The prevalence of Stafne bone cavity: A meta-analysis of 355,890 individuals.

Background/purpose: A Stafne bone cavity (SBC) is an incidental depression in the lingual surface of the mandible. The aim of this study is to provide pooled estimates of the frequency of Stafne bone cavity and to correlate its presence with such variables as sex, laterality, diagnostic methods and population. Materials and methods: Potential studies were searched through four electronic databases: Google Scholar, PubMed, Scopus, and Journal Storage. Titles, abstracts, and full texts of the articles were screened. Results: A total of 54 studies relating to 355,890 subjects met the inclusion criteria for meta-analysis. A meta-analysis using the DerSimonian-Laird model revealed an overall prevalence of 0.17% (CI:0.14%-0.21%, I 2 = 80.7%). SBC was four times more common in males than females (z = 6.94, P < 0.01), and was unilateral in almost all cases (z = 12.90, P < 0.01). Radiographic studies yielded a lower SBC prevalence at 0.12% (CI:0.09%-0.15%, I 2 = 71.7%) than computed tomography studies, skeletal studies and excavation studies. Ancient populations had three times higher SBC prevalences (0.47%, CI:0.21%-0.73%, I 2 = 89.5%) than the average populations today (z = 3.21, P < 0.01). Conclusion: The prevalence of Stafne bone cavity is approximately 0.17%, and was four times more prevalent in males than females. This variant bone cavity was also present unilaterally in the majority of cases. Awareness of SBC is important for dentists, maxillofacial surgeons and other practitioners performing routine dental practices and interpreting panoramic radiographs.

Associations of CB1 cannabinoid receptor (CNR1) gene polymorphisms with risk for alcohol dependence: Evidence from meta-analyses of genetic and genome-wide association studies.

OBJECTIVES: Reported associations of the cannabinoid receptor 1 (CNR1) single nucleotide polymorphisms (SNPs) with alcohol dependence (AD) have been inconsistent, prompting a meta-analysis to obtain more precise estimates. METHODS: A Boolean search of 4 databases (PubMed, Scopus, Google Scholar, and Mednar) sought articles that evaluated the association between CNR1 polymorphisms and risk of AD. We selected the articles with sufficient genotype frequency data to enable calculation of odds ratios (ORs) and 95% confidence intervals (CIs). Using the Population Intervention Comparators Outcome elements, AD patients (P) were compared by genotype data between AD-participants (I) and non-AD-participants (C) in order to determine the risk of AD (O) attributed to the CNR1 SNPs. Analyzing 4 SNPs (rs1049353, rs1535255, rs2023239, and rs806379) using standard genetic models, we examined associations where multiple comparisons were Holm-Bonferroni corrected. The pooled ORs were assessed for aggregate statistical power and robustness (sensitivity analysis). Subgroups were Caucasians and African-Americans. RESULTS: From 32 comparisons, 14 were significant indicating increased risk, from which 5 outcomes (P-value for association [Pa] = .003 to <.001) survived the Holm-Bonferroni-correction, which were deemed robust. In the rs1535255 outcomes, the codominant effect (OR = 1.43, 95% CIs = 1.24-1.65, Pa < .001) had greater statistical power than the dominant effect (OR = 1.30, 95% CI = 1.08-1.57, Pa = .006). In contrast, the rs2023239 codominant outcome was underpowered. Significance of both rs806379 Caucasian outcomes (ORs = 1.20-1.43, 95% CIs = 1.07-1.57, Pa = .003) contrasted with the null effects in African-Americans (ORs = 0.98-1.08, 95% CIs = 0.70-1.53). CONCLUSIONS: Three CNR1 SNPs (rs1535255, rs2023239, and rs806379) were implicated in their associations with development of AD: based on aggregate statistical power, rs1535255 presented greater evidence for associations than rs2023239; rs806379 implicated the Caucasian subgroup. Multiple statistical and meta-analytical features (consistency, robustness, and high significance) underpinned the strengths of these outcomes. Our findings could render the CNR1 polymorphisms useful in the clinical genetics of AD.