Clinical observations demonstrate that dysregulated expression of specific adipokines—including visfatin, APN, and leptin—within periodontal tissues of periodontitis patients correlates significantly with local inflammatory pathology and alveolar bone metabolic dysregulation, revealing a reciprocal pathological circuit that links obesity and periodontitis via metabolic pathways such as lipid/glucose metabolism and oxidative stress (Figure 2D) (10). The gene discussed is LEP; the disease is obesity due to melanocortin 4 receptor deficiency.