- Aggressive periodontitis generally affects systemically healthy individuals under 30 years old and is distinguished from chronic periodontitis by its earlier age of onset, rapid progression, microbial flora, and familial aggregation. - Localized aggressive periodontitis (LAP) clinically presents as localized bone loss around first molars and incisors beginning at puberty with minimal inflammation. Generalized aggressive periodontitis (GAP) presents as generalized interproximal attachment loss affecting at least three teeth. - Both LAP and GAP are associated with small amounts of bacterial plaque containing pathogens like Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans. Genetic and

2. Prof Dr. Eman Abd El-Sattar Tella.

3. 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.

5. 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".

7. 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.

8. - 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.

10. 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“.

11. 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.

13. 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.

15. 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.

17. 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.

19. 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:

20. 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.

21. 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.

22. 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.

23. 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.

24. 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.