Prof Dr. Eman Abd El-Sattar Tella.

Aggressive periodontitis generally affects systemically

healthy individuals less than 30 years old although patients
may be older.
Aggressive periodontitis may be distinguished from chronic
periodontitis by the age of onset, the rapid rate of disease
progression, the nature and composition of the subgingival
microflora, alterations in the host's immune response and a
familial aggregation of diseased individuals.
 LOCALIZED AGGRESSIVE
PERIODONTITIS

Clinical Characteristics

Localized aggressive periodontitis (LAP) 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".
A striking feature of LAP is the lack of clinical
inflammation despite the presence of deep

periodontal pockets. Furthermore, the amount of plaque

on the affected teeth is minimal and 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. 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.
- Other clinical features of LAP may include:
* Distolabial migration of maxillary incisors with
diastema formation.
* Increasing mobility of first molars.
* Sensitivity of denuded root surfaces to thermal and
tactile stimuli.
* Deep dull radiating pain during mastication
because of irritation of the supporting structures by
mobile teeth and impacted food.
* Periodontal abscesses.
* Regional lymph node enlargement.
Radiographic Findings:
Vertical loss of alveolar bone around the first molars and
incisors, beginning around puberty in healthy
teenagers,
is a classic diagnostic sign of LAP.
Radiographic findings may include an "arc-shaped loss
of alveolar bone extending from distal surface of second
premolar to mesial surface of second molar“.
 GENERALIZED AGGRESSIVE
PERIODONTITIS
Clinical Characteristics
Generalized aggressive periodontitis (GAP) usually affects individuals
under the age of 30 but older patients also may be affected.
Clinically, GAP is characterized by "generalized interproxirnal
attachment loss affecting at least three permanent teeth other than
first molars and incisors".
- As seen in LAP, patients with GAP have small amounts of bacterial
plague associated with
the affected teeth. Quantitatively, the amount of plaque seems
inconsistent with the amount of periodontal destruction.
Qualitatively, Porphyromonas gingivalis. A. actinomycetem-
comitans and Bacteroides forsythus frequently are detected in the
plaque that is present. In contrast to LAP, individuals affected with
GAP produce a poor antibody response to the pathogens present.
The destruction occurs episodically with periods of
advanced destruction followed by stages of
quiescence of variable length (weeks to months or
years). Radiographs show bone loss that has
progressed since the previous evaluation.
In cases of GAP, the gingival tissue response 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 occurs in the destructive stage in
which attachment and bone are actively lost.
In other cases, the gingival tissues may appear pink, free
of inflammation. However, deep pockets can be
demonstrated by probing. This tissue response coincide
with periods of quiescence in which the bone level
remains stationary.
In other cases, the gingival tissues may appear pink,
free of inflammation. However, 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 GAP may have systemic
manifestations such as weight loss, mental depression
and general malaise. They should receive medical
evaluations to rule out possible systemic involvement.
 The radiographic picture in GAP range from
severe bone loss associated with minimal number
of teeth to advanced bone loss affecting the
majority of teeth in the dentition.

Sites in GAP patients demonstrated osseous

destruction of 25 to 60 % during a 9-week period.
Despite this extreme loss, other sites in the same
patient showed no bone loss.
 RISK FACTORS FOR AGGRESSIVE
PERIODONTITIS

Microbiologic Factors
- Although several specific microorganisms are
detected in patients with LAP (A
actinomycetemcomitans (A. a.), Capnocytophaga sp.
Eikenella corrodens, Prevotella intermedia and
Campyiobacter rectus), A. a. is implicated as the primary
pathogen associated with this disease is based on the
following evidence:
1- High frequency of A. a. (approximately 90%) in
lesions characteristic of LAP.
2- Elevated levels of A. a. were showed in sites
with evidence of disease progression.
3- Elevated serum antibody titers to A.
actinomvcetemcomitans is showed in many
patients with LAP.
4- A correlation between reduction in the
subgingival load of A. a. during treatment and
a» successful clinical response.
5- A. a. produces a number of virulence factors
that may contribute to the disease process.
Immunologic Factors:
Some immune defects are implicated in the pathogenesis
of aggressive periodontitis.
The human leukocyte antigens (HLA), which regulate
immune responses, were evaluated as markers for
aggressive periodontitis. HLA-A9 and B15 antigens are
consistently associated with aggressive periodontitis.
Patients with aggressive periodontitis display functional
defects of PMNs which can impair either the chemotactic
attraction of PMN to the site of infection or their ability to
phagocytose and kill microorganisms.
Genetic Factors
- All individuals are not equally susceptible to
aggressive periodontitis. A familial pattern of
alveolar bone loss have implicated genetic factors
in aggressive periodontitis.
- Genetic predisposition for LAP suggest that a major
gene plays a role in this disease, which is
transmitted through an autosomal dominant mode
of inheritance.
Environmental Factors
- The amount and duration of smoking can influence
the extent of destruction seen in young adults.
 TREATMENT OF AGGRESSIVE
PERIODONTITIS

Localized Aggressive Periodontitis

- Standard periodontal therapy:
Such therapy has included scaling and root planing, flap surgery
with and without bone grafts, root amputations, hemisections,
occlusal adjustment and strict plaque control. However, response
was unpredictable. Frequent maintenance visits appear to be most
important.
Lack of response of aggressive periodontitis to local therapy alone
is the result of the presence of A. actinomycetemcomitans in the
tissues where it remains after therapy to reinfect the pocket.
Systemic use of antibiotics eliminates bacteria from the tissues.
 Current Approach to Therapy. Patients who are diagnosed
as having an early form of aggressive periodontitis may
respond to standard periodontal therapy. In almost all
cases, systemic tetracycline (250 mg of tetracycline 4 times
daily for at least 1 week) should be given in conjunction with
local mechanical therapy. If surgery is indicated, systemic
tetracycline should be taken approximately 1 hour before
surgery. Doxycycline 100 mg/day may also be used.
Chlorhexidine rinses should also be prescribed and
continued for several weeks to aid healing and augment
plaque control.
In refractory localized aggressive periodontitis cases,
tetracycline- esistant Actinobacilfus species have been
suspected. After performing antibiotic susceptibility tests,
the clinician may consider a combination of amoxicillin and
metronidazole.