ABSTRACT
Inflammatory jaw bone diseases are common in stomatology, including periodontitis, peri-implantitis, medication-related osteonecrosis of the jaw, radiation osteomyelitis of the jaw, age-related osteoporosis, and other specific infections. These diseases may lead to tooth loss and maxillofacial deformities, severely affecting patients' quality of life. Over the years, the reconstruction of jaw bone deficiency caused by inflammatory diseases has emerged as a medical and socioeconomic challenge. Therefore, exploring the pathogenesis of inflammatory diseases associated with jaw bones is crucial for improving prognosis and developing new targeted therapies. Accumulating evidence indicates that the integrated bone formation and dysfunction arise from complex interactions among a network of multiple cell types, including osteoblast-associated cells, immune cells, blood vessels, and lymphatic vessels. However, the role of these different cells in the inflammatory process and the 'rules' with which they interact are still not fully understood. Although many investigations have focused on specific pathological processes and molecular events in inflammatory jaw diseases, few articles offer a perspective of integration. Here, we review the changes and mechanisms of various cell types in inflammatory jaw diseases, with the hope of providing insights to drive future research in this field.
ABSTRACT
The common functional CYP2E1 Rsa I/Pst I polymorphism may influence the risk of esophageal cancer. However, the published results are conflicting. We therefore conducted a meta-analysis comprised of 11 published case-control studies with 1,088 cases and 2,238 controls. Odds ratios (ORs) with 95% confidence interval (CIs) were used to assess the strength of the association. Overall, the pooled ORs were 0.53 (95% CI = 0.31-0.89, P (heterogeneity) < 0.001) and 0.57 (95% CI = 0.34-0.96, P (heterogeneity) < 0.001), for the heterogeneity c1/c2 and c2 allele carriers (c1/c2 + c2/c2) compared with the homozygous c1/c2, respectively. In subgroup analysis by race, the same significant risks were found among Asians (for c2 vs. c1: OR = 0.64, 95% CI = 0.43-0.95, P (heterogeneity) < 0.001; for c1/c2 vs. c1/c1: OR = 0.48, 95% CI = 0.28-0.82, P (heterogeneity) < 0.001; for c1/c2 + c2/c2 vs. c1/c1: OR = 0.51, 95% CI = 0.30-0.86, P (heterogeneity) < 0.001). In conclusion, our meta-analysis demonstrates that CYP2E1 Rsa I/Pst I c2 allele may be a decreased risk factor for developing esophageal cancer among Asians populations.