Drugs the Dentist Meets in Medical History MCQ

This is the capstone where pharmacology meets the dental medical history. The drugs the patient brings in change the chairside plan more often than the drugs the dentist writes. Anticoagulants and antiplatelets are usually continued for simple extractions with local hemostasis. Antihypertensives change the epinephrine plan, and three drug classes cause the classic gingival enlargement triad. Chronic corticosteroids suppress the adrenal axis and require stress-dose attention in severe physiologic stress. Bisphosphonates and denosumab raise MRONJ risk, best prevented by completing extractions before therapy begins. Diabetes medications bring chairside hypoglycemia risk plus the SGLT2 and GLP-1 wrinkles. Chemotherapy, chronic NSAIDs/PPIs, and immunosuppressants round out the medical-history review every dentist must do before instrumenting.

Anticoagulants and Antiplatelets

• Warfarin inhibits vitamin K epoxide reductase, lowering vitamin K-dependent clotting factors (II, VII, IX, X) and proteins C and S; effect is monitored by the INR.
• Direct oral anticoagulants (DOACs) include apixaban and rivaroxaban (direct factor Xa inhibitors) and dabigatran (direct thrombin inhibitor); they do not require INR monitoring and have shorter half-lives; reversal agents are andexanet alfa (Xa inhibitors) and idarucizumab (dabigatran).
• Heparins activate antithrombin III (unfractionated raises both anti-IIa and anti-Xa; low-molecular-weight enoxaparin is mostly anti-Xa); protamine is the reversal agent.
• Antiplatelets include aspirin (irreversibly acetylates platelet COX-1 for the platelet lifespan, 7-10 days), clopidogrel and prasugrel (P2Y12 ADP-receptor antagonists; clopidogrel needs CYP2C19 activation), and ticagrelor (reversible P2Y12 antagonist).
• For simple extractions, warfarin (INR in range) and the usual antiplatelets are typically continued with local hemostasis (pressure, oxidized cellulose, sutures, tranexamic acid rinse where appropriate) rather than stopped, because stopping risks thromboembolism that usually outweighs controllable bleeding risk.

Antihypertensives

• Beta-blockers split into non-selective (propranolol, nadolol, timolol) and cardioselective (metoprolol, atenolol, bisoprolol, esmolol); non-selective agents create the classic dental epinephrine interaction (hypertensive response with reflex bradycardia from unopposed alpha-1 vasoconstriction).
• ACE inhibitors (lisinopril, enalapril) block conversion of angiotensin I to II and inhibit bradykinin breakdown; the dry cough comes from bradykinin accumulation, and angioedema is the dangerous version that can present in the oral cavity and airway.
• Angiotensin II receptor blockers (ARBs: losartan, valsartan) are used when ACE inhibitors are not tolerated (less cough; angioedema possible but less common).
• Calcium channel blockers split into dihydropyridines (amlodipine, nifedipine, peripheral vasodilation, ankle edema) and non-dihydropyridines (verapamil, diltiazem, more cardiac effects); nifedipine is the classic CCB cause of gingival enlargement.
• Thiazides and loop diuretics drop intravascular volume; NSAIDs blunt their antihypertensive effect.

Statins, Diabetes Drugs, Corticosteroids

• Statins inhibit HMG-CoA reductase, lowering LDL; myopathy and rhabdomyolysis are the headline adverse effects, and CYP3A4 inhibitors (macrolides, azoles, grapefruit) raise simvastatin/atorvastatin levels and rhabdomyolysis risk.
• Metformin lowers hepatic gluconeogenesis (does not cause hypoglycemia on its own); rare lactic acidosis is the headline. Sulfonylureas (glipizide, glyburide) raise insulin release and CAN cause hypoglycemia chairside. Insulin causes hypoglycemia. The hypoglycemia caveat: confirm the patient has eaten, monitor symptoms, and keep oral glucose ready.
• SGLT2 inhibitors (empagliflozin, dapagliflozin) cause urinary glucose loss and rare euglycemic DKA (especially around surgery, fasting, and illness); current peri-procedural guidance is to hold them before major surgery.
• GLP-1 receptor agonists (semaglutide, liraglutide, tirzepatide) delay gastric emptying; current guidance addresses aspiration risk under deep sedation or general anesthesia; coordinate hold timing with the medical team.
• Chronic corticosteroid use (more than ~5 mg prednisone/day for more than ~3 weeks) suppresses the hypothalamic-pituitary-adrenal axis; in major physiologic stress (severe surgery, sepsis), stress-dose steroids may be needed to prevent adrenal crisis. Routine dental work generally does NOT require stress dosing; continue the usual dose.

Bisphosphonates, Denosumab, and the Gingival Enlargement Triad

• Bisphosphonates (alendronate, zoledronate) and the RANKL inhibitor denosumab suppress osteoclast activity and bone remodeling; MRONJ (medication-related osteonecrosis of the jaw) is the dental risk, much higher with intravenous antiresorptives for cancer than with oral bisphosphonates for osteoporosis.
• MRONJ prevention is the answer: complete any needed extractions and bony procedures BEFORE antiresorptive therapy begins; once on therapy, conservative care, atraumatic technique, and informed consent for any bony procedure.
• Three drug classes cause the classic gingival enlargement triad: phenytoin (anti-seizure), cyclosporine (immunosuppressant after transplant), and calcium channel blockers (especially nifedipine).
• Management is plaque control plus medication review with the physician to consider a substitute (when possible); surgical excision (gingivectomy) for residual fibrotic overgrowth.

Chemotherapy, Chronic Acid Suppression, Immunosuppressants

• Chemotherapy produces oral mucositis (5-FU, methotrexate are particularly notorious), neutropenia (raising infection risk; check absolute neutrophil count before invasive dentistry), and thrombocytopenia (check platelet count; usually want >50,000 for simple extractions in coordinated cancer care).
• Methotrexate is also used at lower doses for rheumatologic disease; folate supplementation reduces mucositis and other side effects.
• Long-term proton pump inhibitors (omeprazole) and H2 blockers (famotidine) reduce gastric acid; pure dental implications are modest, but they contribute to vitamin B12 and calcium concerns over years.
• Immunosuppressants beyond cyclosporine include tacrolimus (the modern transplant standard; gingival enlargement is uncommon with tacrolimus, distinguishing it from cyclosporine), mycophenolate, basiliximab (induction), and the corticosteroid taper. Active immunosuppression raises infection risk; coordinate elective dental work with the transplant team.

The Capstone Message

• Most dental drug interactions live in the medical history, not in the new prescription.
• A thorough medication review at every visit is the single highest-yield intervention in dental pharmacology safety.
• Coordinate with the physician for major changes (anticoagulant adjustment, steroid stress dosing, antiresorptive therapy before extractions, oncology timing).
• Local hemostasis, capped epinephrine, plaque control, and early recognition of angioedema, hypoglycemia, adrenal crisis, and MRONJ make up the everyday pharmacology of the dental chair.