Anticoagulants and antiplatelet drugs reduce the ability of blood to form clots, or coagulate.
Blood clotting is a process triggered naturally in response to damage to blood vessels from injury or invasive procedures.
Platelets within the blood become activated locally, resulting in an increased tendency to adhere to each other and to damaged blood vessel endothelium (primary haemostasis).
At the same time a cascade of reactions is initiated converting inactive coagulation factors to their active forms, ultimately leading to the production of the protein fibrin.
Fibrin stabilises the primary platelet plug by cross-linking the platelets to each other and to the damaged blood vessel wall to prevent further blood loss (secondary haemostasis).
Anticoagulants and antiplatelet drugs exert their effects at different stages in the coagulation process.
Antiplatelet drugs interfere with platelet aggregation by reversibly or irreversibly inhibiting various steps in the platelet activation required for primary haemostasis.
Anticoagulant drugs inhibit the production or activity of the factors that are required for the coagulation cascade and in this way impair secondary haemostasis.
Certain medical conditions can predispose individuals to the risk of a thrombosis, where a blood clot (thrombus) blocks a blood vessel, either at the site of formation or after travelling to another critical site (thromboembolism), with potentially catastrophic consequences such as heart attack, pulmonary embolism or stroke.
Anticoagulants and antiplatelet drugs are prescribed to reduce the risk of such an event:
However, this reduction in risk of thromboembolic events comes at the cost of an increased risk of bleeding, either spontaneously or associated with invasive procedures.
The balance of these risks for an individual patient is the primary consideration in the management of dental patients who are taking anticoagulants or antiplatelet drugs and require dental treatment.