A dental student’s guide to…anticoagulants and antiplatelets

AnticoagulantsIn this month’s column, Hannah Hook explores the impact anticoagulants and antiplatelets has on dental patients.

It is a common occurrence to treat a patient in general practice who is on anticoagulant or antiplatelet medications.

The primary reason for prescription of these medications is to prevent those who are at high risk for, or who have previously had, a thromboembolic event such as a blood clot.

Examples of patients at an increased risk of thromboembolic events include those who have experienced pulmonary embolism, deep-vein thrombosis, non-valvular atrial fibrillation, or cardiac arrythmia.

Without an antiplatelet or anticoagulant medication these patients are at a higher risk of developing a blood clot. This could consequently result in a thromboembolism, stroke or myocardial infarction.

Due to decreased clotting ability, the treatment of these patients raises various safety concerns regarding the potential risk of bleeding complications following invasive dental procedures.

It is therefore important to have an understanding of the numerous medications a patient may take that will affect their ability to clot.


Anticoagulants prevent the formation of blood clots by inhibiting the production or activity of coagulation factors required for clotting in the coagulation cascade.

There are two main types of anticoagulants:

  • Vitamin K antagonists (VKAs)
  • The newer direct oral anticoagulants (DOACs).

Examples of DOACs include dabigatran, rivaroxaban, apixaban and edoxaban, whilst the most frequently prescribed VKA is warfarin.



Mechanism of action: vitamin K antagonist. Inhibits vitamin K dependent modification of prothrombin and other coagulation factors (II, VII, IX, X).

Tests: INR is a test used for patients taking warfarin. It is used to determine the time it takes for the blood to clot. Patients record their INR in a yellow book, which can show how well their INR has been controlled over the last two months.

Considerations: extractions may be carried out if a patient’s INR is less than four. INR should be carried out 24 hours before extraction (max 72 hours prior to procedure if the patient’s INR is stable).

Half-life: 20-60 hours (DeLoughery, 2015).

Warnings: azole antifungals potentiate the effects of warfarin. Do not prescribe to a patient taking warfarin. Avoid NSAIDs and aspirin.

Antidote: vitamin K.


Mechanism of action Half-life
Dabigatran Reversibly binds to thrombin, preventing thrombin mediated activation of coagulation factors in the coagulation cascade (Comin and Kallmes, 2012). Rapid onset of action is within 0.5-2 hours (Hankey and Eikelboom, 2011). eight hours
Rivaroxaban Reversibly inhibits free and clot bound factor Xa, preventing the formation of thrombin. Onset of action is between 2.5-4 hours (Ansell, 2019). 11-13 hours
Apixaban Reversibly inhibits free and clot bound factor Xa, preventing the formation of thrombin. Rapid onset of action, with peak effects at around one to two hours (Hurst, O’Callaghan and Handa, 2017). 12 hours
Edoxaban Reversibly inhibits free and clot bound factor Xa, preventing the formation of thrombin. Rapid onset of action around one to two hours (Ansell, 2019). 10-14 hours


Antiplatelet drugs act to reversibly or irreversibly block various sites on platelets, therefore decreasing platelet aggregation.

Platelet aggregation is an early stage of haemostasis; therefore inhibition of the platelets leads to prevention of thrombus formation.

  Mechanism of action
Aspirin Irreversibly inhibits cyclo-oxygenase, blocking prostaglandin synthesis and therefore stopping the production of thromboxane. Thromboxane is a hormone released from platelets which stimulates platelet aggregation and vasoconstriction.

  • Clopidogrel
  • Prasugrel
  • Ticagrelor
Thienopyridines inhibit the binding of adenosine diphosphate to its P2Y12 receptor on the platelet surface. Consequently, this blocks the activation of the glycoprotein IIb/IIIa pathway, which is required for the final stages of platelet aggregation.

Clopidogrel and prasugrel are both irreversible, whereas ticagrelor is a reversible antagonist (Dobesh and Oestreich, 2014).

Dipyridamole It is thought that dipyridamole blocks the uptake of adenosine into erythrocytes, endothelial cells and platelets. Adenosine is a potent inhibitor of platelet aggregation, therefore by stopping its uptake an increased extracellular concentration of adenosine occurs.
Glycoprotein IIb/IIIa inhibitors Bind to glycoprotein IIb/IIIa receptors on the platelet’s plasma membrane, preventing the binding of von Willebrand factor and fibrinogen (Valgimigli and Cangiano, 2012). This results in inhibition of platelet aggregation and thrombus formation.

Other considerations

Some patients taking antiplatelets or anticoagulants may also suffer from another medical condition that affects their ability to clot, such as those listed below.

Patients at an increased risk of bleeding:

  • Chronic liver failure
  • Liver disease
  • Haematological malignancy
  • Chemotherapy patients
  • Advanced heart failure
  • Inherited bleeding disorders
  • Idiopathic thrombocytopenic purpura.

If a patient is taking single or multiple antiplatelet or anticoagulant medications who have additional co-morbidities, it would be wise to liaise with their doctor to illicit their advice on planning any invasive dental treatments.

Dental procedures that carry a higher risk of post-operative bleeding complications are shown below.

Procedures with an increased risk of bleeding

  • Complex extractions
  • Adjacent extractions (which will result in a large wound)
  • More than three extractions in one appointment
  • Procedures that require a flap to be raised (surgical extractions, periodontal surgery, crown lengthening, implants)
  • Biopsies
  • Gingival recontouring.


  • There are various antiplatelet and anticoagulant medications patients may take
  • The main reason patients are taking these medications is to reduce the risk of suffering from a thromboembolic event
  • It is important to understand the implications these medications have on the dental management of a patient
  • Some patients may also have pre-existing co-morbidities along with receiving antiplatelet or anticoagulant medications which can further impact their ability to clot
  • Dental procedures placing a patient at an increased risk of bleeding are largely surgical, with the exception of multiple extractions.

Catch up with previous Student’s guide

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Ansell JE (2019) Outpatient Oral Anticoagulant Therapy. Consultative Hemostasis and Thrombosis. Elsevier. 747-77

Comin J and Kallmes DF (2012) Dabigatran (Pradaxa). American Journal of Neuroradiology 33: 426-8

DeLoughery TG (2015) Hemostasis and Thrombosis, Third Edition. Springer International Publishing. 125–131

Dobesh PP and Oestreich JH (2014) Ticagrelor: Pharmacokinetics, pharmacodynamics, clinical efficacy, and safety. Pharmacotherapy 34: 1077-90

Hankey GJ and Eikelboom JW (2011) Dabigatran etexilate: A new oral thrombin inhibitor. Circulation 123: 1436-50

Hurst KV, O’Callaghan JM and Handa A (2017) Quick reference guide to apixaban. Vascular Health and Risk Management 13: 263-7

Valgimigli M and Cangiano E (2012) Therapeutic Advances in Thrombosis, Second Edition. Blackwell Publishing Ltd. 87-110

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