The effect of antiretroviral therapyon the periodontal conditions of patients with HIV infection: A systematic review and meta-analysis.

AIM: To assess any differences (1) in the prevalence of periodontitis and necrotizing periodontal diseases, specifically necrotizing gingivitis (NG) and necrotizing periodontitis (NP) between HIV patients receiving antiretroviral therapy (HAART) and those not receiving the therapy and (2) in the severity of periodontitis based on probing depths (PDs) and clinical attachment loss (CAL) between the two groups. MATERIALS AND METHODS: Systematic electronic search on five databases (PubMed, Google Scholar, Scopus, Web of Science and Scielo) was conducted to identify cross-sectional and longitudinal studies reporting on prevalence of NG, NP and periodontitis among HIV patients who either receive or do not receive HAART treatment. The differences in clinical parameters of PDs and CAL among these patients were assessed. RESULTS: Eighteen articles were considered. The meta-analysis for NG showed that the overall assessment for the relative frequency ratio in the two groups was 0.45 (n = 7; 95% confidence interval [CI]: [0.21, 0.97]; p < .042). Regarding NP, the overall assessment for the relative frequency ratio in both groups was 0.60 (n = 5; 95% CI [0.22, 1.64]; p = .321). With regard to periodontitis, the overall assessment for the relative frequency ratio in the two groups was 1.17 (n = 9; 95% CI [0.90, 1.52]; p = .248). No significant differences in PD and CAL were found between the two groups 0.00 (n = 3; 95% CI [-0.52, -0.53]; p = .985) and 0.32 (n = 3; 95% CI [-0.19, 0.82]; p = .22), respectively. CONCLUSIONS: The prevalence of NG appeared to be significantly reduced in patients receiving antiretroviral therapy. No statistical significant difference was found in the prevalence of NP or periodontitis between the two groups.

IL-1B(3954) polymorphism and red complex bacteria increase IL-1ß (GCF) levels in periodontitis.

OBJECTIVE: The aim of this study was to compare IL-1ß levels in gingival crevicular fluid (GCF) from healthy and periodontitis sites of IL-1B(3954)-Single Nucleotide Polymorphism (SNP) positive and IL-1B(3954)-SNP negative periodontitis subjects in association with their bacterial profiles. BACKGROUND: Susceptibility to periodontitis has been associated with several risk factors, including allelic variants at multiple gene loci. Variations in the IL-1 gene cluster have been linked with increased risk for periodontitis. IL-1B(3954)-SNP has been previously associated with increased levels of IL-1ß in GCF or periodontal tissues in chronic periodontitis patients, as well as higher levels of specific periodontal pathogens. There is insufficient evidence to conclude if IL-1B gene polymorphisms affect the susceptibility to periodontitis by ultimately modulating the levels of IL-1ß in GCF, the subgingival microbial profile or both. MATERIALS AND METHODS: GCF, subgingival plaque, and buccal epithelial cells were collected from 32 individuals with periodontitis. GCF IL-1ß levels were measured by an enzyme-linked immunosorbent assay (ELISA). Bacterial plaque samples were analyzed for 11 periodontal pathogens using polymerase chain reaction (PCR) analysis with specific primers for the 16SrRNA gene of each bacterium. IL-1B(3954)-SNP status was determined by identifying the carriers of the polymorphic T allele. RESULTS: A significant association was shown between IL-1B(3954)-SNP and IL-1ß GCF levels (amount and concentration). The concomitant presence of two or three red complex bacterial species was associated with increased IL-1ß GCF levels in periodontitis sites (site-level analysis). The concurrent presence of all three red complex periodontal pathogens and IL-1B(3954)-SNP was associated with the highest IL-1ß GCF levels in periodontitis sites. CONCLUSIONS: Our results indicate an independent association of both IL-1B(3954)-SNP and red complex bacterial species with increased IL-1ß levels in GCF of periodontitis sites. A better understanding of the interaction between genetics, bacteria, and inflammation is essential to develop more effective diagnostic, prognostic, and therapeutic tools for periodontitis.