Existing evidence suggests that periodontitis may contribute to systemic comorbidities by inducing low-grade chronic inflammation, with individuals suffering from severe periodontitis exhibiting elevated levels of proinflammatory mediators such as interleukin-1 (IL-1), interleukin-6 (IL-6), C-reactive protein (CRP), and fibrinogen, along with increased neutrophil counts, compared with healthy controls [23,24]. This evidence concerns the gene CRP and periodontitis.