Use of Drugs in Dentistry & Drug Reactions in the Mouth – Key Review

A comprehensive set of 50 Q&A flashcards covering definitions, classifications, common oral adverse effects, implicated drug classes, pathophysiology, and significant drug interactions relevant to dentistry.

According to WHO, how is an Adverse Drug Reaction (ADR) defined?

A noxious and unintended drug response that occurs at doses normally used in humans for prophylaxis, diagnosis, therapy, or modification of physiological function.

Which ADR pharmacologic type is dose-related and predictable?

Type A (Augmented) reactions.

Approximately what percentage of ADRs are Type A?

About 80 %.

Which ADR type is non–dose-related, unpredictable, and often includes idiosyncratic reactions?

Type B (Bizarre) reactions.

Name the two broad subdivisions of Type B reactions.

Immunological and non-immunological.

List the additional ADR categories C through F.

C = Dose- and time-related, D = Time-related, E = Withdrawal, F = Unexpected failure of therapy.

Give three common oral ADRs produced by systemic drugs.

Hyposalivation, oral ulcerations, gingival hyperplasia (others include burning mouth, EM, lichenoid reaction, angioedema, etc.).

Roughly how many drugs are known to cause hyposalivation?

More than 500.

Which two large therapeutic classes most frequently cause hyposalivation?

Antihypertensives and psychotropic drugs.

Name four other drug classes that commonly cause dry mouth.

Anticholinergics, antihistamines, benzodiazepines, diuretics (others: PPIs/H2 antagonists, opioids, bronchodilators, etc.).

What oral condition can develop from chronic hyposalivation and present as tongue depapillation?

Atrophic glossitis.

Define hypogeusia, dysgeusia, and ageusia.

Hypogeusia = reduced taste acuity; Dysgeusia = distorted taste perception; Ageusia = complete loss of taste.

State two mechanisms by which drugs alter taste.

(1) Excretion of drug/metabolite in saliva altering its composition or flow; (2) Direct effect on taste receptors or signal transduction.

Which ACE inhibitor commonly causes salty or metallic dysgeusia?

Captopril (others include enalapril).

Burning mouth symptoms are most often associated with which drug class?

ACE inhibitors (e.g., lisinopril, captopril, enalapril).

How soon can burning mouth symptoms appear after starting an offending ACE inhibitor?

A few days to several years after initiation.

Which widely used analgesic class and cardiovascular drug class can induce oral ulceration?

NSAIDs and beta-blockers.

Which antianginal agent is notorious for delayed oral ulcers via its metabolites?

Nicorandil.

Name two immunosuppressive-related mechanisms for oral ulceration.

Viral reactivation (e.g., herpes, CMV) and agranulocytosis (e.g., with phenylbutazone).

List three drug groups frequently linked to drug-related oral ulcerations.

Antihypertensives (nicorandil, captopril), antibiotics (penicillamine, vancomycin), anticonvulsants (carbamazepine, phenytoin).

What is the typical oral presentation of erythema multiforme (EM)?

Bullae and erosions on lips and oral mucosa with possible conjunctival involvement.

Give three drug categories capable of triggering EM.

Analgesics (e.g., diclofenac), anticonvulsants (carbamazepine), antimicrobials (penicillins, tetracyclines).

Which three major drug groups classically cause gingival hyperplasia?

Antihypertensives (calcium channel blockers), anticonvulsants, and cyclosporine.

Which anticonvulsant produces gingival overgrowth via sensitive fibroblast interaction?

Phenytoin.

How does poor oral hygiene influence drug-induced gingival hyperplasia?

It worsens the hyperplasia; frequent dental check-ups are recommended.

State two cardiovascular calcium-channel blockers that can enlarge gingiva.

Amlodipine and nifedipine (others: diltiazem, verapamil).

Describe the latency period for medication-induced oral lichenoid reactions.

Variable; from several weeks to several years after drug initiation.

Name two common drug classes producing oral lichenoid reactions.

NSAIDs and ACE inhibitors.

What pathologic event completes the lichenoid drug reaction cascade?

Apoptosis of basal keratinocytes after T-cell-mediated inflammation.

Identify one antidiabetic and one antimalarial drug associated with lichenoid lesions.

Antidiabetic: metformin; Antimalarial: chloroquine.

Differentiate the three main mechanisms of drug-induced angioedema.

(1) IgE-mediated β-lactam allergy, (2) Non-allergic COX inhibition by NSAIDs/aspirin causing leukotriene excess, (3) Bradykinin accumulation from ACE-inhibitor therapy.

Which mediator’s impaired degradation is implicated in ACE inhibitor angioedema?

Bradykinin.

Give two antibiotics and two NSAIDs that can cause angioedema.

Antibiotics: penicillin derivatives, clindamycin; NSAIDs: aspirin, ibuprofen.

List three heavy metals whose intoxication can discolor oral mucosa.

Bismuth, lead, silver (others: copper, iron, gold).

Explain two general mechanisms of drug-induced oral pigmentation.

(1) Accumulation/deposition of drug or metabolites; (2) Melanin or iron deposition following vascular damage or stimulated pigment synthesis.

Which tetracycline analogue is notorious for oral mucosal pigmentation?

Minocycline.

Define oral mucositis and name three chemotherapeutic agents that cause it.

Inflammation/ulceration of oral mucosa due to chemotherapeutic damage to rapidly dividing epithelial cells; examples: 5-fluorouracil, methotrexate, doxorubicin.

Which two antiresorptive drug classes are linked to osteonecrosis of the jaws?

Bisphosphonates and denosumab.

What oral presentation characterizes medication-related osteonecrosis?

Exposed bone or a non-healing extraction socket.

Why do anti-VEGF agents like bevacizumab heighten osteonecrosis risk?

They possess anti-angiogenic properties, impairing blood supply and healing.

How can broad-spectrum antibiotics predispose to oral candidiasis?

They disturb normal oral flora, allowing Candida overgrowth.

Which biologic TNF-α inhibitor therapy raises risk for TB and meningitis?

TNF-α inhibitors (e.g., infliximab, etanercept).

Why should dentists warn patients on oral contraceptives who receive rifampin?

Rifampin lowers estrogen plasma levels, reducing contraceptive effectiveness.

What serious interaction exists between macrolide antibiotics and statins?

Inhibition of statin metabolism increases risk of myalgia, rhabdomyolysis, and renal failure.

Which dental antibiotic should be avoided in a patient on theophylline and why?

Erythromycin—raises theophylline levels leading to toxicity (nausea, arrhythmias, seizures).

What precaution accompanies metronidazole use concerning alcohol?

Avoid alcohol due to severe disulfiram-like reaction.

Name one NSAID interaction that diminishes antihypertensive control.

NSAIDs reduce the effect of beta-blockers or ACE inhibitors, elevating blood pressure.

Why should high-dose methotrexate patients not receive doxycycline?

Doxycycline can raise methotrexate levels, risking toxicity.

State the risk of combining SSRIs with chronic NSAID therapy.

Increased risk of peptic ulcers and GI bleeding.

How can acetaminophen >2 g daily for >1 week affect a patient on warfarin?

It may increase bleeding risk; INR monitoring is advised.

What anesthetic–analgesic pair may precipitate seizures, especially in elders?

Lidocaine with tramadol.

List two drugs that slow benzodiazepine metabolism, heightening sedation.

Cimetidine and azole antifungals (e.g., ketoconazole).