Chronic Periodontitis
Chronic periodontitis occurs most frequently in adults. Also known as adult
periodontitis or chronic adult periodontitis.
Systemic inflammatory markers, such as the C-reactive protein (CRP), are
elevated in patients with periodontitis.
“An infectious disease resulting in inflammation within the supporting
tissues of the teeth, progressive attachment loss, and bone loss.
Clinical and etiological factors: (1) microbial biofilm formation (dental
plaque), (2) periodontal inflammation (gingival swelling, bleeding on probing),
and (3) attachment as well as alveolar bone loss.
Clinical Features General Characteristics
Characteristic clinical findings in patients with untreated chronic periodontitis
include the following symptoms: • Supra-gingival and subgingival plaque (and
calculus) • Gingival swelling, redness, and loss of gingival stippling • Altered
gingival margins (rolled, flattened, cratered papillae, recessions) • Pocket
formation • Bleeding on probing • Attachment loss • Bone loss
(angular/vertical or horizontal) • Root furcation involvement • Increased
tooth mobility • Change in tooth position • Tooth loss
Can be clinically revealed by means of periodontal screening and recording
(PSR), diagnosed by an assessment of the clinical attachment level, and there
with the detection of inflammatory changes in the marginal gingiva.
Measurements of periodontal probing pocket depth in combination with the
location of the marginal gingiva.
Dental radiographs reveal the extent of bone loss indicated by the distance
between the cemento-enamel-junction and the alveolar bone crest
Aggressive and chronic periodontitis may be differentiated by the rate of
disease progression over time, familial nature of aggressive disease, and
presence of local as well as systemic factors.
Classification
Chronic periodontitis can be classified into the following categories:
• Localized chronic periodontitis, meaning that less than 30% of the teeth show
attachment and bone loss • Generalized chronic periodontitis, meaning that 30%
or more of the teeth show attachment and bone loss.
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 intra-bony pocket formation,
horizontal bone loss is usually associated with supra-bony (supra-alveolar)
pockets.
Disease Severity
If untreated and oral hygiene behaviors remain unchanged, chronic
periodontitis eventually leads to tooth loss and may negatively impact distant
organs by the uncontrolled progression of periodontal inflammation and by
the systemic spread of infection.
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Relative to the degree of attachment and bone loss, disease severity can be
described as: Mild chronic periodontitis: clinical attachment loss of 1 to 2 mm
• Moderate chronic periodontitis: clinical attachment loss of 3 to 4 mm. •
Severe chronic periodontitis: clinical attachment loss of 5 mm or more.
Symptoms
Chronic periodontitis is commonly a slowly progressing complex disease
without a pain experience.
Gingival bleeding during oral hygiene procedures or eating may be the first
sign of disease occurrence. Areas with advanced periodontal inflammation
may present with purulence emanating from the periodontal pocket.
Due to gingival recession, patients may notice black triangles between teeth
or tooth sensitivity in response to temperature changes (cold and heat). Food
impaction may occur in the space of interdental triangles, leading to
increased discomfort and bad breath. Rarely tooth loss may occur.
In cases with advanced disease progression, areas of localized dull pain or
pain sensations radiating to other areas of the mouth or head may occur.
Disease Progression
In general, the progression rate of chronic periodontitis is slow, so that
symptoms of the disease appear around the age of 40 or later in life.
Onset and the rate of disease progression, however, may be influenced by a
number of modifiable (e.g., smoking, diet) and non-modifiable (e.g., genetic
disorders and risk issues) factors.
Interproximal sites, in general, are more prone to periodontal destruction,
compared to buccal/facial sites.
Plaque control becomes more difficult, and interproximal furcation areas,
interproximal caries, root caries, overhanging restoration margins, and tooth
crowding may further promote interproximal attachment loss.
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The continuous model: Describes slow and continuous disease progression
and suggests that sites exhibit a constant progression rate of attachment loss
throughout the duration of the disease.
The random or episodic-burst model: Describes the episodic occurrence of
short progressive bursts of periodontal destruction followed by periods of
stagnation. Sites, teeth, and the chronology of bursts and stagnation are
subject to random effects.
The asynchronous, multiple-burst model: Describes the occurrence of
periodontal destruction (bursts) during defined periods, which are
asynchronously interrupted by periods of stagnation or remission for
individual sites and teeth.
The prevalence and severity of the disease increases with age equally in both
genders. In general, 40% of patient ≥50 years old and almost 50% of patient
≥65 years old show signs of mild to moderate periodontal destruction. From
11% to 30% of patients develop severe periodontitis at the age of 40 years or
older
Risk Factors for Disease
Microbiologic Aspects: Plaque accumulation on tooth and gingival surfaces
(dental biofilm formation) at the dento-gingival junction is considered the
primary and most common etiology of gingivitis and chronic periodontitis.
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. P. gingivalis as a
poly-microbial synergistic effect.
There is a symbiotic relation between mirobes and host as microbes increase
this relation changes to dysbiotic and result in host response causing
inflammation and disease progression if not treated early.
Local factors: Factors that facilitate plaque accumulation or prevent plaque
removal by oral hygiene procedures can be detrimental to the patient.
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Calculus is considered the most important plaque-retentive factor because of
its ability to retain and harbor plaque bacteria on its rough surface as well as
inside.
Systemic Factors: Haim–Munk syndrome, Papillon–Lefèvre syndrome,
Ehlers–Danlos syndrome, Kindler syndrome, and Cohen syndrome,HIV/AIDS
may also show periodontal destruction, osteoporosis, severe unbalanced diet,
and stress, as well as dermatologic, hematologic, and neoplastic factors,
diabetes mellitus, cardiovascular disorders, stroke, and lung disorders,an
increased body weight (obesity).
Genetic factors: Papillon–Lefèvre syndrome is a well-known genetic disorder
(a defect on chromosome 11) that exhibits not only palmoplantar
hyperkeratosis but also severe periodontitis. Haim–Munk syndrome, Ehlers–
Danlos syndrome, Down syndrome, Kindler syndrome, Cohen syndrome, and
congenital neutropenia (Kostmann syndrome) are other genetic disorders that
have been related to periodontal disease.
Environmental and Behavioral Factors: Smoking is a major risk factor for
the development and progression of generalized chronic periodontitis.
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
Psychological factors, such as stress and depression, also negatively influence
the progression of chronic periodontitis. Patients with periodontitis often
report the experience of family- or work-related stress. Positive correlations
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between cortisol levels and periodontal indices (plaque index, gingival index),
bone loss, and missing teeth were recorded.
In addition, stress as an etiologic factor was even strongly associated with
periodontitis when patients were smokers compared to nonsmokers.
Immunologic Factors: In periodontal lesions, MMPs contribute to soft and
hard tissue degradation during active inflammatory processes. RANKL binds to
its receptor RANK on the cell surface of premature osteoclasts, and it initiates
osteoclast differentiation leading to degradation of alveolar bone.
Osteoprotegerin (OPG) is an inhibitor of RANKL, and during periodontitis, an
imbalance between OPG and RANKL promotes further bone degradation.
Reduced counts in neutrophils (polymorphonuclear neutrophils [PMNs])
inluence the degree of periodontal inflammation. Congenital neutropenia
(Kostmann syndrome) leads not only to an increased susceptibility to infection
in general, but also to severe chronic periodontitis.
Patients with Kostmann syndrome show reduced levels of antimicrobial
peptides, such as the cathelicidin (LL-37) and neutrophil peptides (alpha
defensins), which impair their innate immune response.
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