From Gums to Brain: Unveiling the Hidden Inflammatory Connection Between Periodontal and Cerebrovascular Diseases

Periodontal disease (PD) encompasses inflammatory conditions affecting the supporting structures of the teeth, with gingivitis and periodontitis being the most prevalent forms. Gingivitis, characterized by gum inflammation and bleeding, can progress to periodontitis, which involves the destruction of connective tissue and alveolar bone. PD is a global health burden, affecting over a billion individuals, with 42.2% of adults aged ≥30 years in the United States experiencing some form of periodontitis. Without proper management, PD can lead to severe systemic consequences. The cause of PD is multifactorial, involving bacterial biofilm, systemic diseases, aging, smoking, high-fat diets, and immune deficiencies. These risk factors act independently or synergistically, accelerating disease progression. Prevention and treatment strategies focus on biofilm control, nonsurgical therapy, improved oral hygiene, and risk factor management to halt disease progression and restore tooth support. Recent research suggests a strong link between PD and cardiovascular diseases, including stroke, due to systemic inflammation. Periodontitis-induced inflammation triggers the release of cytokines and CRP (C-reactive protein), which can enter systemic circulation, promoting atherosclerosis and endothelial dysfunction. Bacterial translocation from the oral cavity into the bloodstream further exacerbates vascular disease, increasing stroke risk. Epidemiological studies indicate that individuals with periodontitis have a significantly higher risk of stroke, with case-control and cohort studies showing strong associations. However, some interventional studies suggest that periodontal treatment alone may not significantly reduce cardiovascular events, highlighting the complexity of this relationship. This review aimed to summarize existing literature on the association between PD and cerebrovascular diseases, emphasizing underlying pathophysiological mechanisms and epidemiological evidence.