeneration of the surrounding
connective tissue, including the gingival fibers.
• Just apical to the junctional epithelium,
collagen fibers are destroyed and the area is
occupied by inflammatory cells and edema.

24. Development of Periodontal
Pocket

25. Pocket Formation
The two mechanisms associated with collagen loss are as follows:
• (1) collagenases and other enzymes secreted by various cells in
healthy and inflamed tissue, such as fibroblasts, PMNs and
macrophages, become extracellular and destroy collagen
(enzymes that degrade collagen and other matrix macromolecules
into small peptides are called matrix metalloproteinases); and
• (2) fibroblasts phagocytize collagen fibers by extending cytoplasmic
processes to the ligament–cementum interface and degrading the
inserted collagen fibrils and the fibrils of the cementum matrix.
• As a consequence of the loss of collagen, the apical cells of the
junctional epithelium proliferate along the root surface and extend
finger-like projections that are two or three cells in thickness

26. Correlation of clinical and histopathological
features of chronic periodontitis
s.no Clinical features Histopathologic features
1 Gingival wall of pocket presents a
various degrees of bluish red
discoloration; flaccidity; a smooth,
shiny surface; and pitting on
pressure.
The discolouration is caused by
circulatory stagnation, the flaccidity by
destruction of gingival fibers and
surrounding tissues;
the smooth, shiny surface ,by atrophy
of epithelium and oedema; and the
pitting on pressure, by edema and
degeneration
2 Less frequently, gingival wall may be
pink and firm
In such cases, fibrotic changes
predominate over exudation and
degeneration

27. 4 Bleeding is elicited by gently
probing soft tissue wall of pocket
Ease of bleeding results
from increased vascularity,
thinning and degeneration
of epithelium, and proximity
of engorged vessels to inner
surface.
5 When explored with a probe,
inner aspect of pocket is generally
painful
Pain on tactile stimulation is
caused by ulceration of
inner aspect of pocket wall
6 In many cases, pus may be
expressed by applying digital
pressure.
Pus occurs in pockets with
suppurative inflammation of
inner wall.

28. Risk factors for
Chronic Periodontitis

29. I. Prior history of Periodontitis
• A disease predictor (associated with, not causative of) rather than a true
risk factor. Puts the patient at the 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 continuous disease if plaque is allowed to accumulate.
• This emphasizes the need for continuous monitoring and maintenance of
periodontitis patients to prevent recurrence of disease.
• Factors associated with the initiation of chronic periodontitis may also
influence disease progression.
• Furthermore, the extent and severity of disease within an individual are
good predictors of future disease occurrence.

30. II. Microbiologic Aspects
• Plaque accumulation on tooth and gingival surfaces (dental
biofilm formation) at the dentogingival junction is considered
the primary initiating agent in the etiology of gingivitis and
chronic periodontitis.
• Attachment and bone loss are associated with an increase in
the proportion of gram-negative organisms in the subgingival
biofilm,with specific increases in organisms known to be
pathogenic and virulent.
• Porphyromonas gingivalis, Tannerella forsythia, and
Treponema denticola, otherwise known as the red complex
bacteria, are frequently associated with ongoing attachment
and bone loss in chronic periodontitis.
• Periodontal pathogens like P. gingivalis may then invade the
periodontal tissue and therewith induce further immune
responses with increasing concentrations of proinflammatory
mediators that may enhance periodontal breakdown.

31. III. Local factors
• Microbial plaque is a crucial factor in the inflammation of
periodontal tissues, but the progression of gingivitis to
periodontitis is largely governed by host-response and
cumulative risk factors that predispose an individual to
periodontal tissue destruction and attachment loss.
• Microbial biofilms of particular compositions will initiate chronic
periodontitis in certain individuals whose host response and
cumulative risk factors predispose them to periodontal tissue
destruction and attachment loss.

32. Plaque retentive factors – calculus – most important
Others, subgingival and over hanging margins of restorations,
Subgingivally extending carious lesions,
Furcation involvements, cervical enamel projection.,
Crowded and mal-aligned teeth,
Root grooves and concavities

33. IV. Age
• CHRONIC PERIODONTITIS is AGE ASSOCIATED and not age
related disease.
• Both the prevalence and severity of periodontal disease increase
with age. It is possible that degenerative changes related to aging
may increase susceptibility to periodontitis.
• It is suggested that periodontal disease is not an inevitable
consequence of the aging process and that aging alone does not
increase disease susceptibility.
• The attachment loss and bone loss seen in older individuals are
the result of prolonged exposure to other risk factors over a
person's life, creating a cumulative effect over time. Therefore
young individuals with periodontal disease may be at greater risk
for continued disease as they age.

34. V. Environmental factors
• The positive association exist between smoking and periodontitis
• Risk attributable to tobacco for chronic periodontitis is between 2.5
and 7.0. Also the response to periodontal therapy is impaired in
smokers.
• A further feature in smokers is that their signs and symptoms of both
gingivitis and chronic periodontitis, viz., gingival redness and bleeding
on probing (BoP), are masked by the dampening of inflammation
seen for smokers as compared to non-smokers
• Smoking has been shown to affect the vasculature, the humoral and
cellular immune responses, cell signalling processes, and tissue
homeostasis.

35. Effects of smoking on etiology and
pathogenesis of periodontal disease
Etiologic factor Impact of smoking
Microbiology No effect on the rate of plaque accumulation
Increased colonization of periodontopathic
microorganisms
Immunology Altered neutrophil functions
Increased GCF levels of TNF-a, PGE2, neutrophil
collagenase, and elastase
Physiology Decreased gingival blood vessels,
Decreased GCF flow and BoP,
Decreased subgingival temperature
Increased inflammatory mediators
Increased LA recovery time

36. • Smoking is a major risk factor for the development and
progression of generalized chronic periodontitis.
• Periodontitis is influenced by smoking in a dose dependent
manner. The intake of more than 10 cigarettes per day
tremendously increases the risk of disease progression when
compared to nonsmokers and former smokers, respectively.
• Compared to nonsmokers, the following features are found in
smokers:
• Increased periodontal pocket depth with more than 3 mm
• Increased attachment loss
• More recessions Increased loss of alveolar bone
• Increased tooth loss
• Fewer signs of gingivitis (less bleeding upon
• probing)
• A greater incidence of furcation involvement

37. VI. Systemic factors
• In several instances periodontitis is also associated with other systemic
disorders, such as Papillon–Lefèvre syndrome, Ehlers–Danlos syndrome,
Kindler syndrome, and Cohen syndrome.
• Patients who suffer from diseases that impair host immune responses
(e.g., HIV/AIDS) may also show periodontal destruction. it is also known
that osteoporosis, severe unbalanced diet, and stress, as well as
dermatologic, hematologic, and neoplastic factors, interfere with
periodontal inflammatory responses.
• In addition to defined syndromes, periodontitis is also associated with
severe systemic diseases, such as diabetes mellitus, cardiovascular
disorders, stroke, and lung disorders.
• In the context of diabetes mellitus, a number of patients exhibit an
increased body weight (obesity), which also correlates with the
prevalence and severity of periodontal attachment and bone loss.

38. Diabetes mellitus --
• Periodontitis is now considered as the sixth complication of diabetes
mellitus. For diabetes mellitus and periodontitis, there is a known
interaction during which both diseases mutually correlate to each
other.
• Patients with diabetes mellitus exhibit a higher risk to develop
periodontitis, and the periodontal infection/inflammation may
negatively interfere with the glycemic control of the diabetic patient
• The diabetic state is associated with:
• Decreased collagen synthesis
• Increased collagenase activity
• Altered neutrophil function
• Elevated blood sugar levels suppress the host’s immune response
and results in:
• Poor wound healing
• Susceptibility to recurrent infections

39. VII. 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.
• Not only B cells and macrophages, but also periodontal
ligament cells, gingival fibroblasts, and epithelial cells
synthesize proinflammatory mediators—such as interleukin-1
beta (IL-1 beta), IL-6, IL-8, prostaglandin-E2 (PGE2), tumor-
necrosis factor alpha (TNF-alpha), and many others—that
modify innate and adaptive immune responses at periodontal
sites

40. VIII. Behavioral factors and stress
• Influence physiologic systems like the endocrine and immune system,
leading to health changes. , inflammatory conditions and impaired wound
healing.
• The association between stress and disease is particularly strong for
infectious diseases, inflammatory conditions and impaired wound healing.
• Specific periodontal conditions associated with psychosocial variables,
including chronic periodontitis, NUG , chronic and experimental gingivitis.
• Patients with periodontitis often report the experience of family- or work-
related stress. Positive correlations between cortisol levels and periodontal
indices (plaque index, gingival index), bone loss, and missing teeth were
recorded
• Stress and Periodontal Disease: Potential Mechanisms
• 1. Immunosuppression via cortisol secretion
• 2. Poor oral hygiene compliance in patients with chronic stress
• 3. Patients with stress are less likely to seek professional care
• 4. Patients with stress may smoke more frequently

41. IX. Genetic factors
• There is convincing evidence from twin studies for a
genetic predisposition to the periodontal diseases.
Indicated that risk of chronic periodontitis has a high
inherited component.
• Much attention has been focused on polymorphisms
associated with genes involved in cytokines production.
• Patients with the IL-1 genotype increased the risk for
tooth loss by 2.7 times
• The combined effect of the IL-1 genotype & smoking
increased the risk of tooth loss by 7.7 times.

42. TREATMENT
Periodontal Evaluation
Comprehensive periodontal examination
Diagnosis and prognosis
Patient education
• Clinical findings and disease status
• Disease pathogenesis and prevention
• Personalized oral hygiene instruction
Reduction of systemic and environmental risk factors
• Physician consultation
• Smoking cessation
Periodontal treatment plan
• Oral hygiene assessment and education
• Nonsurgical therapy
• Periodontal reevaluation
• Periodontal supportive maintenance

43. Nonsurgical Therapy
Oral hygiene assessment and education
Infection control
• Nonsurgical periodontal therapy
• Supragingival and subgingival scaling and root planing
• Extraction of hopeless teeth
Reduction of local risk factors
• Removal or reshaping of overhangs and over contoured
restorations
• Restoration of carious lesions
• Restoration of open contacts

44. Periodontal Reevaluation
Inquiry of new concerns or problems
Inquiry of changes in patient's medical and oral health
status
Oral hygiene assessment and education
Comprehensive periodontal examination
Assessment of outcome of nonsurgical therapy
Determination of required additional nonsurgical and
adjunctive therapy

45. Surgical Therapy
Adjunct to nonsurgical therapy
Should only occur once patient demonstrates proficient biofilm control
Objectives:
• Primary: Access for root instrumentation
• Secondary: Pocket reduction through soft tissue resection, osseous
resection, or periodontal regeneration
Periodontal access surgery
• Resective
• Regenerative
Extraction of hopeless teeth
Periodontal plastic surgery
• Mucogingival surgery
• Aesthetic crown lengthening
Preprosthetic surgery
• Prosthetic crown lengthening
• Implant site preparation and implant placement

46. Periodontal Maintenance Therapy
Inquiry of new concerns or problems
Inquiry of changes in patient's medical and oral health
status
Oral hygiene assessment and education
Comprehensive periodontal examination
Professional maintenance care
• Supragingival and subgingival biofilm and calculus removal
• Selective scaling and root planing
Assessment of recall interval and plan for next visit

49. Bibliography
• Carranza’s Clinical Periodontology 10th Edition.
• Carranza And Newmann’s Clinical Periodontology 13th Edition.
• Jan Lindhe. Clinical Periodontology And Implant Dentistry, 6th Edition.
• T. F. Flemming. Periodontitis. Annals. 1991. 4. 1.32.
• Shaju jp, zade rm, das m (2011) prevalence of periodontitis in the Indian
population: a literature review. J Indian soc periodontology 15: 29-30
• Periodontal disease and diabetes: A two-way street; Brian L. Mealey, DDS, MS;
JADA, Vol. 137 October 2006
• Global burden of severe periodontitis in 1990-2010: A systematic review and
meta-regression. J Dent Res. 2014;93:1045–1053.)