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Detection of Aggregatibacter actinomycetemcomitans clone JP2 in subjects with Aggressive Periodontitis and its correlation with clinical parameters

Grant number: 14/16315-3
Support Opportunities:Scholarships in Brazil - Scientific Initiation
Effective date (Start): February 01, 2015
Effective date (End): December 31, 2015
Field of knowledge:Health Sciences - Dentistry - Periodontology
Principal Investigator:Luciana Saraiva
Grantee:Marcela Giudicissi
Host Institution: Faculdade de Odontologia (FO). Universidade de São Paulo (USP). São Paulo , SP, Brazil


Aggregatibacter actinomycetemcomitans(Aa) is an important periodontal pathogen that may be associated with aggressive periodontitis (AP) which is characterized by rapid attachment and bone loss. Aa possesses many virulence factors that can suppress or inactivate the host immune system. Aa shows several serotypes, including serotype b that is often associated with PA. The Aa JP2 clone (serotype b) is highly virulent and its pathogenicity is characterized by increased leukotoxin production due of the 530-bp deletion (”530) in the promoter lkt / ltx gene region. The objective of this study will be looking for Aa JP2 clones in patients with PA, correlating these data with the clinical findings of these patients. Forty patients with AP and ten periodontally healthy patients will be selected. Subgingival biofilm samples will be sampled from two sites per individual. The patients will receive periodontal treatment and then they will enter into a periodontal maintenance and control program each three months. Aa strains of JP2 and non-JP2 clones will be grown in specific media and recombinant plasmids will be constructed harboring a single copy of the 16S rRNA gene of each of the strains. To obtain the standard curve (used as a parameter to quantify the samples) successive dilutions of the plasmids will be used presenting a cloned copy of each gene analyzed (16S rRNA Aa). After extraction of the DNA from the clinical samples, the copy number of microorganisms will be quantified by qPCR using specific probes and primers. Our hypothesis is that carriers of the Aa clone JP2 exhibit greater severity of periodontal disease compared to patients with other clones non-JP2.

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