Aggressive Periodontitis Question And Answers

Aggressive Periodontitis

According to the recent classification of periodontitis [International Workshop for the Classification of the Periodontal Diseases organized by the American Academy of Periodontology (AAP) in 1999], the term aggressive periodontitis is used to denote the early onset periodontitis (prepubertal, juvenile, and rapidly progressing periodontitis).

Question 1: Define aggressive periodontitis. Describe the etiopathogenesis and risk factors associated with it.
Answer:

Aggressive periodontitis encompasses distinct types of periodontitis that affect people, who, in most cases, otherwise appear healthy.

• It tends to have a familial aggregation and there is a rapid rate of disease progression. Aggressive periodontitis occurs in localized and generalized forms.
• Aggressive periodontitis may be distinguished from chronic periodontitis based on several

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• criteria: local factors lower than chronic periodontitis, rapid attachment loss of over 2 mm in under a year with larger quiescent periods, rapid bone destruction documented by X-rays made throughout the year, composition of the associated subgingival microflora, appearance in healthy subjects and detection in families.
• It can occur in patients around puberty and under the age group of 30 years.

Etiology

• Aggressive periodontitis patients display an increased susceptibility to periodontal disease due to an inadequate host response to highly virulent strains of periodontopathogenic bacteria, which is due to the increased expression of a wide variety of immunological and genetic risk factors.
• The complex interplay between the host risk factors and periodontal microflora induces a high susceptibility to periodontal disease, yet these patients appear healthy otherwise.
• Since some systemic conditions can mimic aggressive periodontitis, these diseases must be excluded before the diagnosis of aggressive periodontitis can be established.
• The specific periodontopathic microbial populations associated with aggressive periodontitis are Aggregatibacter actinomycetemcomitans (previously Actinobacillus actinomycetemcomitans) and Capnocytophaga species.

Risk Factors for Aggressive Periodontitis

1. Microbial factors: A. actinomycetemcomitans has been implicated as the primary pathogen associated with LAP.
2. Immunological factors: Some immune defects have been implicated in the pathogenesis of aggressive periodontitis.
3. The human leukocyte antigens A9 and B15 have shown a consistent association with aggressive periodontitis. Patients with aggressive periodontitis display functional defects in neutrophils, monocytes, etc.
4. which can impair the Chemotactic and phagocytic ability of these cells. Some studies have demonstrated hyper-responsiveness of these cells, resulting in excessive production of prostaglandin E₂ which can result in connective tissue destruction.
5. Polymorphisms in the receptors for immunoglobulin (IgG₂) have been shown in patients with localized aggressive periodontitis. Autoimmunity also is said to play a role in generalized aggressive periodontitis.
6. Genetic factors: A familial pattern of alveolar bone loss has implicated genetic factors in aggressive periodontitis. It has been suggested that certain immunologic defects may be inherited. LAP is transmitted through an autosomal dominant mode of inheritance.
7. Environmental factors: Smoking and stress may have an impact on attachment loss in young patients with localized aggressive periodontitis.

Based on extent and severity, aggressive periodontitis can be classified broadly into

1. Localized aggressive periodontitis
2. Generalized aggressive periodontitis.

When less than 30% of periodontal sites are involved the condition is said to be localized, while if 30% or more of sites are involved, the condition is labeled as generalized. Severity is measured by the amount of clinical attachment loss as slight (1–2 mm CAL), moderate (3–4 mm CAL) or severe ≥5 mm CAL).

Diagnosis

To distinguish aggressive periodontitis from other forms of periodontitis the following general criteria are useful:

• Clinical features
  • Presence or absence of signs of gingival inflammation
  • Rate of attachment loss
  • Limited amount of local factors concerning the amount of destruction
• Examination of siblings
• Microbial testing
• Immunity
  • Antibody response to infecting agent
  • Defective or hyperresponsive immunity.

Question 2: Discuss localized aggressive periodontitis.
Answer:

Localized Aggressive Periodontitis

Clinical Characteristics

1. Although age is not a criterion for diagnosis according to the 1999 AAP classification of periodontal disease the onset is usually between puberty and 20 years of age.
2. Affects both males and females with a predilection for female patients.
3. Localized to fist molar/incisor presentation with interproximal attachment loss on at least two permanent teeth, one of which is a fist molar, and involving no more than two teeth other than first molars and incisors.
4. Least destruction in the cusped-premolar area.
5. Rapid progression of the disease. Bone loss is three to four times faster than in chronic periodontitis.
6. Lack of clinical inflammation despite the presence of deep periodontal pockets and advanced bone loss.
7. The amount of plaque on the affected teeth is minimal in most cases. The limited plaque contains elevated amounts of A.actinomycetemcomitans and in some patients Porphyromonas gingivalis.
8. Distolabial migration of the maxillary incisors results in diastema formation.
9. Increased mobility of the maxillary and mandibular incisors and first molars.
10. Sensitivity of the denuded root surfaces.
11. Deep, dull, radiating pain during mastication.

Radiographic Findings

1. Vertical bone loss around the first molars and incisors. Radiographically seen as an arc-shaped loss of alveolar bone extending from the distal surface of the second premolar to the mesial surface of the second molar.
2. Bilateral symmetric pattern of bone loss (mirror image).

Possible reasons for the localization of periodontal destruction suggested are:

1. A. actinomycetemcomitans during the initial colonization of the first permanent molar is thought to evade the host defense mechanisms, thus enabling the bacteria to initiate periodontal tissue destruction.
2. After the initial attack, the body develops adequate immune defenses by the production of opsonic antibodies which can phagocytosis and clear the invading bacteria. A strong antibody response to infecting agents is characteristic of localized aggressive periodontitis.
3. Bacteria antagonistic to A. actinomycetemcomitans may colonize the periodontal tissue and inhibit A. actinomycetemcomitans from further colonizing the periodontal sites.
4. A. actinomycetemcomitans may have lost its leukotoxin-producing ability for unknown reasons.
5. A defect in the cementum formation may be responsible for the localization of the lesions.

Question 3: Discuss generalized aggressive periodontitis.
Answer:

Generalized Aggressive Periodontitis

Clinical Characteristics

1. It usually affects individuals under age 30, but older patients may also be affected. Male adolescents are more likely to be affected.
2. GAP produces poor antibody response to pathogens present.
3. Presence of generalized interproximal attachment loss affecting at least three permanent teeth other than fist molar and incisors.
4. The destruction is episodic with periods of advanced destruction followed by periods of quiescence.
5. The gingival tissue response in GAP can be severe, acutely inflamed tissue that is proliferating, ulcerated, and fiery red, bleeding on the slightest provocation.
6. This tissue response occurs in the destructive stage of the disease. In some cases, the gingiva may be pink, free of inflammation with deep pockets. This tissue response is believed to coincide with periods of quiescence.
7. The amount of plaque is inconsistent with the amount of destruction. P.gingivalis, A.actinomycetemcomitans, and Tannerella forsythia are frequently detected in the plaque present.

Radiographic Findings 

It ranges from severe bone loss associated with a minimal number of teeth to advanced bone loss affecting a majority of the teeth.

Question 4: Describe in detail the treatment modalities of aggressive periodontitis.
Answer:

Therapeutic Goals

The goals of periodontal therapy are to:

1. Alter or eliminate the microbial etiology and contributing risk factors for periodontitis, thereby arresting the progression of the disease preserving the dentition in comfort, function, and appropriate esthetics, and preventing the recurrence of the disease.
2. Regeneration of the periodontal attachment apparatus.
3. Due to the complexity of aggressive periodontal diseases systemic factors, immune defects, and microbial flares, control of disease may not be possible in all instances.
4. In such cases, the treatment objective is to slow the progression of the disease.

Treatment Considerations

In general, treatment methods for aggressive periodontal diseases are similar to those used for chronic periodontitis, which includes oral hygiene instruction and reinforcement and evaluation of the patient’s plaque control; supra- and subgingival scaling and root planing to remove microbial plaque and calculus; control of other local factors; occlusal therapy as necessary; periodontal surgery as necessary; and periodontal maintenance.

In addition to the parameters for chronic periodontitis, patients who have aggressive periodontitis need:

1. A general medical evaluation to determine if systemic disease is present in children and young adults who exhibit severe periodontitis, particularly if aggressive periodontitis appears to be resistant to therapy. Environmental risk factors if present are modified.
2. Initial periodontal therapy alone is often ineffective. In the early stages of disease, lesions are treated with adjunctive antimicrobial therapy combined with scaling and root planning with or without surgical therapy following microbiological identification and antibiotic sensitivity testing.
3. In very young patients, the use of tetracyclines may be contraindicated. Alternative antimicrobial agents or delivery systems may be considered.

Antimicrobial Dosage

Tetracycline 250 mg qid for 2 weeks

Metronidazole 250 mg and amoxicillin 250 mg thrice daily for 10 days

Amoxicillin with clavulanic acid (augmentin) 375 mg twice daily.

The long-term outcome may depend upon patient compliance and delivery of periodontal maintenance at appropriate intervals. If primary teeth are affected, the eruption of permanent teeth should be monitored to detect possible attachment loss.

Due to the potential familial nature of aggressive diseases, evaluation and counseling of family members may be indicated.

Outcomes Assessment

The desired outcomes of periodontal therapy in patients with aggressive periodontitis should include:

Signifiant reduction of clinical signs of gingival inflmmation

Reduction of probing depths (<5 mm)

Stabilization or gain of clinical attachment

Radiographic evidence of resolution of osseous lesions

Progress toward occlusal stability

Progress toward the reduction of clinically detectable plaque to a level compatible with periodontal health.

Conclusion

Aggressive periodontitis is today recognized as an independent disease category that manifests as an entity across all age groups though in lesser levels when compared to chronic periodontitis.

• The category included several types of periodontal disease that were formerly classified independently and used criteria that are not currently applicable.
• Generally, aggressive periodontitis is characterized by rapid progression of disease along with a diminished or deficient host response that further aggravates the rate of progression.
• The treatment of aggressive periodontitis is less predictable due to its rapid progression and characteristics of the disease.