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AGGRESSIVE PERIODONTITIS
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AGGRESSIVE PERIODONTITIS
y LOCALIZED AGGRESSIVE PERIODONTITIS
Historical Background
Clinical Characteristics
Radiographic Findings
y GENERALIZED AGGRESSIVE PERIODONTITIS
Clinical Characteristics
Radiographic Findings
y RISK FACTORS FOR AGGRESSIVE PERIODONTITIS
Microbiologic Factors Immunologic Factors
Genetic Factors
Environmental Factors
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AGGRESSIVE vs CHRONIC
The rapid rate of disease progression,
The nature and composition of the associated
subgingival microflora, Alterations in the host's immune response,
Familial aggregation of diseased individuals.
Aggressive periodontitis generally affectssystemically healthy individuals less than 30
years old, although patients may be older.
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AGGRESSIVE PERIODONTITIS
Aggressive periodontitis describes three of the
diseases formerly classified as early onset
periodontitis.
LJP
GJP
RPP
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AGGRESSIVE PERIODONTITIS
Localized aggressive periodontitis was
formerly classified as localized juvenile
periodontitis (LJP).
Generalized aggressive periodontitis
encompasses the diseases previously
classified as
Generalized juvenile periodontitis (GJP)
Rapidly progressive periodontitis (RPP)
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LOCALIZED AGGRESSIVE PERIODONTITIS
y Historical Background
y In 1923, Gottlieb called diffuse atrophy o f the alveolar bone anddeep cementopathia
y In 1938, Wannenmacher described incisor-first molar involvement
and called the diseaseparodontitis marginalis progressivay In 1966 the World Workshop in Periodontics concluded that the
concept of periodontosis as a degenerative entity wasunsubstantiated and that the term should be eliminated fromperiodontal nomenclature.
y
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LOCALIZED AGGRESSIVE
PERIODONTITIS The termjuvenile periodontitis was introduced byChaputand colleagues in 1967 and by Butler' in1969.
In 1971, Baer' defined it as "a disease of theperiodontium occurring in an otherwise healthyadolescent which is characterized by a rapid lossof alveolar bone about more than one tooth ofthe permanent dentition.
The amount of destruction manifested is notcommensurate with the amount of localirritants."
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LOCALIZED AGGRESSIVE
PERIODONTITIS In 1989 the World Workshop in ClinicalPeriodontics categorized this disease as localized
juvenile periodontitis (LJP), a subset of the broad
classification of early onset periodontitis (EOP). Under this classification system, age of onset and
distribution of lesions were of primaryimportance when making a diagnosis of LJP
Most recently, disease with the characteristics ofLJP has been renamed localized aggressive
periodontitis.
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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 .
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WHY INCISORS & FIRSTMOLARS
The localized distribution of lesions in
localized aggressive periodontitis is
characteristic but as yet unexplained.
The following possible reasons for the
limitation of periodontal destruction to certain
teeth have been suggested:
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WHY INCISORS & FIRSTMOLARS
1. After initial colonization of the first permanentteeth to erupt (the first molars and incisors),Actinobacillus actinomycetemcomitans evades
the host defenses by differentmechanisms, production of polymorphonuclear leukocyte
chemotaxis-inhibiting factors,
endotoxin,
collagenases,
leukotoxin,
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WHY INCISORS & FIRSTMOLARS
y These factors allow the bacteria to colonize the pocketand initiate the destruction of the periodontal tissues.
y After this initial attack, adequate immune defenses are
stimulated to produce opsonic antibodies to enhancethe clearance and phagocytosis of invading bacteria andneutralize leukotoxic activity.
y In this manner, colonization of other sites may beprevented.
y A strong antibody response to infecting agents is onecharacteristic of localized aggressive periodontitis.
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WHY INCISORS & FIRSTMOLARS
2. Bacteria antagonistic to A.
actinomycetemcomitans maycolonize 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."
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WHY INCISORS & FIRSTMOLARS
3.A. actinomycetemcomitans may lose its
leukotoxin producing ability for unknown
reasons.
If this happens, the progression of the disease
may become arrested or retarded and
colonization of new periodontal sites averted.
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WHY INCISORS & FIRSTMOLARS
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.
This was true not only of root surfaces exposedto periodontal pockets but also of roots still
surrounded by their periodontium.
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CLINICAL CHARACTERISTICS
A striking feature of localized aggressive
periodontitis is the lack of clinical inflammation
despite the presence of deep periodontal pockets
Furthermore, in many cases the amount of
plaque on the affected teeth is minimal, which
seems inconsistent with the amount of
periodontal destruction present . The plaque that is present forms a thin biofilm on
the teeth and rarely mineralizes to form calculus."
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CLINICAL CHARACTERISTICS
Although the quantity of plaque may be
limited, it often contains elevated levels ofA.
actinomycetemcomitans, and in some
patients, Porphyromonas gingivalis.
Localized aggressive periodontitis progresses
rapidly.
The rate of bone loss is about three to four
times faster than in chronic periodontitis.
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CLINICAL CHARACTERISTICS
Other clinical features of localized aggressiveperiodontitis may include
Distolabial migration of the maxillary incisors
with concomitant diastema formation . Increasing mobility of the first molars,
Sensitivity of denuded root surfaces to thermaland tactile stimuli, and
Deep, dull, radiating pain during mastication,probably because of irritation of the supportingstructures by mobile teeth and impacted food.
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CLINICAL CHARACTERISTICS
Periodontal abscesses may form at this stage,
and regional lymph node enlargement may
occur.
It should be noted that not all cases of
localized aggressive periodontitis progress to
the degree described previously.
In some patients, the progression of
attachment loss and bone loss may be self-
arresting.
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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 fromthe distal surface of the second premolar to
the mesial surface of the second molar
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GENERALIZED AGGRESSIVE
PERIODONTITIS
Clinical Characteristics
Generalized aggressive periodontitis usually
affects individuals under the age of 30, butolder patients also may be affected.
In contrast to localized aggressive
periodontitis, evidence suggests that
individuals affected with generalized
aggressive periodontitis produce a poor
antibody response to the pathogens present.
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GENERALIZED AGGRESSIVE
PERIODONTITIS
Clinically it is 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 evaluation22
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GENERALIZED AGGRESSIVE
PERIODONTITIS
As seen in localized aggressive periodontitis,
patients with generalized aggressive
periodontitis often have small amounts of
bacterial plaque associated with the affected
teeth .
Quantitatively, the amount of plaque seems
inconsistent with the amount of periodontaldestruction.
Qualitatively, P. gingivalis, A.
actinomycetemcomitans, and Bacteriodes23
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GENERALIZED AGGRESSIVE
PERIODONTITIS
Two gingival tissue responses can be found in
cases of generalized aggressive periodontitis.
One is a severe, acutely inflamed tissue, oftenproliferating, ulcerated, and fiery red
Bleeding may occur spontaneously or with
slight stimulation.
Suppuration may be an important feature.
This tissue response is considered to occur in
the destructive stage, in which attachment
and bone are activel lost.24
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GENERALIZED AGGRESSIVE
PERIODONTITIS
y 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
yHowever, despite the apparently mild clinical
appearance, deep pockets can be demonstrated
by probing.y This tissue response coincide with periods of
quiescence in which the bone level remains
stationary.
y Some atients with eneralized a ressive25
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GENERALIZED AGGRESSIVE
PERIODONTITIS Patients with a presumptive diagnosis ofgeneralized aggressive periodontitis must
have their medical histories updated and
reviewed.
These patients should receive medical
evaluations to rule out possible systemic
involvement.
As seen with localized aggressive
periodontitis, cases of generalized aggressive
periodontitis may be arrested spontaneously26
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RADIOGRAPHOC FINDINGS
The radiographic picture in generalized
aggressive periodontitis can range from severe
bone loss associated with the minimal number
of teeth, as described previously, to advanced
bone loss affecting the majority of teeth in the
dentition
Despite this extreme loss, other sites in thesame patient showed no bone loss.
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RISK FACTORS FOR AGGRESSIVE
PERIODONTITIS
MICROBIOLOGICAL FACTORS
IMMUNOLOGICAL FACTORS
GENETIC FACTORS ENVIRONMENTAL FACTORS
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RISK FACTORS FOR AGGRESSIVE
PERIODONTITIS
yMicrobiologic Factors
yAlthough several specific microorganisms
frequently are detected in patients with localized
aggressive periodontitis
y A. actinomycetemcomitans,
y Capnocytophaga sp.,
y Eikenella corrodens,y Prevotella intertnedia, and
y Campylobacter rectus),
yA. actinomycetemcomitans has been implicated as
the rimar atho en associated with this29
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RISK FACTORS FOR AGGRESSIVE
PERIODONTITIS
As summarized by Tonetti and Mombelli, this
link is based on the following evidence:
(1)A. actinomycetemcomitans is foundin highfrequency (approximately 90%) in lesions
characteristic of localized aggressive
periodontitis,
(2) sites with evidence of disease progression
often show elevated levels ofA.
actinomycetemcomitans,
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RISK FACTORS FOR AGGRESSIVE
PERIODONTITIS
y (3) many patients with the clinicalmanifestations of localized aggressiveperiodontitis have significantly elevated serum
antibody titers to A. actinomycetemcomitans,y (4) clinical studies show a correlation between
reduction in the subgingival load ofA.actinomycetemcomitans during treatment anda successfulclinical response, and
y (5)A. actinomycetemcomitans produces anumber of virulence factors that may
contribute to the disease process31
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IMMUNOLOGIC FACTORS
Some immune defects have been implicated in
the pathogenesis of aggressive periodontitis.
The human leukocyte antigens (HLA), whichregulate immune responses, have been
evaluated as candidate markers for aggressive
periodontitis.
HLA-A9 and B15 antigens are consistently
associated with aggressive periodontitis
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IMMUNOLOGIC FACTORS
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.
Current studies have also demonstrated a
hyper responsiveness of monocytes from
localized aggressive periodontitis patients33
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IMMUNOLOGIC FACTORS
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 bedisproportionately present in patients with
localized aggressive periodontitis.
These PMN and monocyte defects may be34
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Autoimmunity
yAutoimmunity has been considered to have a role
in generalized aggressive periodontitis ,antibodies
to collagen, DNA, and immunoglobulin G (IgG).
y Possible immune mechanisms include
yAn increase in the expression of type II major
histocompatibility complex (MHC) molecules, HLA
DR43 ,yAltered helper or suppressor T-cell function,
y Polyclonal activation of B cells by microbial
plaque, and 35
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Genetic Factors
Results from several studies support the
concept that all individuals are not equally
susceptible to aggressive periodontitis
Currently, specific genes have not been
identified that are responsible for these
diseases.
However, segregational analyses and linkage
analyses of families with a genetic
predisposition for localized aggressive
periodontitis suggest that a major gene plays a36
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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 generalizedaggressive periodontitis.
However, smoking may not have the same
impact on attachment levels in younger37
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Palmar and plantar hyperkeratosis associated
with Papillon-Lefevre syndrome.
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Radiograph of patient with Papillon-
Lefevre syndrome
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Patient with Papillon-Lefevre
syndrome
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Probe extends deep into pocket on mesial of
molar. Gingiva is healthy looking(LJP)
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Radiograph demonstrating deep localized circumferential bone
loss on first molar in 18-year-old.
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Radiograph showing semilunar bone defect on
mesial of first molar in a patient with LJP
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Rapidly progressive adult periodontitis in
a 28-year-old
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Rapidly progressive adult periodontitis in a 28-year-
old female, pocket depth recordings.
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Rapidly progressive adult periodontitis in
a 28-year-old female, radiographs
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Rapidly progressive adult periodontitis in a
29-year-old
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Rapidly progressive adult periodontitis in a 29-year-
old female.
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Prepubertal periodontitis: 13-year-old boy
with agranulocytosis.
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Prepubertal periodontitis: 13-year-old
boy with agranulocytosis
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Prepubertal periodontitis: 10-year-old boy with
S cyclic neutropenia.
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Prepubertal periodontitis: 10-year-old boy with
agammaglobulinemia and cyclic neutropenia.
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LJP IN 19 YR OLD
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LJP IN 19 YR OLD
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LJP IN 19 YR OLD
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Radiograph of a case of juvenile periodontitis
showing typical molar-incisor lesions.
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Lingual view of the left mandibular molar are in a
patient with juvenile periodontitis.
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Lingual view of the left mandibular molar are in a patient with
juvenile periodontitis., after flap elevation
9