Periodontitis is a chronic inflammatory disease that is initiated by bacteria. Pathogens and their virulence factors alter normal cellular metabolic activity and deteriorate periodontal microconditions. Owing to the complexity of tooth structure and the limitation of conventional treatment, we may not live up to all patients’expectations, especially those with grade C and stage Ⅲ or Ⅳ periodontitis. With the advantages of bactericidal effects, high safety, inhibition of bacterial drug resistance and promotion of tissue healing, photodynamic therapy (PDT)seems to be an ideal technology in periodontal treatment. However, it cannot remove subgingival stones and still cannot replace mechanical treatment to preliminarily control periodontal inflammation. Therefore, near-infrared low-energy light combined with traditional photosensitizers is mostly used in clinical periodontal adjuvant treatment. In periodontal maintenance treatment on a regular basis, a single application can also reduce the sensitivity of patients and effectively control plaque, but its effect will be affected by the degree of periodontal inflammation, the concentration and type of photosensitizer, the energy of the light source, etc. With the further development of material science, the performance of photosensitizers to accelerate oxides and target bacteria will be optimized. In the future, parameters of PDT need to be designed in large-scale studies in accord with different stages and grades of 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.