The Coagulation–Immune Axis in Oral Squamous Cell Carcinoma: Mechanisms, Prognostic Significance, and Therapeutic Opportunities

Oral squamous cell carcinoma (OSCC) develops in a microbe-rich, injury-prone mucosa in which coagulation, inflammation, and tissue repair are closely coupled. Tumor and host cells can activate tissue factor-thrombin signaling, platelets, fibrin turnover, extracellular vesicles, and neutrophil extracellular traps, thereby reshaping myeloid-cell recruitment, cytotoxic immunity, angiogenesis, and invasion. However, local procoagulant biology does not necessarily predict systemic venous thromboembolism. We therefore organize the evidence using a compartmentalized immunothrombosis model that distinguishes intratumoral coagulation-immune remodeling, systemic thrombosis, and treatment-dependent perioperative events. Direct OSCC studies support several components of this network, but much of the evidence linking coagulation to immune escape and treatment response remains preclinical or extrapolated from other tumors. Circulating D-dimer, fibrinogen, platelet indices, and inflammatory ratios show prognostic associations, yet their incremental value beyond established clinicopathologic factors has not been established. Anticoagulant, antiplatelet, protease-activated receptor, podoplanin-CLEC-2, fibrinolytic, and NET-directed strategies are biologically plausible but should not be used as OSCC treatment without a standard indication or clinical trial. Future studies should pair longitudinal blood measurements with spatial tumor profiling and match interventions to a verified mechanism, anatomical compartment, and safe treatment window.