AGGRESSIVE PERIODONTITIS

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 AGGRESSIVE PERIODONTITIS
LOCALIZED AGGRESSIVE PERIODONTITIS
 Historical Background
 Clinical Characteristics
 Radiographic Findings

GENERALIZED AGGRESSIVE PERIODONTITIS

 Clinical Characteristics
 Radiographic Findings
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 affects
systemically 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
Historical Background
In 1923, Gottlieb“ called diffuse atrophy o f the alveolar bone and
deep cementopathia
In 1938, Wannenmacher described incisor-first molar involvement
and called the disease parodontitis marginalis progressiva
In 1966 the World Workshop in Periodontics concluded that the
concept of periodontosis as a degenerative entity was
unsubstantiated and that the term should be eliminated from
periodontal nomenclature.

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 LOCALIZED AGGRESSIVE
PERIODONTITIS
• The term juvenile periodontitis was introduced by
Chaput and colleagues in 1967 and by Butler' in
1969.
• In 1971, Baer' defined it as "a disease of the
periodontium occurring in an otherwise healthy
adolescent which is characterized by a rapid loss
of alveolar bone about more than one tooth of
the permanent dentition.
• The amount of destruction manifested is not
commensurate with the amount of local
irritants."

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 LOCALIZED AGGRESSIVE
PERIODONTITIS
• In 1989 the World Workshop in Clinical
Periodontics 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 primary
importance when making a diagnosis of LJP
• Most recently, disease with the characteristics of
LJP 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 & FIRST MOLARS

• 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 & FIRST MOLARS

• 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,
• production of polymorphonuclear leukocyte
chemotaxis-inhibiting factors,
• endotoxin,
• collagenases,
• leukotoxin,

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 WHY INCISORS & FIRST MOLARS

These factors allow the bacteria to colonize the

pocket and initiate the destruction of the periodontal
tissues.
After this initial attack, adequate immune defenses are
stimulated to produce opsonic antibodies to enhance
the clearance and phagocytosis of invading bacteria
and neutralize leukotoxic activity.
In this manner, colonization of other sites may be
prevented.
 A strong antibody response to infecting agents is one
characteristic of localized aggressive periodontitis.

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 WHY INCISORS & FIRST MOLARS

• 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."

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 WHY INCISORS & FIRST MOLARS

• 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 & FIRST MOLARS

• 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 exposed
to 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 of A.
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 aggressive
periodontitis may include
• Distolabial migration of the maxillary incisors
with concomitant diastema formation .
• Increasing mobility of the first molars,
• Sensitivity of denuded root surfaces to thermal
and tactile stimuli, and
• Deep, dull, radiating pain during mastication,
probably because of irritation of the supporting
structures 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 from
the 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, but older
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 evaluation
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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 periodontal
destruction.
• Qualitatively, P. gingivalis, A. actinomycetemcomitans,
and Bacteriodes forsythus frequently are detected in
the plaque that is present.
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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, often
proliferating, 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
actively lost.
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 GENERALIZED AGGRESSIVE
PERIODONTITIS
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
However, despite the apparently mild clinical appearance,
deep pockets can be demonstrated by probing.
This tissue response coincide with periods of quiescence
in which the bone level remains stationary.
Some patients with generalized aggressive periodontitis
may have systemic manifestations such as weight loss,
mental depression, and general malaise

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 GENERALIZED AGGRESSIVE
PERIODONTITIS
• Patients with a presumptive diagnosis of generalized
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 spontaneously or after therapy, whereas
others may continue to progress inexorably to tooth
loss despite intervention with conventional treatment
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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 the
same 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
Microbiologic Factors
Although several specific microorganisms frequently are
detected in patients with 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.

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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 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,
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 RISK FACTORS FOR AGGRESSIVE
PERIODONTITIS
(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, and
(5) A. actinomycetemcomitans produces a number of
virulence factors that may contribute to the disease
process
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 IMMUNOLOGIC FACTORS
• Some immune defects have been implicated in
the pathogenesis of aggressive periodontitis.
• The human leukocyte antigens (HLA), which
regulate 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 patients with respect to their production
of PGE 2 in response to lipopolysaccharide (LPS).

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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 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.
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 Autoimmunity
Autoimmunity has been considered to have a role in
generalized aggressive periodontitis ,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.

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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 a role in this disease, which is transmitted
through an autosomal dominant mode of inheritance
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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
generalized aggressive periodontitis.
• However, smoking may not have the same impact on
attachment levels in younger patients with localized
aggressive periodontitis.
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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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Localized juvenile periodontitis in a 16-year-old male.
Maxillary and mandibular incisors have severe bone
loss causing them to spread.

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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

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