The relationship between FOSB and SOCS3 gene polymorphisms and the susceptibility to periodontitis and osteopenia in...

The aim is to analyze the relationship and significance of the FOS, FOSB, Suppressors of cytokine signaling (SOCS), and hypoxia-inducible factor 1 (HIF1) gene loci and their polymorphisms with periodontitis and osteopenia in the Chinese population. In this case-control study, data on questionnaires, periodontal examination, bone mineral density, and FOS, FOSB, SOCS3, and HIF1 gene loci and their polymorphisms were obtained from 474 participants. The data were analyzed using the analysis of variance, Kruskal-Wallis test, χ² test, and logistic regression. The incidence of osteopenia was significantly increased in patients with periodontitis compared to controls (58.6 vs. 34.4%, P < 0.001). Accordingly, the risk was increased 2.21-fold compared with controls (95% CI 2.09-4.95). Osteopenia patients had a significantly higher risk of periodontitis than patients with normal bone density (OR = 3.22, 95% CI 2.09-4.94). There were significant positive associations between FOSB and SOCS3 polymorphisms and periodontitis and osteopenia susceptibility. Individuals carrying the G/G genotype of the FOSB gene rs708905 locus had an increased risk of periodontitis (OR = 5.06, 95% CI 2.36-10.86) and osteopenia (OR = 3.26, 95% CI 1.34-7.96). Compared with the C/C genotype, the A/A genotype of the FOSB rs8105114 locus was associated with a significantly higher risk of periodontitis (OR = 2.14, 95% CI 1.02-4.53) and osteopenia (OR = 2.85, 95% CI 1.12-7.22). Compared with the A/A genotype, the risk of periodontitis in the G/G genotype of the SOCS3 rs7207782 locus was increased 3.10-fold (P < 0.001), and the risk of osteopenia was increased 2.01-fold (P = 0.023). There was a bidirectional relationship between periodontitis and osteopenia. The rs708905 G/G and rs8105114 A/A genotypes of FOSB and the rs7207782 G/G genotype of SOCS3 were risk factors for both periodontitis and osteopenia in the Chinese population, which could increase knowledge about disease‑specific and cross‑disease genetic pattern.