[2] Therefore, the prevalence of LAP varies considerably between continents, and differences in race or ethnicity seem to be a major contributing factor.
Of the microflora characterised in aggressive periodontitis, approximately 65-75% of bacteria are Gram-negative bacilli, with few spirochaetes or motile rods present.
An early study dating back to 1983 explains its prevalence and documents its role in localised aggressive periodontitis.
[9] Samaranayake notes the evidence for the specific involvement of Aggregatibacter actinomycetemcomitans includes: an increased incidence of it found in subgingival plaque obtained from lesional sites, high level of its antibody which tends to fall following successful treatment, its possession of a wide range of potentially pathogenic products and its elimination with concordant disease regression, following treatment with successful periodontal therapy and adjunctive tetracycline.
Greater numbers of both Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans were found in active, destructive periodontal lesions in comparison to non-active sites.
[11][12] An impaired ability of peripheral blood lymphocytes to react to chemotactic stimuli is found in the majority of patients with aggressive periodontitis.
[7] Aggressive periodontitis is a multifactorial disease with many complex interactions including host factors, microbiology and genetics.
[13] The plasma cells produce specific antibodies in response to the periodontal pathogens, which diffuse into the gingival crevicular fluid.
However, patients with generalized aggressive periodontitis have decreased ability to mount high titres of IgG to Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans.
[13] Studies of families, twins and sibling pairs have provided strong evidence for a genetic basis for aggressive periodontitis.
[15] A person's genetic predisposition to the condition is determined by a single gene of major effect, inherited as an autosomal dominant trait.
However, for the disease process to initiate the person must be exposed to the presence of periodontal pathogens and potentially also various environmental factors.
[26] In this case, the manifestation of aggressive periodontitis is believed to be the result of genetic mutation, combined with environmental factors.
[34][17] The periodontal tissue also exhibits minimal signs of inflammation clinically[35] and show a robust response with serum antibodies to pathogens.
A healthy periodontium in a Caucasian would appear stippled and pink with a knife edge margin where it abuts the tooth (pigmentation may differ in other races).
[40] On probing, patients with AgP should have evidence of significant periodontal pocket depths and loss of attachment (LOA).
Dental practitioners should also be aware of false pocketing around erupting/newly erupted teeth in the mixed dentition phase and also in the presence of gingival inflammation.
Radiographic assessment should be carried out for patients with evidence of periodontitis to observe alveolar bone levels which can help to identify signs of AgP.
[40] In healthy periodontal tissues, the distance from the amelocemental junction (ACJ) to the alveolar bone crest is typically in the order of 1mm in young people.
In addition to that, presence of angular or vertical bone loss (especially at 6's) and arrowhead or furcation lesions are also a strong suggestion of AgP.
[44][45] Early detection of AgP allows intervention to be carried out before extensive periodontal destruction has taken place which further simplifies treatment.