Download aggressive periodontitis

AGGRESSIVE
PERIODONTITIS
LOGIEN AL GHAZAL
17/11/2015
General characteristics
•Generally affects systemically healthy individuals less than 30 years old.
•Aggressive periodontitis may be universally distinguished from
chronic periodontitis by the age of onset, the rapid rate of disease progression.
•The nature and composition of the associated subgingival microflora, alterations
in the host's immune response, and a familial aggregation of
•diseased individuals.
•Strong racial influence is observed (African).
The two subtypes are:
•Localized aggressive periodontitis:
localized juvenile periodontitis (LJP).
•Generalized aggressive periodontitis:
Generalized juvenile periodontitis (GJP) and
Rapidly progressive periodontitis (RPP)
LOCALIZED AGGRESSIVE PERIODONTITIS
Clinical Characteristics
•Localized aggressive periodontitis usually has an age of
onset around puberty.
•Clinically, it is characterized as having:
"localized first molar/incisor presentation with interproximal attachment
loss on at least two permanent teeth, one of which is a first molar, and
involving no more than two teeth other than first molars and incisors“
•The localized distribution of lesions in localized aggressive periodontitis is
characteristic
.
The following possible reasons for the limitation of periodontal destruction to
certain teeth have been suggested:
1. After initial colonization of the first permanent teeth to erupt (the first molars
and incisors), Actinobacillus actinomycetemcomitans evades the host defenses
by different mechanisms:
•Including production of polymorphonuclear leukocyte chemotaxis-inhibiting
factors
•endotoxin
•Collagenases
•leukotoxin
•Other factors allow the bacteria to colonize the pocket and initiate the
destruction of the periodontal tissues.
A strong antibody response to infecting agents is one characteristic
of localized aggressive periodontitis.
2. Bacteria antagonistic to A. actinomycetemcomitans may
colonize the periodontal tissues and inhibit A. actinomycetemcomitans
from further colonization of periodontal sites in the mouth.
This would localize A. actinomycetemcomitans infection and tissue
destruction.“
3. A. actinomycetemcomitans may lose its leukotoxin producing
ability for unknown reasons." If this happens, the progression of the disease
may become arrested or retarde
4. The possibility that a defect in cementum formation may be responsible for
the localization of the lesions.
Root surfaces of teeth extracted from patients with localized aggressive
periodontitis have been found to have hypoplastic or aplastic cementum.
Clinical Characteristics
•A striking feature of localized aggressive periodontitis is the lack of clinical
inflammation despite the presence of deep periodontal pockets.
•The amount of plaque on the affected teeth is minimal, which seems
inconsistent with the amount of periodontal destruction present.
•The quantity of plaque may be limited, it often contains elevated levels of A.
actinomycetemcomitans, and in some patients, Porphyromonas gingivalis.
•Progresses rapidly.
•Evidence suggests that the rate of bone loss is about three to four times
faster than in chronic periodontitis.
•Distolabial migration of the maxillary incisors with concomitant diastema
Formation.
Clinical Characteristics
•Increasing mobility of the first molars.
•Sensitivity of denuded root surfaces to thermal and tactile stimuli.
•Deep, dull, radiating pain during mastication, probably because of irritation
of the supporting structures by mobile teeth and impacted food.
•Periodontal abscesses may form at this stage, and regional lymph node
enlargement may occur.
•Not all cases of localized aggressive periodontitis progress to the degree
described previously.
•Some patients, the progression of attachment loss and bone loss may be
self-arresting.
Radiographic Findings
•Vertical loss of alveolar bone around the first molars and
incisors.
•Beginning around puberty in otherwise healthy teenagers, is a classic
diagnostic sign of localized aggressive periodontitis.
•Radiographic findings may include an "arc-shaped loss of alveolar bone
extending from the distal surface of the second premolar to the mesial surface
of the second molar""
Prevalence and Distribution
by Age and Sex
A clinical and radiographic study of 7266 English adolescents 15 to 19 years
old also showed a prevalence rate of 0.1%.
In the U.S., a national survey of adolescents age 14 to 17 reported that 0.53%
had localized aggressive periodontitis.
Gender: Blacks were at much higher risk for localized aggressive periodontitis.
Black males were 2.9 times more than females.
In contrast, white females were more likely to have localized aggressive
periodontitis than white males.
Age: puberty and 20 years of age.
GENERALIZED AGGRESSIVE
PERIODONTITIS
Clinical Characteristics
Generalized aggressive periodontitis usually affects individuals
under the age of 30, but older patients also may be affected.
Evidence suggests that individuals affected with generalized aggressive
periodontitis produce a poor antibody response to the pathogens present.
Characterized by:
"generalized interproximal attachment loss affecting at least three
permanent teeth other than first molars and incisors"
The destruction appears to occur episodically with periods of advanced
destruction followed by stages of quiescence of variable length (weeks to
months or years).
Radiographs often show bone loss that has progressed since the previous
Evaluation.
•Quantitatively, the amount of plaque seems inconsistent with the amount of
periodontal destruction.
•Qualitatively, P. gingivalis, A. actinomycetemcomitans, and Bacteriodes
forsythus frequently are detected in the plaque that is present.
Two gingival tissue responses can be found in cases of generalized
aggressive periodontitis:
1. One is a severe, acutely inflamed tissue, often proliferating, ulcerated,
and fiery red. ,bleeding may occur spontaneously or with slight stimulation.
Suppuration.
2. In other cases, the gingival tissues may appear pink, free of
inflammation, and occasionally with some degree of stippling, although
the last feature may be absent.
•Despite the apparently mild clinical gingival appearance, deep pockets
can be demonstrated by probing.
•Systemic manifestations such as weight loss, mental depression, and general
Malaise.
•Generalized aggressive periodontitis atients must have their medical
histories updated and reviewed.
Radiographic Findings
•The radiographic picture in generalized aggressive periodontitis can range
from severe bone loss associated with the minimal number of teeth.
•Advanced bone loss affecting the majority of teeth in the dentition
•A comparison of radiographs taken at different times illustrates the aggressive
nature of this disease.
•Despite the extreme bone loss at certain sites, other sites in the same
patient may show no bone loss.
Prevalence and Distribution by Age and Sex
•In a study of untreated periodontal disease conducted in Sri Lanka by Loe
and colleagues,36 8% of the population had rapid progression of periodontal
disease characterized by a yearly loss of attachment of 0.1 to 1.0 mm.
•In the U.S., a national survey of adolescents aged 14 to 17 reported that
0.13% had generalized aggressive periodontitis.
•In addition, blacks were at much higher risk than whites for all forms of
aggressive periodontitis and males were more likely to have generalized
aggressive periodontitis than females.
RISK FACTORS FOR AGGRESSIVE
PERIODONTITIS
1. Microbiologic Factors
Localized aggressive periodontitis (A. actinomycetemcomitans,
Capnocytophaga sp., Eikenella corrodens, Prevotella intertnedia, and
Campylobacter rectus).
A. actinomycetemcomitans has been implicated as the primary
pathogen associated with this disease.
Tonetti and Mombelli this link is based on the following evidence:
(1) A. actinomycetemcomitans is found in high frequency (approximately
90%) in lesions characteristic of localized aggressive periodontitis.
(2) Sites with evidence of disease progression often show elevated levels
of A. actinomycetemcomitans.
.
(3) many patients with the clinical manifestations of localized aggressive
periodontitis have significantly elevated serum antibody titers to
A. Actinomycetemcomitans
(4) clinical studies show a correlation between reduction in the subgingival
load of A. actinomycetemcomitans during treatment and a successful
clinical response.
(5) A. actinomycetemcomitans produces a number of virulence factors that
may contribute to the disease process.
•Another study found elevated levels of P. gingivalis, P. intermedia,
Fusobacterium nucleatum, C. rectus, and Treponema denticola.
•Electron microscopic studies of localized aggressive periodontitis have
revealed bacterial invasion of connective tissue.
2. Immunologic Factors
•The human leukocyte antigens (HLA), which regulate immune responses,
have been evaluated as candidate markers for aggressive periodontitis.
•Patients with aggressive periodontitis display functional defects of
polymorphonuclear leukocytes (PMNs), monocytes, or both.
•These defects can impair either the chemotactic attraction of PMN to the site
of infection or their ability to phagocytose and kill microorganisms.
•Hyperresponsiveness of monocytes from localized aggressive periodontitis
patients with respect to their production of PGE 2 in response to
lipopolysaccharide (LPS).
•This hyperresponsive phenotype could lead to increased connective tissue or
bone loss due to excessive production of these catabolic factors.
•Additionally, poorly functional inherited forms of monocyte FcyRII, the receptor
for human IgG2 antibodies, have been shown to be disproportionately present
in patients with localized aggressive periodontitis.
•These PMN and monocyte defects may be induced by the bacterial infection
or may be genetic in origin.
•Autoimmunity :
Host antibodies to collagen, DNA, and immunoglobulin G (IgG).
Possible immune mechanisms include an increase in the expression
of type II major histocompatibility complex (MHC) molecules,
HLA DR43 .
Altered helper or suppressor T-cell function, polyclonal activation of B
cells by microbial plaque, and genetic predisposition.
3. Environmental Factors
•The amount and duration of smoking are important variables that can
influence the extent of destruction seen in young adults .
•Patients with generalized aggressive periodontitis who smoke have more
affected teeth and more loss of clinical attachment than nonsmoking
patients with generalized aggressive periodontitis.
• Smoking may not have the same impact on attachment levels in younger
patients with localized aggressive periodontitis.
4. Genetic Factors
•All individuals are not equally susceptible to aggressive periodontitis.
•Familial pattern of alveolar bone loss and have implicated genetic factors in
aggressive periodontitis.
•Localized aggressive periodontitis suggest that a major gene plays a role in
this disease, which is transmitted through an autosomal dominant mode of
Inheritance.
•Familial clustering of the neutrophil abnormalities seen in localized
aggressive periodontitis.
•The antibody response to periodontal pathogens, particularly A.
actinomycetemcomitans, is under genetic control and that the ability to
mount high titers of specific, protective antibody (primarily IgG2) against
A. actinomycetemcomitans may be race dependent.
•Gene of major effect exists for aggressive periodontitis.