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CHRONIC PERIODONTITIS
INTRODUCTION
• Chronic periodontitis, formerly known as “adult periodontitis”
or “chronic adult periodontitis,” is the most prevalent form of
periodontitis.
• A slowly progressing disease.
• However, in the presence of systemic or environmental factors
that may modify the host response to plaque accumulation
DEFINITION
“An inflammatory disease of the supporting tissues
of the teeth caused by specific microorganisms or
groups of specific microorganisms, resulting in
progressive destruction of the periodontal ligament
and alveolar bone with increased probing depth
formation, recession, or both”
CLINICAL FEATURES
General Characteristics:
• Supragingival and subgingival plaque accumulation with
calculus formation
• Gingival inflammation
• Pocket formation
• Loss of periodontal attachment
• Loss of alveolar bone
• Occasional suppuration
• Gingival bleeding
• Tooth mobility
GINGIVAL FEATURES
• Slightly to moderately swollen
• Alterations in color ranging from pale red to magenta.
• Loss of gingival stippling
• Changes in the surface topography may include blunted or
rolled gingival margins and flattened or cratered papillae
Disease Distribution
Site-specific disease
• Clinical signs of chronic periodontitis—inflammation, pocket
formation, attachment loss, and bone loss—are believed to be
caused by the direct, site-specific effects of subgingival plaque
accumulation
• As a result of this local effect, pocketing, attachment, and
bone loss may occur on one surface of a tooth while other
surfaces maintain normal attachment levels
• Localized periodontitis: Periodontitis is considered localized
when less than 30% of the sites assessed in the mouth
demonstrate attachment loss and bone loss
• Generalized periodontitis: Periodontitis is considered
generalized when 30% or more of the sites assessed in the
mouth demonstrate attachment loss and bone loss
 Vertical bone loss - when attachment
and bone loss on one tooth surface is
greater than that on an adjacent
surface, associated with angular bony
defects and intrabony pocket
formation
 Horizontal bone loss - when
attachment and bone loss proceeds at
a uniform rate on the majority of
tooth surfaces, associated with
suprabony pockets
Disease Severity
• Slight (mild) periodontitis: Periodontal destruction is
generally considered slight when no more than 1 to 2 mm of
clinical attachment loss has occurred.
• Moderate periodontitis: Periodontal destruction is generally
considered moderate when 3 to 4 mm of clinical attachment
loss has occurred.
• Severe periodontitis: Periodontal destruction is considered
severe when 5 mm or more of clinical attachment loss has
occurred.
Symptoms
• Gums bleed when brushing or eating
• Spaces occur between their teeth as a result of tooth
movement; or that teeth have become loose
• Areas of localized dull pain, sometimes radiating deep into the
jaw
• The presence of areas of food impaction may add to the
patient’s discomfort.
• Gingival tenderness or “itchiness” may also be found.
Disease Progression
• Rate of disease progression is usually slow but may be
modified by systemic or environmental and behavioral factors
• Onset of chronic periodontitis can occur at any time, and the
first signs may be detected during adolescence in the
presence of chronic plaque and calculus accumulation.
• Because of its slow rate of progression, however, chronic
periodontitis usually becomes clinically significant in the mid-
30s or later
suggests that disease progression is slow
and continuous, with affected sites
showing a constantly progressive rate of
destruction throughout the duration of the
disease.
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.
MODELS OF DISEASE PROGRESSION
Continuous
model
Random model
or episodic-burst
model
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
Asynchronous,
multiple-burst
model
Prevalence
• Chronic periodontitis increases in prevalence and severity
with age, generally affecting both genders equally.
Periodontitis is an age-associated, not an age-related, disease.
• In other words, it is not the age of the individual that causes
the increase in disease prevalence, but rather the length of
time that the periodontal tissues are challenged by chronic
plaque accumulation
RISK FACTORS FOR DISEASE
Prior History of Periodontitis
• A prior history of periodontitis puts patients at greater risk for
developing further loss of attachment and bone
Local Factors
• Plaque accumulation on tooth and gingival surfaces at the
dentogingival junction
• Attachment and bone loss are associated with an increase in
the proportion of gram-negative organisms
• Porphyromonas gingivalis (formerly Bacteroides gingivalis),
Tannerella forsythia (formerly Bacteroides forsythus), and
Treponema denticola, otherwise known as the “red complex”
• Plaque-retentive factors are important in the development
and progression of chronic periodontitis because they retain
plaque microorganisms in proximity to the periodontal
tissues, providing an ecologic niche for plaque growth and
maturation.
• Calculus is considered the most important plaque-retentive
factor because of its ability to retain and harbor plaque
bacteria on its rough surface. As a result, calculus removal is
essential for the maintenance of a healthy periodontium.
Other factors are
• Subgingival and overhanging margins of restorations;
• Carious lesions that extend subgingivally
• Furcations exposed by loss of attachment and bone;
• Crowded and malaligned teeth
• Root grooves and concavities
Systemic Factors
• Diabetes is a systemic condition that can increase the severity
and extent of periodontal disease in an affected patient.
• Type 2 diabetes is most likely to develop in an adult
population at the same time as chronic periodontitis.
• The synergistic effect of plaque accumulation and modulation
of an effective host response through the effects of diabetes
can lead to severe and extensive periodontal destruction that
may be difficult to manage with standard clinical techniques
without controlling the systemic condition
Environmental and Behavioral Factors
• Smoking has been shown to increase the severity and extent
of periodontal disease smokers with chronic periodontitis
have more attachment and bone loss, more furcation
involvements, and deeper pockets
• Emotional stress has previously been associated with
necrotizing ulcerative disease, perhaps because of the effects
of stress on immune function
Genetic Factors
• Periodontitis is considered to be a multifactorial disease in
which the normal balance between microbial plaque and host
response is disrupted
• A genetic variation or polymorphism in the genes encoding
interleukin-1α (IL-1α) and IL-1β is associated with an
increased susceptibility to a more aggressive form of chronic
periodontitis

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chronic periodontitis.pptx

  • 2. INTRODUCTION • Chronic periodontitis, formerly known as “adult periodontitis” or “chronic adult periodontitis,” is the most prevalent form of periodontitis. • A slowly progressing disease. • However, in the presence of systemic or environmental factors that may modify the host response to plaque accumulation
  • 3. DEFINITION “An inflammatory disease of the supporting tissues of the teeth caused by specific microorganisms or groups of specific microorganisms, resulting in progressive destruction of the periodontal ligament and alveolar bone with increased probing depth formation, recession, or both”
  • 4. CLINICAL FEATURES General Characteristics: • Supragingival and subgingival plaque accumulation with calculus formation • Gingival inflammation • Pocket formation • Loss of periodontal attachment • Loss of alveolar bone • Occasional suppuration • Gingival bleeding • Tooth mobility
  • 5. GINGIVAL FEATURES • Slightly to moderately swollen • Alterations in color ranging from pale red to magenta. • Loss of gingival stippling • Changes in the surface topography may include blunted or rolled gingival margins and flattened or cratered papillae
  • 6. Disease Distribution Site-specific disease • Clinical signs of chronic periodontitis—inflammation, pocket formation, attachment loss, and bone loss—are believed to be caused by the direct, site-specific effects of subgingival plaque accumulation • As a result of this local effect, pocketing, attachment, and bone loss may occur on one surface of a tooth while other surfaces maintain normal attachment levels
  • 7. • Localized periodontitis: Periodontitis is considered localized when less than 30% of the sites assessed in the mouth demonstrate attachment loss and bone loss • Generalized periodontitis: Periodontitis is considered generalized when 30% or more of the sites assessed in the mouth demonstrate attachment loss and bone loss
  • 8.  Vertical bone loss - when attachment and bone loss on one tooth surface is greater than that on an adjacent surface, associated with angular bony defects and intrabony pocket formation  Horizontal bone loss - when attachment and bone loss proceeds at a uniform rate on the majority of tooth surfaces, associated with suprabony pockets
  • 9. Disease Severity • Slight (mild) periodontitis: Periodontal destruction is generally considered slight when no more than 1 to 2 mm of clinical attachment loss has occurred. • Moderate periodontitis: Periodontal destruction is generally considered moderate when 3 to 4 mm of clinical attachment loss has occurred. • Severe periodontitis: Periodontal destruction is considered severe when 5 mm or more of clinical attachment loss has occurred.
  • 10. Symptoms • Gums bleed when brushing or eating • Spaces occur between their teeth as a result of tooth movement; or that teeth have become loose • Areas of localized dull pain, sometimes radiating deep into the jaw • The presence of areas of food impaction may add to the patient’s discomfort. • Gingival tenderness or “itchiness” may also be found.
  • 11. Disease Progression • Rate of disease progression is usually slow but may be modified by systemic or environmental and behavioral factors • Onset of chronic periodontitis can occur at any time, and the first signs may be detected during adolescence in the presence of chronic plaque and calculus accumulation. • Because of its slow rate of progression, however, chronic periodontitis usually becomes clinically significant in the mid- 30s or later
  • 12. suggests that disease progression is slow and continuous, with affected sites showing a constantly progressive rate of destruction throughout the duration of the disease. 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. MODELS OF DISEASE PROGRESSION Continuous model Random model or episodic-burst model
  • 13. 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 Asynchronous, multiple-burst model
  • 14. Prevalence • Chronic periodontitis increases in prevalence and severity with age, generally affecting both genders equally. Periodontitis is an age-associated, not an age-related, disease. • In other words, it is not the age of the individual that causes the increase in disease prevalence, but rather the length of time that the periodontal tissues are challenged by chronic plaque accumulation
  • 15. RISK FACTORS FOR DISEASE Prior History of Periodontitis • A prior history of periodontitis puts patients at greater risk for developing further loss of attachment and bone
  • 16. Local Factors • Plaque accumulation on tooth and gingival surfaces at the dentogingival junction • Attachment and bone loss are associated with an increase in the proportion of gram-negative organisms • Porphyromonas gingivalis (formerly Bacteroides gingivalis), Tannerella forsythia (formerly Bacteroides forsythus), and Treponema denticola, otherwise known as the “red complex”
  • 17. • Plaque-retentive factors are important in the development and progression of chronic periodontitis because they retain plaque microorganisms in proximity to the periodontal tissues, providing an ecologic niche for plaque growth and maturation. • Calculus is considered the most important plaque-retentive factor because of its ability to retain and harbor plaque bacteria on its rough surface. As a result, calculus removal is essential for the maintenance of a healthy periodontium.
  • 18. Other factors are • Subgingival and overhanging margins of restorations; • Carious lesions that extend subgingivally • Furcations exposed by loss of attachment and bone; • Crowded and malaligned teeth • Root grooves and concavities
  • 19. Systemic Factors • Diabetes is a systemic condition that can increase the severity and extent of periodontal disease in an affected patient. • Type 2 diabetes is most likely to develop in an adult population at the same time as chronic periodontitis.
  • 20. • The synergistic effect of plaque accumulation and modulation of an effective host response through the effects of diabetes can lead to severe and extensive periodontal destruction that may be difficult to manage with standard clinical techniques without controlling the systemic condition
  • 21. Environmental and Behavioral Factors • Smoking has been shown to increase the severity and extent of periodontal disease smokers with chronic periodontitis have more attachment and bone loss, more furcation involvements, and deeper pockets
  • 22. • Emotional stress has previously been associated with necrotizing ulcerative disease, perhaps because of the effects of stress on immune function
  • 23. Genetic Factors • Periodontitis is considered to be a multifactorial disease in which the normal balance between microbial plaque and host response is disrupted • A genetic variation or polymorphism in the genes encoding interleukin-1α (IL-1α) and IL-1β is associated with an increased susceptibility to a more aggressive form of chronic periodontitis