The document provides an overview of chronic periodontitis, including its definition, classification, etiology, clinical features, disease progression, risk factors, diagnosis, and treatment. It discusses how chronic periodontitis is caused by an inflammatory response to bacterial plaque biofilm and is influenced by both local and systemic risk factors. Key points include that it is a slowly progressive disease involving loss of attachment and bone, and that risk is increased by factors like smoking, diabetes, genetic predispositions, and a prior history of periodontitis.

2. •Introduction
•Definition
•History
•Classification
•Etiopathogenesis
•Clinical features
•Disease progression
•Risk factors
•Prognosis
•Diagnosis
•Treatment planning
•Conclusion
•references

3. According to the most recent classification that resulted from a 1999
international workshop , diseases of the periodontium comprise a long list of
conditions involving the supporting structures of the tooth.
The two most prevalent and most investigated periodontal diseases are dental
plaque– induced gingivitis and chronic periodontitis.
INTRODUCTION

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

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

7. •Slow progressive disease.
•Formerly known as adult periodontitis or chronic adult
periodontitis.
•Changed to a more universal description of chronic
periodontitis-occur at any age

9. CLASSIFICATION

12. Host
susceptibility
Host cell and
molecules
Dental
plaque

13. Dental
plaque
Biofilm
development
Gene transfer- horizontal gene transfer- competence stimulating
peptide
Antimicrobial resistance.
Regulation of gene expression.-exposure of S gordonii to saliva
results in the induction of genes (sspA/B) that mediate host-surface
binding and coaggregation with Porphyromonas gingivalis and
Actinomyces.
Bacterial antigens and virulence factors in the biofilm
Cell–cell communication.-quorum sensing, or cell density–mediated
gene expression. mediated by autoinducer 1 and autoinducer.

14. •Porphyromonas gingivalis,
• Tannerella forsythia,
•Prevotella intermedia,
•Campylobacter rectus,
•Eikenella corrodens,
•F nucleatum,
• Actinobacillus actinomycetemcomitans,
• Peptostreptococcus micros,
•and Treponema spp
species

15. Desulfobulbus sp oral clone R004,
Deferribacteres sp oral clones BH017 and
D084, and Bacteroides sp oral clone AU126

16. Host susceptibility
•Ample evidence suggests that susceptibility to periodontitis varies
considerably among individuals, with approximately 10% being
highly susceptible and 10% being highly resistant.
•This difference in susceptibility has largely been attributed to
genetic factors
Host susceptibility

17. Host cells and molecules implicated in
periodontal pathogenesis
Dental plaque
Indirect
damage
Depend on
initiation and
progression
direct damage
Matrix degrading
enzymes and
molecules that impair
the functions of host
cell

18. PMNs
plasma
cells
macrophagesLymphocytes
acute
chronic
Host Defense
cells

19. Cytokines
IL-1a,
IL-1b,
TNF-a,
IL-10
Lipid molecules
Prostaglandin E2,
thromboxane B2
Host molecules regulating
the inflammatory response

20. Anti-inflammatory
•cytokines - Interleukin-10.
•lipid mediators- lipoxin A4
Lesser in periodontitis
patients

21. React with
Cellular
structural
component of
the periodontal
structures
Molecular
structural
elements
epithelial cells
• the periodontal
ligament
gingival fibroblasts
the cells of the alveolar bone
(e.g., osteoblasts and
osteoclasts)
Extracellular
component
•collagens
•Non collagenous
proteins
(e.g., elastin and
connective tissue
proteoglycans).

22. The initial, early, and established lesions are sequential stages in gingivitis and
they, rather than the advanced lesion which is manifest clinically as
periodontitis, make up the major portion of inflammatory gingival and
periodontal disease in humans.
Page and Schroeder provided the basic understanding
of gingivitis and periodontitis histopathology and
inflammation.

24. CLINICAL FEATURES
Plaque
formation
• Supragingival
• Subgingival
• Gingival inflammation
• Pocket formation
• Loss of periodontal attachment
• Loss of alveolar bone
• Occasional suppuration
Calculus
formation

25. In patients with poor oral hygiene- the gingiva
appears slight to moderate swollen .
Exhibit pale red to magenta .
Loss of gingival stippling
Changes in surface topography
rolled or blunted gingival margin
flattened or cratered papilla

26. ,consistency
Patients with regular
home care
 The changes in colour, contour, consistency frequently
associated with gingival inflammation may not be visible
clinically
 Only bleeding on probing in response to examination of the
periodontal pocket formation with a periodontal probe.

27. Infection
Long standing cases , in low grade inflamation,thickened ,fibrotic
marginal tissues may obscure the underlying inflammatory changes.
Pocket depths are variable.
suprabony and intrabony pockets can be found
Horizontal and vertical bone loss can be found.
Tooth mobility appears in advanced cases with
extensive attachment loss and bone loss

28. DISEASE DISTRIBUTION
•Site specific.
• classified as localized or generalized.
Less than 30% of site involved more than 30 %
of site involved

29. a
DISEASE SEVERITY
Considered as function of time.
With increasing age –more attachment loss.
Can be described as
Slight (mild) -no more than 1 to 2 mm of CAL
Moderate - 3to 4 mm CAL
Severe - more than 5 mm CAL

30. a
SYMPTOMS
Bleeding gums when brushing
Space occur as their teeth
movement occurs or teeth become
loose.
Usually painless, but dull, radiating
type of pain occurs.
Food impaction
Gingival tenderness or itchiness.

31. Differential
diagnosis

32. Comparison of chronic and
aggressive periodontitis
Clinical features
Histopathology
Immunopathology
Microbiology
Neutrophil functions
Response to treatment

33. Chronic
periodontitis
Aggressive
periodontitis
Age
Rate of disease
progression
Local factors
- Familial nature present
Comparison of clinical features

34. Comparison of Histopathology
Chronic periodontitis Aggressive
periodontitis
Stages of
disease
progression
X
Plasma cells
Inflammatory
infiltrate
Plasma cells with
neutrophils migrating
through the pocket-
lining epithelium and
forming a layer
between the tissues
and the plaque biofilm
Note: his profile is identical to the histopathology of chronic periodontitis, it does not
necessarily mean that they are not different diseases. This profile may just represent the
response of the periodontium to varying plaque biofilms in susceptible individuals with
the subsequent loss of tooth support being a consequence of this inflammatory process.

35. Chronic
periodontitis
Th_1 Aggressive
periodontitis
Th-2
b cell
Th-17
production of
metalloproteinases
with resultant
osteoclast formation
and bone destruction.
Comparison of immuno pathological features

36. Comparison of microbiology
Comparisons of the microbiology of chronic and generalized
aggressive forms of periodontitis are in the early phases.
gram-negative anaerobic infections, but that gram-positive bacteria
and even non-bacterial microbes from the Archaea domain may
have an etiological role.
Co-infection with Epstein-Barr virus and cytomegalovirus shows a
particularly close link with progressive periodontitis.
Based on the available preliminary data, generalized aggressive
periodontitis and chronic periodontitis appear to be different from a
microbiological perspective

37. Comparison of neutrophil
Chronic periodontitis Aggressive
periodontitis
- number Decrease in cyclic
neutropenia.
Increase in GAP
Normal or elevated chemotaxis
response
suppress
- Phagocytosis
response
more
- Hyperactive ⁄
"primed"
neutrophil
Present
increased neutrophil
adhesion, enzyme
release, and perhaps
most importantly, an
elevated oxidative burst.

38. a
DISEASE PROGRESSION
•Rate of disease progression is usually slow-
0.2mm/year facially.
o.3mm/year interproximally.
•Modified by systemic or environmental factors.
•Onset at any age, but first sign may be detected
during adolescent in the presence of chronic
plaque and accumulation.
•Significant in mid thirties
•or later.

39. at era
•Does not progress at an equal rate in all affected
sites throughout the mouth.
•Some remain static for long periods-Lindhe et al.
Whereas other progress at rapid rate.
•More progressive lesions affected at interproximal
areas- Lang et al and Lindhe et al.
•Furcation areas
•Overhanging restorations
•Malposed teeth
•Food impaction.

40. ….prevalence

41. Models proposed for disease
progression
Continuous
model
socransky et
al
Random or
episodic model
Goodson et al
Asynchronous
or multiple
burst model.

43. of the time
PREVALANCE
•Increases in prevalence with increasing in
age.
•Periodontitis is an age associated ,not age
related disease.
•Length of the time that the periodontal
tissues are challenged by chronic plaque
accumulation.

44. Risk - is the probability that an individual will get a specific
disease in a given period. The risk of developing the disease
will vary from individual to individual.

45. Risk factors for disease:
Risk factor - is a characteristic, an aspect of behavior, or an
environmental exposure that is associated with destructive
periodontitis.
Prior history of
periodontal
disease
Local factors
Systemic
factors
Environmental
and behavior
factors
Genetic
factors

46. Prior history of periodontal
disease:
As a risk predictor.
Puts patient at greater risk for developing loss of attachment and bone loss-
Mc Guire et al and Papapanou et al.
Persistent gingivitis
or periodontitis with
pocketing
,attachment loss
and bone loss.
Continue to lose
periodontal
support.
Not
treated Patient with
periodontitis who
had successfully
treated
Develop continuing
disease if plaque is
allowed to
accumulate.
treated
Emphasis for
continuous
monitoring,
treatment and
maintenance of
patients

47. Local
factors
Plaque accumulation at tooth
and gingival surfaces at
dentogingival surfaces
considered as primary initiating
agent-Lang et al.
Plaque retentive factors is
important factor in development
and progression of periodontitis.
As they retain plaque micro
organism in the proximity to the
periodontal tissues
Providing etiological niche to
plaque growth and maturation.
Attachment and bone loss
are associated with Gram
negative anerobes.
Red complex
These bacteria impart local effect on
the cells and tissues of the host
,resulting in a local site specific
process.

48. Systemic factors
Chronic periodontitis+ systemic factors = increase the rate of
progression.
Non genetic
•Smoking –a major risk factor
•Diabetes
•HIV
•Nutritional disorders
•Osteoporosis
•Medication
•Stress
•Hematological
•Dermatological factors
•Neoplastic disorders
Genetic factors

49. DIABETES
0%
50%
100%
type 2 type 1
prevalance
prevalanc
e
•a disease of metabolic dysregulation.
Pathogenesis:
• Microvascular changes caused by
hyperglycemia leads to glycosylation of
basement membrane proteins.
• Thickening of basement membrane
•Altered structural and physical properties of
BM.
•Disruption of collagen fibers in BM, swelling
of endothelium, Impedes oxygen diffusion,
metabolic waste elimination, PMN migration
diffusion of serum factor including antibodies
Susceptible to infection Brownlee et al 1994
.
•Hyperglycemia + collagen AGEs -Increases
cross linking between collagen molecules
•Reduced solubility and turnover of collagen
results in failure in periodontal repair and
regeneration (Brownlee 1994)

50. Ronic periodi
Chronic periodontitis associated with many
syndromes
•Haim –Munk syndrome
•Papillon Lefevre syndrome
•Ehlers Danos syndrome
•Kindlers syndrome
•Cohen syndrome

51. AGE:
•Both the prevalence and severity of periodontal
disease increases with age. (Burt 1994, Papapanou
1994, 1998).
•Lindhe (1991, 1992) – minimal loss of attachment in
aging subjects enrolled in preventive programs
throughout their lives.

52. GENDER
United States national surveys.. Abdellatif et al (1987) have shown
that males have poorer oral hygiene.
• Gender differences in prevalence and severity of chronic
periodontitis are related to preventive practices rather than any
genetic factor.
RACE
• In USA – prevalence, severity and extent of chronic periodontitis is
more in Black, intermediate in Mexican African and least in Whites.
CAL • Whites – more on facial aspect and associated with gingival
recession. • Blacks – interproximal areas.

53. NUTRITION:
Vitamin C or ascorbic acid is essential for the formation of collagen and
intercellular material, bone and teeth.
•Altered nutritional status interaction
•Decreased immune function, and Intake of medications.

54. OSTEOPOROSIS
disease -characterized by low bone mass and deterioration of bone
structure that causes bone fragility and increases the risk of fracture.
A direct association between skeletal and mandibular osteopenia and
destructive periodontal disease as measured by loss of interproximal
alveolar bone in postmenopausal women has been reported.
(Wactawski-Wende and coworkers 1996).
• Studies in animal models indicate that osteoporosis does not initiate periodontitis;
there is evidence that the reduced bone mass seen in osteoporosis may aggravate
periodontal disease progression (Krook 1975, Aufdemorte 1993).
•Both osteoporosis and periodontal diseases are bone resorptive
diseases……hypothesized that osteoporosis could be a risk factor for the progression
of chronic periodontal disease

55. Environmental and
behavior factor
•Smoking increase the severity and extent of periodontal disease.
•Dose dependent
Compare to the non smokers, smokers have
•Have more attachment and bone loss
•More recession
•Increase tooth loss
•Less bleeding on probing
•Furcation involvement

56. Smokers demonstrating the composite IL-1 genotype are
at greater risk for periodontal disease.
Role of IL-1 genotype:
Increase the risk for tooth loss 2.7 times-those who are
heavy smokers.
IL-1 negative influence the risk for tooth loss by 2.9 times.
The combined effort of IL-1genotype and smoking
increased the risk of tooth loss by 2.2 times –Febig et al

57. As a result of consumption of tobacco ,reactive
oxygen species(i.e radicals) is released
Chemically the periodontal tissues
Via DNA damage
Lipid peroxidation of cell membrane
Damage of endothelial cells
Induction of smooth muscle cell growth

58. Psychological factors( stress and depression)
•Negatively influence the progression of the
disease.
•Positive correlation between cortisol levels and
periodontal index (eg plaque index, gingival
index, bone loss and missing teeth have been
recorded.
•Strongly associated with periodontitis when
patients wee smokers as compared with non
smokers.

59. Immunological factors
•Chronic periodontitis –onset, progression and
severity of periodontal disease depend on the
individuals host response.
•Patients may show alteration in peripheral monocytes-
related to reduced reactivity of lymphocytes or an
enhanced b cell response.
•B cells,macrophage ,periodontal ligament cells, gingival
fibroblast and epithelial cells synthesize pro inflammatory
mediators ) eg interluekin 1 β,interluekin 6,interluekin
8,prostoglandin E2,tumor neecrosis factor-α) that modify innate and
adaptive immunity responses at periodontal sites.

60. Genetic factors
Genetic variations such as Single Nucleotide Polymorphisms
and genetic copy variations influence innate and adaptive
immune response as well as structure of periodontal tissues.
Hereditabilty 50%
Studies:
Genetic variations or polymorphism is in the genes encoding IL-1α and IL
–β associated with incresae risk for chronic periodontitis-
Kornman et al.
Genome wide association studies : Significant association between
periodontitis and coronary artery disease.

61. DIAGNOSIS
clinical radiographical
Inflammatory changes in
the marginal gingiva.
Loss of clinical attachment
.
bone loss
conventional

62. DISEASE ACTIVITY:
Consistent with the view of periodontitis as a
highly localized infection of the periodontium,
disease activity is perceived as the condition under
which periodontal attachment loss increases
abruptly at discrete sites over a relatively short
period of time in a small percentage of sites
(Socransky et al 1984).

63. ADVANCED
DIAGNOSTIC
TESTS

64. CHAIR SIDE DIAGNOSTIC KITS :
The ideal diagnostic test should be
•Quantitative.
• Highly sensitive method capable of analyzing a single periodontal site
in health as well as disease.
• Reproducible.
•Highly specific.
• Simple to perform.
•A rapid, one or two stage procedure.
•Non-invasive.
•Versatile in terms of sample handling, storage and transport.
• Amendable to chairside use.
• Economical

65. Chairside periodontal test kits can be
categorized as
•Microbiological test kits
•Biochemical test kits
• Genetic kits

66. PERIOSCAN

67. detects elevated levels (>IU) of Asparate Aminotransferase (AST) in GCF
POCKET- WATCH
(Periodontal Tissue Monitor
System) :
•PERIOCHECK:
This system (Pro Dentec Bates ville) detects the presence of neutral
proteinases such as collagenase in GCF.

68. PROGNOSTIK [Dentsply]:
It detects the presence of serine
proteinases and elastase in GCF samples.
PERIOGARD [Colgate] :
It detects the presence of Aspartate
Aminotransferase in GCF sample.

69. •EVALUSITE :
This chair side immunoassay detects periodontal pathogens
such as Aa commitans , P gingivalis , P intermedia .
. Increased levels of human inflammatory proteins,Increased levels of
bacterial toxins.
•CRP LATEX KIT:
C- Reactive Protein (CRP) latex slide test (Serology kit) is used for the
qualitative and semi-quantitative measurement of C-reactive protein
(CRP) in human serum.

70. •Topas- I (Toxicity Pre Screening Assay)
Introduced to detect two markers of infection: &
bacterial proteins.
BIOLISE :
Recently software has been made Biolise [SLT-Lab
instruments, Craitsheim, Germany] which is used to
detect the elastase activity in GCF. [Hermann et al
2001].
GLUCOMETER It is used for Blood glucose
measurements using gingival crevicular blood.

71. PERIODONTAL SUSCEPTIBILITY TEST:
IL GENETICS INC. WALTHAM.MASS-
Detects the presence of a specific form of 2 IL genes; Allele 2 at
IL1A+4845 & IL1B+3954.
Test also used to correlate the IL-1 production with other
clinical parameters; BOP, Bone & attachment loss and tooth &
implant loss.

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

73. TREATMENT PLANNING
1) Procedures designed to halt the progression of disease.
2) Procedures designed to regenerate structures destroyed
by disease. Pihlstrom BL.
Successful periodontal therapy is dependent on anti- infective procedures aimed at
eliminating pathogenic organisms found in dental plaque associated with the tooth surface
and within other niches in the oral cavity. Slots J.
• Since periodontal disease is a plaque-induced infection and most patients are not skilled
in mechanical plaque removal, professional cleaning is almost universally indicated to
sustain long-term stability of the periodontium.
• Anti-infective therapy includes both mechanical and chemotherapeutic approaches to
minimize or eliminate microbial biofilm (bacterial plaque), the primary etiology of
gingivitis and periodontitis.

74. The traditional modality as an initial periodontal treatment phase has been to
perform scaling and root planing by jaw quadrant (Q-SRP) at a series of
appointments (Badersten et al. 1984).
More recently, Quiynen et al. (1995) advocated the benefit of performing full-
mouth SRP within 24h in order to prevent re-infection of the treated sites from
the remaining untreated periodontal pockets.
Mechanical approach

75. Chemotherapeutic approaches include topical application
of antiseptics or sustained-release local drug delivery
agents that are designed to prevent plaque accumulation
and to disinfect the root surfaces and adjacent periodontal
tissues.
Chemical approach

76. SURGICAL THERAPY:
Surgery is indicated where nonsurgical methods fail.
Advantages of periodontal surgery :
Pocket elimination procedures gave the greatest probing
depth reduction.
Pocket elimination was defined as gingivectomy or a flap
procedure with or without osseous re-contouring.

77. Surgical techniques includes Gingivectomy Undisplaced flap ,Modified
Widman flap with and without osseous re- contouring, apically
positioned flap with and without osseous re-contouring.

78. CONCLUSION:
Chronic periodontitis an infectious disease resulting in
inflammation with in supporting tissues of the teeth,
progressive attachment loss and bone loss”.
With all emerging technologies, a successful
diagnosis and treatment will only be achieved
through open sharing of ideas, research
findings and thorough testing.

79. REFERENCES:
•Carranza. Clinical periodontology 9th , 10th and 11th edition.
•Outline of periodontics Manson, Eley, 4th edition.
•Clinical periodontology and implant surgery :Lindhe-5 th edition
•Textbook of periodontics-Shallu bathla
•Comparative between chronic and aggressive periodontitis: Perio 2000
vol 53,2010 7-11.
•Relationship between periodontal disease and systemic health
Periodontology 2000, Vol. 25, 2001, 21–36.
•Periodontal risk assessment, diagnosis and treatment planning
Periodontology 2000, Vol. 25, 2001, 37–58
•Non-surgical periodontal therapy Periodontology 2000, Vol. 25, 2001,
77–88 .
•Surgical periodontal therapy Periodontology 2000, Vol. 25, 2001, 89–99
120