Resumo O presente estudo avaliou a associação da predisposição clínica e dos fatores genéticos com a presença de doenças peri-implantares. Cento e quatorze pacientes com implantes dentais instalados na Clínica de Especialização do Amazonas, Brazil, foram incluidos no estudo. Após exame clínico e radiográfico, a amostra foi categorizada em 4 grupos, de acordo com o Status peri-implantar: saúde (n=71), mucosite (n=30), peri-implantite (n=13) e doentes (mucosite + peri-implantite). DNA genômico foi extraído de células orais da saliva, e o polimorfismo genético em osteoprotegerina (OPG), ligante do receptor ativador do fator Kappa nuclear (RANKL) e receptor ativador do fator Kappa nuclear (RANK) foram genotipados por PCR em tempo real. O estudo se propôs a avaliar se os polimorfismos em RANK, RANKL e OPG estão envolvidos na patogênese da mucosite e da peri-implantite, e avaliar também a presença de fatores de risco moduladores da resposta em uma população brasileira. Idade, biotipo peri-implantar, diabetes e presença de biofilme peri-implantar foram associados a mucosite (p<0.05) e peri-implantite (p<0.05). Tabagismo, alcoolismo e biofilme periodontal também foram associados com a presença de peri-implantite (p<0.05). Análise univariada e multivariada não demonstraram associação de peri-implantite ou mucosite com os polimorfismos genéticos em RANK (rs3826620), RANKL (rs9594738) e OPG (rs2073618) (p>0.05). Os polimorfismos genéticos estudados não foram associados com mucosite e peri-implantite em uma população brasileira da região Amazônica.

Abstract The present study evaluated polymorphisms in RANK, RANKL and OPG-encoding genes to assess whether they are associated with mucositis and peri-implantitis in a population from the Brazilian Amazon region. One hundred and fourteen patients with dental implants were included in the study. After clinical and radiographic examination, the sample was categorized into 4 groups, according to the peri-implant status: Healthy (n=71), Mucositis (n=30), Peri-implantitis (n=13) and Diseased (Mucositis + Peri-implantitis, n=43). Genomic DNA was extracted from buccal cells from saliva, and the genetic polymorphism in osteoprotegerin (OPG), Kappa nuclear factor activator receptor (RANKL) and nuclear kappa factor activator receptor (RANK) were genotyped by the real time PCR. Univariate and multivariate statistical analyses were performed to compare clinical variables among groups and to evaluate genotypes and alleles distributions and the established alpha was 5%. Age, peri-implant biotype, diabetes and presence of peri-implant biofilm were associated with mucositis (p<0.05) and peri-implantitis (p<0.05). Smoking, alcoholism, and periodontal biofilms were also associated with the presence of peri-implantitis (p<0.05). Univariate and multivariate analysis did not demonstrate an association of peri-implantitis or mucositis with any genetic polymorphism in RANK (rs3826620), RANKL (rs9594738) and OPG (rs2073618) (p>0.05). The studied genetic polymorphism in RANK, RANKL and OPG were not associated with mucositis and peri-implantitis in a Brazilian population from the Amazon region.

Abstract This study was performed to evaluate the interplay between dental caries, nutritional status, and genetic polymorphisms in TAS1R1 and TAS1R2 (taste receptor, type 1, member 1 and 2) in preschool children and pre-adolescents. We included 525 subjects (306 preschool children and 219 pre-adolescents). Parents/caregivers answered a self-administered questionnaire about their children’s systemic health, characteristics, oral hygiene habits, and diet. Clinical examination was performed to evaluate dental caries and nutritional status. Saliva samples were collected for DNA extraction. The genotyping of rs17492553 ( TAS1R1 ), rs3935570, and rs4920566 ( TAS1R2 ) polymorphisms was performed using real-time PCR with Taqman Genotyping Master Mix and SNP assay. Both univariate and multivariate Poisson regression analyses with robust variance were used for the data analysis. In preschool children, consumption of sweets between meals increased the prevalence of dental caries by 85% (PR c = 1.85; 95%CI 1.39–2.46; p < 0.001), whereas in pre-adolescents, this prevalence increased by 34% (PR a = 1.34; 95%CI 1.11–1.62; p = 0.002), regardless of genetic polymorphisms . Moreover, individuals carrying at least one allele C in rs17492553 presented 23% more prevalence of dental caries (PR a = 1.23; 95%CI 1.02–1.49 p = 0.030). Nutritional status was not associated with dental caries, neither with genetic polymorphisms . Consumption of sweets between meals increased the prevalence of dental caries. In pre-adolescents, rs17492553 genetic polymorphism in TAS1R1 was associated with dental caries.