Chronic periodontitis

1. CHRONIC
PERIODONTITIS
PRESENTED BY:
DR. THASLIM FATHIMA
DEPARTMENT OF PERIODONTOLOGY

2. CONTENTS
• INTRODUCTION
• DEFINTION
• HISTORY
• COMMON CHARACTERISTICS
• DISEASE DISTRIBUTION
• PREVALENCE
• RISK FACTORS FOR DISEASE
• MICROBIOLOGICAL ASPECTS
• LOCAL FACTORS
• SYSTEMIC FACTORS
• IMMUNOLOGIC FACTORS
• GENETIC FACTORS
• ENVIRONMENTAL AND BEHAVIORAL FACTORS
• DISEASE ACTIVITY
• CLINICAL DIAGNOSIS
• CLINICAL FEATURES
• RADIOGRAPHIC APPEARANCE OF CHRONIC PERIODONTITIS
• TREATMENT PLANNING
• MECHANICAL THERAPY
• SURGICAL THERAPY
• PROGNOSIS
• CONCLUSION

3. CHRONIC PERIODONTITIS
• Chronic – (Greek – Kronos means time) long lasting.
• Chronic periodontitis, formerly known as “adult
periodontitis” or “chronic adult periodontitis” is the most
prevalent form of periodontitis.
• Most commonly seen in adults.

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.”

5. History
• Fauchard recognized the relationship between oral
hygiene and the etiology of periodontal disease.
• John W. Riggs (1811-1885)
Periodontitis or alveolar pyorrhea was known as ‘Riggs
disease’ and he was the first individual to limit his practice
to periodontics.

6. COMMON CHARACTERISTICS
• Prevalent in adults but
can occur in children
• Amount of destruction
consistent with local factors
• Associated with a variable
microbial pattern
• Subgingival calculus
frequently found
• Slow to moderate rate of
progression, with possible
periods of rapid
progression
• Systemic diseases (e.g.,
diabetes mellitus, human
immunodeficiency virus)
• Local factors that
predispose an individual to
periodontitis
• Environmental factors
(e.g., cigarette smoking,
emotional stress)

7. • Localized form:
<30% of sites involved
•Generalized form:
>30% of sites involved
Slight
1 to 2 mm
of clinical
attachment
loss
Moderate
3 to 4 mm
of clinical
attachment
loss
Severe
≥5 mm of
clinical
attachment
loss

8. Disease Distribution
• Chronic periodontitis is considered a site-specific
disease.
• Local inflammation, pocket formation, attachment loss,
and bone loss are the consequences of direct exposure
to the subgingival plaque (biofilm).
• As a result of this local effect, pocket formation and
attachment as well as bone loss may occur on one
surface of a tooth, whereas other surfaces maintain
normal attachment levels.

9. • As a result of the site-specific nature, the number of
teeth with clinical attachment loss classifies chronic
periodontitis into the following types :
Localized chronic periodontitis
• less than 30% of the sites show attachment
and bone loss
Generalized chronic periodontitis
• 30% or more of the sites show attachment and
bone loss

10. • During chronic periodontitis, the local inflammatory
response may lead to different patterns of bone loss,
including vertical (angular) and horizontal bone
destruction.
• Although vertical bone loss is associated with intrabony
pocket formation, horizontal bone loss is usually
associated with suprabony (supra-alveolar) pockets.

11. Disease Severity
• With increasing age, attachment loss and bone loss
become more prevalent and more severe as a result
of an accumulation of destruction.
TIME
systemic
disorders
severity

12. Disease severity may be described as:
mild, moderate, or severe.
• Mild chronic periodontitis: when no more than 1
mm to 2 mm of clinical attachment loss has
occurred
• Moderate chronic periodontitis: when 3 mm to 4
mm of clinical attachment loss has occurred
• Severe periodontitis: when 5 mm or more of
clinical attachment loss has occurred

16. SYMPTOMSGingival
bleeding
black triangles
tooth
sensitivity
tooth mobility,
tooth
movement,
tooth loss. localized dull
pain
food impaction
Gingival
tenderness

17. Disease Progression
• The rate of disease progression is usually slow..
..but it may be modified by systemic, environmental, and
behavioral factors.
• The onset of chronic periodontitis can occur at any time.
• Because of its slow rate of progression, however,chronic
periodontitis usually becomes clinically significant when a
patient reaches his or her mid-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 they may also be associated with
areas of greater plaque accumulation and inaccessibility to
plaque control measures.

19. The continuous model
• 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.

20. The random or episodic-burst model
• The random or episodic-burst model 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.

21. The asynchronous, multiple-burst
model• 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.

22. Prevalence
• Chronic periodontitis increases in prevalence and severity
with age, and it generally affects both genders equally.
• Periodontitis is an age-associated (not an age-related)
disease.
• Nonetheless, the prevalence of periodontitis increases with
age so that 40% of patients who are 50 years old or older
and almost 50% of patients who are 65 years old or older
show moderate periodontal destruction.
• The prevalence of severe forms of periodontitis also
increases with age.

23. Risk Factors for Disease
• Periodontitis is considered to be a multifactorial disease.
• The extent of the periodontal destruction depends on the host’s
immune competence as well as genetic predispositions that
influence individual susceptibility to disease.

24. Microbiological Aspects
• Attachment and bone loss are associated with an increase in the
proportion of gram-negative organisms in the subgingival biofilm.
Dental biofilm
develops
optimal
plaque control
neglected oral
hygiene
gingivitis
complete resolution
of this early gingival
inflammation
inflammation will
progress and
eventually result in
the loss of attachment
Although not all
patients with
gingivitis develop
periodontitis, it is
known that all
patients with
periodontitis
experienced prior
gingivitis

25. • Porphyromonas gingivalis, Tannerella forsythia, and Treponema
denticola—otherwise known as the “red complex”—are
frequently associated with ongoing attachment and bone loss in
patients with chronic periodontitis.
periodontal
breakdown
with increasing
concentration
of pro-
inflammatory
mediators
invade the
periodontal
tissue

26. Local Factors
• Plaque accumulation and biofilm development are
the primary causes of periodontal inflammation and
destruction.
• Calculus is considered the most important plaque-
retentive factor as a result of its ability to retain and
harbor plaque bacteria on its rough surface as well
as inside.

28. • Tooth morphology may influence plaque retention.
• Roots may show grooves or concavities, and, in some
instances, enamel projections on the surface or the
furcation entrances.
• In addition, subgingival and overhanging margins of
restorations, carious lesions that extend subgingivally, and
furcations exposed by loss of bone promote plaque
retention.

29. Systemic Factors
• In several instances, periodontitis is also associated
with other systemic disorders, such as:
• Haim– Munk syndrome, Papillon–Lefèvre syndrome,
Ehlers–Danlos syndrome, Kindlers syndrome, and
Cohen syndrome
• Patients with diseases that impair the host immune
response (e.g., human immunodeficiency virus,
acquired immunodeficiency syndrome) may also
show periodontal destruction.

30. • It is also known that osteoporosis,a severely
unbalanced diet, and stress as well as
dermatologic,hematologic, and neoplastic factors
interfere with periodontal inflammatory responses.
• In addition to being associated with defined
syndromes,
• Periodontitis also occurs with severe systemic
diseases, such as diabetes mellitus, cardiovascular
disorders, stroke, and lung disorders

31. Diabetes mellitus and periodontitis
Patients with diabetes mellitus exhibit a higher risk for the
development of periodontitis, and periodontal infection and
inflammation may negatively interfere with the glycemic
control of the diabetic patient.
A number of studies showed that the prevalence, severity,
and prognosis of periodontitis are associated with the
incidence of diabetes mellitus.
It was found that the average pocket depth as well as the
clinical attachment loss was increased in patients with
diabetes mellitus (independent of the type of diabetes
mellitus).

32. Two way relationship of diabetes and periodontitis

33. • Patients with poor glycemic control (i.e., a glycated
hemoglobin level of >9%) tend to experience a more
severe progression of periodontitis as compared with
patients with good glycemic control (i.e., a glycated
hemoglobin level of <9%).

34. • Periodontal therapy may contribute to the glycemic control of
the diabetic patient.
• It has been shown that systematic periodontal therapy leads
a 0.4% reduction of glycated hemoglobin.
• Each therapy regimen that contributes to achieve a reduction
in the glycated hemoglobin level decreases the risk of
diabetes-related long-term consequences, such as
myocardial infarction, microvascular complications, and many
others.

35. Immunologic Factors
• The onset, progression, and severity of the disease depend
on the individual host’s immune response.
• B-cells, macrophages, periodontal ligament cells, gingival
fibroblasts, and epithelial cells synthesize pro-inflammatory
mediators (e.g., interleukin-1β, interleukin-6, interleukin-8,
prostaglandin E2, tumor necrosis factor-α) that modify
innate and adaptive immune responses at periodontal sites.

36. • Pro-inflammatory mediators regulate the synthesis and
secretion of, for example, matrix metalloproteinases and
receptor activator of nuclear factor-κβ ligand (RANKL)
• In periodontal lesions, matrix metalloproteinases contribute to
soft and hard-tissue degradation during active inflammatory
reactions.
• RANKL binds to its receptor activator of nuclear factor-κβ on
the cell surface of premature osteoclasts, thereby initiating
osteoclast differentiation that leads to the degradation of
alveolar bone.
• Physiologically, osteoprotegerin is the opponent of RANKL;
• During periodontitis, an imbalance between osteoprotegerin
and RANKL promotes further bone degradation.

37. • Reduced neutrophil counts influence the degree of
periodontal inflammation.
• Congenital neutropenia (Kostman syndrome) leads not
only to an increased susceptibility to infection in general
but also to severe chronic periodontitis.
• Patients with Kostman syndrome show reduced levels of
antimicrobial peptides,such as the cathelicidin LL-37 and
neutrophil peptides (α-defensins), which impair the
innate immune response.
• LL-37 is an effective antimicrobial peptide that is
synthesized from inactive precursors.

38. • Mutations in the cathepsin C gene hinder cleavage
and thus the activation of LL-37.
• Such genetic alterations contribute to the severity
and progression of chronic periodontitis (i.e.,
Papillon–Lefèvre syndrome; Haim–Munk syndrome)

39. Genetic Factors
• Genetic variations such as single nucleotide polymorphisms
(SNPs) and genetic copy number variations may directly
influence innate and adaptive immune responses as well as the
structure of periodontal tissues.
• Periodontal destruction has been found among family members
and across different generations within a family, thereby
suggesting a genetic basis for the susceptibility to periodontal
disease.

40. • Porphyromonas gingivalis induces the gene expression of
ANRIL in human gingival fibroblasts, thereby suggesting the
potential regulation of ANRIL during periodontal infection
and inflammation.
• Another study identified a SNP in an untranslated region of
the human β-defensin-1 gene DEFB1, and this genetic
alteration was significantly associated chronic periodontitis.
• Human β-defensin-1 is an antimicrobial peptide that plays
an important role in innate immune responses.

41. Environmental and Behavioral
Factors
• Smoking and psychological stress
• Smoking is a major risk 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
as compared with non-smokers and former smokers.

42. As compared with non-smokers, the following
features are found in smokers:
• Increased periodontal pocket depth of more than 3 mm
• Increased attachment loss
• More recessions
• Increased loss of alveolar bone
• Increased tooth loss
• Fewer signs of gingivitis (e.g., less bleeding with probing)
• Greater incidence of furcation involvement

43. • As a result of the consumption of tobacco, reactive
oxygen (i.e., radicals) is released that chemically
irritates periodontal tissues via DNA damage, the
lipid peroxidation of cell membranes, the damage of
endothelial cells, and the induction of smooth
muscle cell growth.

44. • Psychological factors (e.g.,
stress, depression) also
negatively influence the
progression of chronic
periodontitis.
• Positive correlations between
cortisol levels and periodontal
indices (e.g., plaque index,
gingival index), bone loss, and
missing teeth have been
recorded.
• Stress as an etiologic factor was
even more strongly associated
with periodontitis when patients
were smokers as compared with
non smokers.

45. 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)

46. DIAGNOSIS
CLINICAL
chronic inflammatory
changes in the marginal
gingiva
periodontal pockets
loss of clinical attachment

47. DIAGNOSIS
The primary criterion for bone loss in these
studies was the distance from the
cementoenamel junction (CEJ) to the alveolar
crest, The threshold distance of bone loss has
varied from 1 mm to 3 mm, although most of
the studies have used > 2 mm as the criterion
for bone loss

48. Clinical Features
• Characteristic clinical findings in patients with untreated
chronic periodontitis include the following:
Supragingival and
subgingival plaque and
calculus
Gingival swelling, redness,
and loss of gingival stippling
Altered gingival margins
(e.g., rolled, flattened,
cratered papillae,recessions)
Pocket formation
Bleeding on probing
Attachment loss (angular or
horizontally)
Bone loss
• Root furcation
involvement (exposure)
• Increased tooth mobility • Change in tooth position • Tooth loss Recession

49. Radiographic appearance of chronic
periodontitis

50. 1
• Fuzziness and a break in the continuity of the lamina
dura at the mesial or distal aspect of the crest of the
interdental septum have been considered as the earliest
radiographic changes in chronic periodontitis.
• These result from the extension of gingival inflammation
into the bone, causing widening of the vessel channels
and a reduction in calcified tissue at the septal margin.

51. 2
• A wedge-shaped radiolucent area is formed at the
mesial or distal aspect of the crest of the septal
bone.
• The apex of the area is pointed in the direction of
the root.
• This is produced by resorption of the bone of the
lateral aspect of the interdental septum, with an
associated widening of the periodontal space.

52. 3
• The destructive process extends across the crest of the interdental septum, and
the height is reduced.
• Fingerlike radiolucent projections extend from the crest into the septum .The
radiolucent projections into the interdental septum are the result of the deeper
extension of the inflammation into the bone.
• Inflammatory cells and fluid, proliferation of connective tissue cells, and
increased osteoclasts cause increased bone resorption along the endosteal
margins of the medullary spaces.
• The radiopaque projections separating the radiolucent spaces are the composit
images of the partially eroded bony trabeculae.

53. • The height of the interdental septum is progressively
reduced by the extension of inflammation and the
resorption of bone.

54. Osseous defects as a result of periodontal disease is
classified clinically into horizontal (even) and angular
(vertical) defects
• In horizontal bone loss, the height of alveolar bone is
symmetrical and parallel to an imaginary line joining CEJ
of adjacent teeth.
• There occurs resorption of buccal, lingual cortical walls
including the interdental bone.
• It can be categorized as mild, moderate or severe,
depending on its extent.

55. HORIZONTAL BONE LOSS

56. HORIZONTAL BONE LOSS

57. In the vertical or angular osseous destruction, the bone loss is
unsymmetrical;
alveolar crest is not parallel to the level connecting the CEJ of the
adjacent teeth.
These defects develop when bone loss progresses down the root of
the tooth, resulting in deepening of the clinical periodontal pocket.
The early vertical defects appear as abnormal widening of the PDL
space at alveolar crest.
Further vertical osseous destruction leads to the formation of osseous
defects where the base of the defect is located apically to the alveolar crest.

58. VERTICAL BONE LOSS

59. VERTICAL BONE LOSS

60. TREATMENT PLANNING
Pihlstrom BL, Committee of the American Academy of Periodontology. J
Periodontol 1997
RX
TREATMENT for periodontitis
generally falls into two categories:
1) Procedures designed to halt the
progression of disease
2) Procedures designed to
regenerate structures destroyed by
disease

61. The primary
objectives of
therapy for
patients with
chronic
periodontitis
are to halt
disease
progression
and to resolve
inflammation.
Initial
periodontal
therapy or
basic
treatment of
periodontitis
involves the
removal of
both
supragingival
and subgingival
plaque.
The clinical
outcome is
largely
dependent on
the skill of the
operator in
removing
subgingival
plaque and the
skill and
motivation of
the patient in
practicing
adequate
home care.

62. Mechanical therapy

63. Scaling and root planing
• The beneficial effects of SRP combined with personal
plaque control in the treatment of chronic periodontitis
include reduction of clinical inflammation, microbial shifts
to a less pathogenic subgingival flora, decreased probing
depth, gain of clinical attachment, and less disease
progression. (Morrison EC, Ramfjord SP-1980).
• Studies show that clinical conditions generally improve
following root planing; nonetheless, some sites still do not
respond to this therapy.
(Kaldahl WB, Kalkwarf KL-1988).

64. • In general, clinicians should evaluate post-SRP healing
at 4 to 6 weeks following treatment. After 6 weeks, most
of the healing has taken place but repair and collagen
maturation may continue for an additional 9 months.
[Badersten A-1981].
• Following the completion of root planing re-evaluation
should be conducted to determine the personal plaque
control, and treatment response.

65. Pharmacological therapy
If the patient’s daily personal
plaque control is not adequate
to maintain gingival health,
then additional instruction and
motivation in personal plaque
control and/or the use of
topical chemotherapeutics (eg,
mouthrinses, local drug
delivery devices) may be
indicated.
Antimicrobial products such as
mouthrinses containing
essential oils, triclosan or
chlorhexidine are also useful
adjuncts to brushing and
flossing in gingivitis and
periodontitis patients and can
reduce plaque accumulation
and gingivitis by 75%

66. Pharmacological therapy
• Pharmacotherapeutics may have an adjunctive role in the
management of periodontitis in certain patients.
• These adjunctive therapies are categorized by their route of
administration to diseased sites: systemic or local drug
delivery.
• Systemic drug administration:
• Patients with multiple sites unresponsive to mechanical
debridement,
• Acute infections,
• Medically compromised patients,
• Presence of tissue-invasive organisms and
• Ongoing disease progression.

67. Common Antibiotic Therapies in the
Treatment of Chronic Periodontitis
1. Doxycycline / minocycline : 100-200mg/q.d for 21 days.
2. Azithromycin : 500 mg/ q.d for 4-7 days.
3. Ciprofloxacin : 500 mg/b.i.d for 8 days.
4. Clindamycin : 300 mg/ t.i.d for 8 days.
5. Metronidazole : 500 mg/ t.i.d for 8 days.
6. Metronidazole + Amoxycillin: 250 mg/t.i.d for 8 days.
7. Metronidazole + Ciprofloxacin: 500 mg/b.i.d for 8 days

68. Local delivery
• The greatest potential of local delivery devices may be to
enhance therapy at sites that do not respond to
conventional treatment.
• Controlled delivery of chemotherapeutic agents within
periodontal pockets can alter the pathogenic flora and
improve clinical signs of periodontitis.(Williams RC-2001)
• Local drug delivery systems provide several benefits; the
drug can be delivered to the site of disease activity at a
bactericidal concentration and it can facilitate prolonged
drug delivery.

69. Local delivery modalities have shown beneficial
clinical improvements with regard to probing depth
reduction and gain in clinical attachment.(Newman
MG, Kornman KS-1994
Furthermore, there are limited data to suggest that
local delivery of antibiotics may also be beneficial in
preventing recurrent attachment loss in the absence
of maintenance therapy.(Michalowicz BS-1995)

70. Surgical therapy
• Surgical access to facilitate mechanical
instrumentation of the roots has been utilized to
treat chronic periodontitis for decades.
• A surgical approach to the treatment of periodontitis
is utilized in an attempt to:
• 1) provide better access for removal of etiologic
factors;
• 2) reduce deep probing depths; and
• 3) regenerate or reconstruct lost periodontal tissues.
(Consensus Report: Mucogingival therapy. Ann Periodontol 1996)

71. Regenerative surgical therapy
The optimal goal of therapy for individuals who have lost a significant
amount of periodontal attachment is regeneration of lost tissues.
While root debridement in combination with plaque control has
demonstrated efficacy in resolving inflammation and arresting
periodontitis, healing typically results in the formation of a long
junctional epithelium with remodeling of the alveolus.(Caton J-1980).
Similarly, surgical debridement alone does not induce significant
amounts of new connective tissue attachment. However, some bone
fill may occur in selected sites. (Listgarten MA-1979).

72. Occlusal management
• Excessive occlusal forces may be associated with adverse
effects on the periodontium and affect the response to therapy
with respect to gaining clinical attachment.
• Occlusal therapy may aid in reducing tooth mobility and
gaining some bone lost due to traumatic occlusal forces.
(Burgett FG -1992)

73. Periodontal maintenance procedures
• Periodic monitoring of periodontal status and appropriate
maintenance procedures should be part of the long-term
treatment plan for managing chronic periodontitis.
• Although experimental studies have demonstrated very successful
treatment outcomes when patients are professionally maintained at
2-week intervals, such a program is impractical for most chronic
periodontitis patients. (Rosling B-1976)
• Therefore, to maximize successful therapeutic outcomes, patients
must maintain effective daily plaque control. It also appears that in-
office periodontal maintenance at 3 to 4 month intervals can be
effective in maintaining most patients. (Ramfjord SP-1993)

74. Prognosis for Patients with Chronic
Periodontitis
• Chronic periodontitis is a slowly progressive disease
associated with well-known local environmental factors.
• In cases where the clinical attachment loss and bone loss
are not very advanced (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

75. • In patients with more severe disease as evidenced by
furcation involvement and increasing clinical mobility, or in
patients who are noncompliant with oral hygiene practices,
coupled with Secondary contributing factors such as cigarette
smoking or uncontrolled systemic diseases, the alterations in
host defense, may result in a case that does not respond well
to conventional periodontal therapy (scaling with root planing,
oral hygiene instruction, and surgical intervention).
• Therefore these patients often have a fair, poor, or
questionable prognosis, and the use of systemic
antibiotics should be considered to help control the
disease the prognosis may be downgraded to fair to
poor.

77. REFERENCES
• Clinical periodontology. Carranza 10th edition
• Clinical Periodontology and Implant Dentistry. Lindhe,6th
edition
• Advances in the pathogenesis of periodontitis: summary
of developments, clinical implications and future
directions. Roy C. Page, Steven Offenbach-
Periodontology 2000. Vol. 14, 1997, 216-248.
• Treatment of Plaque-induced Gingivitis, Chronic
Periodontitis, and Other Clinical Conditions- American
Academy of Periodontology - Research, Science, and
Therapy Committee-2004.
• Periodontal diseases: A brief historical Perspective,
Haralld Loe, Periodontology 2000, Vol. 2, 1993, 7-12.