Aggressive periodontitis

Aggressive periodontitis describes a type of periodontal disease and includes two of the seven classifications of periodontitis:

1. Localized aggressive periodontitis (LAP)
2. Generalized aggressive periodontitis (GAP)

Aggressive periodontitis is much less common than chronic periodontitis and generally affects younger patients than does the chronic form.

The localized and generalized forms are not merely different in extent; they differ in etiology and pathogenesis.

Aetiology

Microbiology:

Of the microflora characterised in aggressive periodontitis, approximately 65-75% of bacteria are Gram-negative bacilli, with few spirochaetes or motile rods present [1]. Aggressive periodontitis is often characterised by a rapid loss of periodontal attachment associated with highly pathogenic bacteria and an impaired immune response. Various studies have associated Aggregatibacter actinomycetemcomitans, formerly known as Actinobacillus actinomycetemcomitans, with aggressive periodontitis. An early study dating back to 1983 explains its prevalence and documents its role in localised aggressive periodontitis [2].

Virulence factors are the attributes of microorganism that enable it to colonise a particular niche in its host, overcome the host defences and initiate a disease process [6]. Fives Taylor et al. (2000) have categorised the virulence factors of Aggregatibacter actinomycetemcomitans as follows [6].

Promote colonization and persistence in the oral cavity:	Interfere with host defences:	Destroy host tissues:	Inhibit host repair of tissues:
Adhesins	Leukotoxin	Cytotoxins	Inhibitors of fibroblast proliferation
Invasins	Chemotactic inhibitors	Collagenase
Bacteriocins	Immunosuppressive proteins	Bone resorption agents	Inhibitors of bone formation
Antibiotic resistance	Fc-binding proteins	Stimulators of inflammatory mediators

Features

According to the 1999 International Workshop for the Classification of Periodontal Diseases, aggressive periodontitis was defined according to 3 primary features, in contrast to chronic periodontitis. These features are common for both localized and generalized form of disease. (1,2)

Primary features

• • Patients are clinically healthy.(1)

Patients do not have any underlying systemic disease that would contribute to aggressive periodontitis.(3) For instance, diabetes is proved to be associated with periodontitis- it is a major risk factor when glycaemic control is poor.(4)

• • The rate of loss of attachment and bone loss is rapid.(1)

Loss of attachment refers to the destruction of periodontium whereas the the bone refers to the alveolar bone supporting the teeth.(5) The loss can be determined by using a calibrated periodontal probe and taking radiographs of the dentition.(6) Usually the loss of attachment is greater than 2mm per year.

• • Aggressive periodontitis runs in the patient’s family.(1)

Familial aggregation of aggressive periodontitis is often discovered by taking a thorough medical history of the patient. The patient is said to have a high genetic susceptibility to aggressive periodontitis. Many studies have shown that genetic factors contribute to the pathogenesis of of this disease.(7) In this case, the manifestation of aggressive periodontitis is believed to be the result of genetic mutation, combined with environmental factors.(7)

Secondary features

Secondary features are characteristics which are frequently seen but not always present in every patient diagnosed with aggressive periodontitis.

• • The amount of bacteria is out of proportion to the severity of periodontal tissue destruction.(1)

The amount of bacteria is often indicated by the level of dental plaque.(8) This feature implies that when aggressive periodontitis is present, loss of attachment and bone loss tend to occur even if the plaque level is low.

• • High levels of Actinobacillus actinomycetemcomitans and, in some populations, Porphyromonas gingivalis.

These gram-negative microbes are considered the chief aetiological agent of aggressive periodontitis.(9) They are implicated in the development of aggressive periodontitis by triggering inflammatory response in periodontal tissue.

• • There are abnormalities associated with phagocytes.(1)

Phagocytes are essential in resolving inflammation. The impairment of the their phagocytic activity results in persistent inflammation in periodontal tissues.(10)

• • Hyper-responsive macrophage phenotype. (1)

Due to the increased responsiveness, the macrophages produce excessive levels of inflammatory mediator and cytokine, such as prostaglandin E2 (PGE2) and interleukin-1β (IL-1B).(1) Their hyperactivity is associated with periodontal tissue destruction and bone loss.(11)

• • Progression of attachment loss and bone loss may be self-arresting.(1)

In some patients, the disease may burnout without any cause-related therapy.(12)

Localized vs. generalized forms of aggressive periodontitis

The 1999 Consensus Report published by the American Academy of Periodontology permitted the subdivision of aggressive periodontal disease into localized and generalized forms based on enough individually specific features, as follows:

• Localized aggressive periodontitis
  • circumpubertal (around the time of puberty) onset
  • robust serum antibody response to infective agents: the dominant serotype antibody is IgG2
  • localized first molar/incisor presentation
  • Gingival inflammation, edematous, bleeding, pocketing
• Generalized aggressive periodontitis
  • usually affects patients under 30 years of age
  • poor serum antibody response to infective agents
  • pronounced episodic nature of periodontal destruction
  • generalized presentation affecting at least 3 permanent teeth other than first molars and incisors.
  • More bony destruction and more rapid than the LAP
  • Bleeding, deep pocketing (BPE 4), Periodontal abscess. No gingival inflammation

Severity of periodontal tissue destruction is subclassified in the same fashion as is chronic periodontitis.

Treatment

Treatment generally involves mechanical therapy (non-surgical or surgical debridement) in conjunction with antibiotics. Several studies suggest that these types of cases respond best to a combination of surgical debridement and antibiotics. Regenerative therapy with bone grafting procedures are often selected in these cases due to the favorable morphology of the bony defects which result from the disease.

Aggregatibacter actinomycetemcomitans (Aa) is one of the most efficient causative pathogens in this disease, Tetracycline seems affecting Aa better (250 mg 3 times daily for 2 weeks). However some suggests the use of Metronidazole 400 mg and Amoxicillin 250 mg 4 times daily for 1 week in severe cases. Root planing and maintaining good oral hygiene is required and Periodontal surgery to gain more access to the roots is needed occasionally.