AGGRESSIVE PERIDONTITIS

Aggressive periodontitis (AP) is a destructive periodontal disease that occurs

early in life. Unlike chronic periodontitis, the disease progression rate is higher,
with different microbial etiology and distinctive clinical features.

Note
Aggressive periodontitis is defined based on the following primary features (Lang 1999)

 Rapid attachment loss and bone destruction.

 Familial aggregation of cases.
 Non-contributory medical history.

Secondary features that are generally considered but not universally present are:

 Amount of microflora inconsistent with the severity of periodontal destruction.

 Increased proportions of Aggregatibacter actinomycetemcomitans.
 Phagocyte abnormalities.
 Hyper-responsive macrophage phenotype (increased production of PGE2 and Interleukin-1β).
 Progression of attachment and bone loss may be self-arresting.

Classification
LOCALIZED AGGRESSIVE PERIODONTITIS (LAP)

 Circumpubertal onset
 Localized first molar/incisor involvement 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.
 Robust serum antibody response to infecting agents.

LAP was previously classified as Localized Juvenile Periodontitis (LJP).

GENERALIZED AGGRESSIVE PERIODONTITIS (GAP)

  Mostly involving persons under 30 years of age, but older patients may
also be affected.
 Generalized interproximal attachment loss affecting at least three
permanent teeth other than first molars and incisors.
 Pronounced episodic pattern of destruction of attachment and alveolar
bone.
 Poor serum antibody response to infecting agents.

GAP was previously classified as Generalized Juvenile Periodontitis (GJP) and

Rapidly Progressive Periodontitis (RPP).

(Based on International classification workshop 1999)

Clinical Features
LOCALIZED AGGRESSIVE PERIODONTITIS (LAP)

 Onset- at about puberty.

 Localized first molar/incisor presentation.
 Deep periodontal pockets and advanced bone loss with apparent lack of
clinical inflammation.
 Minimal plaque accumulation around the affected teeth.
 Distolabial migration of maxillary incisors leading to diastema formation.
 Increased mobility of incisors and first molars.
 Sensitivity due to the denuded root surfaces.
 Dull pain during mastication
 Periodontal abscess may be seen occasionally with regional lymph node
enlargement.
 The rate of disease progression is 3 to 4 times faster than in chronic
periodontitis.

GENERALIZED AGGRESSIVE PERIODONTITIS (GAP)

 Mostly affects individuals under 30 years of age.

 Destruction occurs in an episodic pattern with alternate periods of
exacerbation and quiescence.
  Involved teeth have little plaque accumulation around them.
 Deep periodontal pockets, advanced bone loss along with bleeding
and suppuration in affected teeth. Yearly attachment loss of 0.1 to 1
mm is seen.
 Generalized tooth mobility.

PREVALENCE

 Less than 1%.

 More prevalent in black males followed by black females, white females
and white males.

Microbial Factors
 Aggregatibactor actinomycetemcomitans (A.a -->JP-2 clone) was isolated
in periodontal lesions from more than 90% of LAP patients.
 Other dominant microbes are: Capnocytophaga sp., Eikenella corrodens,
Prevotella sp., Campylobacter rectus.

Note
 Tonetti and Mombelli in 1999 based on the following evidences, claimed A.a. to be the
principal pathogen in the etiology of AgP.
 A.a. is found in high frequency (90%) in LAP lesions.
 Active disease progression sites have shown elevated levels of A.a.
 LAP patients have significantly elevated serum antibody titers to A.a.
 A positive correlation is observed between the reduction in the subgingival load of A.a. and
improvement in the clinical parameters.
 A.a. produces numerous virulence factors, that contribute towards the disease progression.

Virulence factors - Aggregatibactor

Actinomycetemcomitans
Leukotoxin Destroys PMNs and macrophages
Endotoxin Activates host cells to produce inflammatory mediators
Bacteriocin Inhibit growth of beneficiary bacteria
Collagenases Degrades host tissue collagen
Immunosuppressive Inhibit antibody production
factors

Radiographic Features
LOCALIZED AGGRESSIVE PERIODONTITIS (LAP)

 Vertical bone loss around first molars and incisors.

 Arc-shaped bone loss extending from distal surface of the second premolar
to the mesial surface of second molar.
 Bone defects are wider than those seen in chronic periodontitis.
 The bony defects are similar on left and right regions – ‘mirror image
pattern’.

GENERALIZED AGGRESSIVE PERIODONTITIS (GAP)

 Generalized horizontal pattern of bone loss.

Other risk factors for Aggressive Peridontitis

IMMUNOLOGIC FACTORS

 Human leukocyte antigens (HLA) A9 and B 15 are associated with AgP.

 Functional defects of PMNs and macrophages.
 Hyperresponsive macrophages producing increased PGE2, causing
increased connective tissue destruction.
 Autoimmunity- increased expression of MHC Class II molecules, altered
helper or suppressor T-cell function.

ENVIRONMENTAL FACTORS

 Smoking
Treatment
 Control of the infection and arresting the disease progression by means of
SRP or surgical periodontal therapy (either respective or regenerative).
 Adjunctive antibiotic therapy.
 Correction of anatomic defects.
 Patient motivation and frequent recall visits.