Table 3.

Potential interactions of oral anticoagulants with drugs used or prescribed in dentistry.

Drug	Via	Dabigatran	Rivaroxaban	Apixaban	Edoxaban
Antacids (H2B; PPI; Al-Mg-hydroxide)	GI absorption	−12/30% PDC (no clinical effect)	No effect	No effect	No effect
Itraconazole Ketoconazole Posaconazole Voriconazole	potent P-gp and BCRP competition; CYP3A4 inhibition	+140/150% PDC CONTRA-INDICATED	Up to +160% PDC CONTRA-INDICATED	+100% PDC CONTRA-INDICATED	+87–95% PDC Reduce DOAC dose
Fluconazole	Moderate CYP3A4 inhibition	No data	+42% PDC Consider DOAC dose reduction	No data	No data
Clarithromycin Erythromycin	moderate P-gp competition and CYP3A4 inhibition	+15–20% PDC Consider DOAC dose reduction	+30–54% PDC Consider DOAC dose reduction	No data	+90% PDC Reduce DOAC dose
Rifampicin	P-gp/ BCRP and CYP3A4 inducer	−66% PDC CONTRA-INDICATED	Up to −50% PDC CONTRA-INDICATED	−54% PDC CONTRA-INDICATED	−35% PDC, but with compensatory Increase of Active Metabolites AVOID IF POSSIBLE
Non-COX-selective NSAIDs (Naproxen Ibuprofen, Ketoprofen, Fenoprofen, Flurbiprofen) and salicylates	P-gp competition and pharmaco-dynamic interaction	GI and peptic ulceration and/or perforation, +60% BR AVOID IF POSSIBLE
NSAIDs	Pharmacodynamic Interaction	Increased BR AVOID IF POSSIBLE	Increased BR AVOID IF POSSIBLE	Increased BR AVOID IF POSSIBLE	Increased BR AVOID IF POSSIBLE
Opioid			Increased BR AVOID IF POSSIBLE

BCRP: breast cancer resistance protein; BR: bleeding risk; NSAID: non-steroidal anti-inflammatory drugs; H2B: H2-blockers; PPI: proton pump inhibitor; GI: gastrointestinal; PDC: plasma drug concentration; P-gp: P-glycoprotein.