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Influence of genetic polymorphisms in the colonization/recolonization patterns in chronic periodontitis patients

Grant number: 14/03276-0
Support type:Scholarships in Brazil - Doctorate
Effective date (Start): June 01, 2014
Effective date (End): August 29, 2017
Field of knowledge:Health Sciences - Dentistry
Cooperation agreement: Coordination of Improvement of Higher Education Personnel (CAPES)
Principal Investigator:Gustavo Pompermaier Garlet
Grantee:Ian Franco Cavalla Ruiz
Home Institution: Faculdade de Odontologia de Bauru (FOB). Universidade de São Paulo (USP). Bauru , SP, Brazil
Associated scholarship(s):15/18163-9 - Potential common genetic susceptibility traits shared by chronic and apical periodontitis: focus on SNPs assessment followed by bioinformatics analysis including clinical, microbiological and inflammatory/immunological data, BE.EP.DR


Periodontal diseases have a complex etiology, involving the interactions of multiple genes controlling the host response to infecting microorganisms. Adult twin studies have suggested a relation between genetic background and periodontitis risk. Population variations on host´s infection response control genes can explain a great proportion of the differential clinical presentation of periodontitis. The ecologic changes of subgingival biofilm leading to increased proportions of Gram (-) rods of the so called red and orange complex are correlated to worsening of the clinical parameters of periodontitis and treatment failure. Recent genome-wide association studies have identified Single Nucleotide Polymorphisms (SNP) associated to an increased risk of infection by red and orange complex microorganism and the putative periodontal pathogen A. actinomycetemcomitans. In this context, the purpose of this study is to investigate the involvement of SNP in the differential pre and post treatment subgingival biofilm profile and to correlate the later with clinical parameters and immunological markers of periodontitis. The study design consider two different population samples: (1) a longitudinal one of 75 chronic periodontitis patients and 50 healthy controls, who will receive cause-related treatment as needed and followed by a period of one year. Subgingival biofilm samples of these volunteers will be collected at baseline, 6 and 12 months; and (2) a cross-sectional sample of 197 chronic periodontitis patients, 193 gingivitis patients and 218 healthy individuals. Affected gingival tissue samples of the chronic periodontitis patients scheduled for surgical treatment will be collected to quantify the expression profiles of immunological markers. The subgingival biofilm samples will be characterized by DNA-DNA hybridization checkerboard for 40 species and quantitative Real Time PCR for 12 species, both pathogenic and commensal. The participants will be genotypified for the SNP of interest and the microbiological, clinical and immunological data will be analyzed to establish correlations between the risk alleles and the response variables. The data analysis will consider a case/control design, using both the "classic" healthy control group and the "resistant" phenotype group of gingivitis-affected individuals. This alternative approach maximizes the possibilities of finding true correlations between genetic profiles and the study variables. Such knowledge might allow the development of diagnostic, preventive and therapeutic strategies in order to improve the clinical management of periodontal diseases. (AU)

Scientific publications
(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)
COLAVITE, PRISCILA MARIA; CAVALLA, FRANCO; GARLET, THIAGO POMPERMAIER; SORIANI AZEVEDO, MICHELLE DE CAMPOS; MELCHIADES, JESSICA LIMA; CAMPANELLI, ANA PAULA; LETRA, ARIADNE; FAVARO TROMBONE, ANA PAULA; SILVA, RENATO MENEZES; GARLET, GUSTAVO POMPERMAIER. TBX21-1993T/C polymorphism association with Th1 and Th17 response at periapex and with periapical lesions development risk. Journal of Leukocyte Biology, v. 105, n. 3, p. 609-619, MAR 2019. Web of Science Citations: 0.
CAVALLA, FRANCO; BIGUETTI, CLAUDIA C.; DIONISIO, THIAGO J.; AZEVEDO, MICHELLE C. S.; MARTINS, JR., WALTER; SANTOS, CARLOS F.; TROMBONE, ANA PAULA F.; SILVA, RENATO M.; LETRA, ARIADNE; GARLET, GUSTAVO P. CCR5 Delta 32 (rs333) polymorphism is associated with decreased risk of chronic and aggressive periodontitis: A case-control analysis based in disease resistance and susceptibility phenotypes. CYTOKINE, v. 103, p. 142-149, MAR 2018. Web of Science Citations: 5.
CAVALLA, FRANCO; BIGUETTII, CLAUDIA CRISTINA; COLAVITE, PRISCILA MARIA; SILVEIRA, ELCIA VARISE; MARTINS, JR., WALTER; LETRA, ARIADNE; FAVARO TROMBONE, ANA PAULA; SILVA, RENATO MENEZES; GARLET, GUSTAVO POMPERMAIER. TBX21-1993T/C (rs4794067) polymorphism is associated with increased risk of chronic periodontitis and increased T-bet expression in periodontal lesions, but does not significantly impact the IFN-g transcriptional level or the pattern of periodontophatic bacterial infection. VIRULENCE, v. 6, n. 3, SI, p. 293-304, APR 2015. Web of Science Citations: 7.

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