Research progress on the relationship between platelets and periodontitis

Platelets, small cell fragments in the blood that prevent bleeding, are closely associated with hemostasis and thrombosis and play an important role in the inflammatory response. Periodontitis is a chronic inflammatory disease caused by periodontopathogenic bacteria, resulting in local and systemic inflammatory responses that are associated with many systemic diseases. In recent years, several animal and human studies have demonstrated the correlation between periodontitis and platelets from three aspects: gingiva, and gingival crevicular fluid, and found that activated platelets play a very important role in the development and progression of periodontitis. Porphyromonas gingivalis and inflammatory mediators S100A8/A9 activate platelets, which then combine with leukocytes to form platelet–leukocyte aggregates. These aggregates can migrate into periodontal tissue, producing proinflammatory cytokines, thereby promoting the development and progression of periodontitis. Available studies also suggest that initial periodontal therapy reduces platelet activation and platelet–leukocyte aggregate formation, which may reduce the risk of cardiovascular diseases (CVDs) in patients with periodontitis. Additionally, studies found that antiplatelet drugs can inhibit periodontal inflammation and promote periodontal tissue repair and that P. gingivalis-induced expression of CD40L on platelets may be an important mediator between periodontitis and CVD. These reports suggest that platelets can serve as novel therapeutic targets for the treatment of periodontitis. This review aims to discuss the current literature on the correlation and interaction mechanisms between periodontitis and platelets.