Periodontics · patient case with 3 questions
Generalized gingival enlargement in a patient on multiple medications
Patient: Male, 45 years old
Chief Complaint: “My gums are growing over my teeth.”
Background: Epilepsy controlled on phenytoin for nine years. Hypertension on amlodipine. Renal transplant six years ago, on ciclosporin. Irregular brushing, no interdental cleaning.
Vital Signs: BP 136/86 mmHg · HR 76 bpm · T 98.2°F
Findings: Firm, pale, stippled gingival enlargement beginning at the interdental papillae and extending to cover up to a third of several clinical crowns, most marked anteriorly and on the labial surfaces. Heavy plaque and calculus. No ulceration, no fever, no lymphadenopathy.
Question 1
Where does drug-influenced gingival enlargement characteristically BEGIN?
Show answer and explanation
Correct answer: D. At the interdental papilla and free gingival margin
- A. The attached gingiva may become involved as the lesion enlarges, but it is not where the process starts, and involvement is secondary.
- B. The mucogingival junction is the boundary between keratinized attached gingiva and alveolar mucosa. Drug-influenced enlargement characteristically STOPS at this line rather than starting there — a useful diagnostic feature, since it distinguishes the condition from diffuse swellings that cross it.
- C. Alveolar mucosa is non-keratinized and lies beyond the mucogingival junction. Drug-influenced enlargement does not involve it.
- D. CORRECT. Enlargement begins as a painless beadlike swelling of the INTERDENTAL PAPILLA and the FREE (marginal) gingiva. The papillae enlarge first, then coalesce with the marginal tissue to produce a lobulated mass that can cover the crowns. The anterior labial gingiva is affected most, and the process does not extend beyond the mucogingival junction.
Note: All three drug classes are represented in this patient and they act on the same target: ANTICONVULSANTS (phenytoin, roughly 50% of users), CALCIUM CHANNEL BLOCKERS (nifedipine, amlodipine, around 10–20%) and IMMUNOSUPPRESSANTS (ciclosporin, about 25–30%; tacrolimus much less). Ciclosporin combined with a calcium channel blocker is the highest-risk combination of all — as here.
Question 2
All of the following belong in the differential diagnosis of gingival ENLARGEMENT of this type EXCEPT:
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Correct answer: A. Primary herpetic gingivostomatitis
- A. CORRECT as the exception. PRIMARY HERPETIC GINGIVOSTOMATITIS is an acute VESICULO-ULCERATIVE infection — a febrile child or young adult with painful vesicles that rupture into shallow ulcers, fiery erythematous gingiva, malaise and cervical lymphadenopathy. It causes acute inflammatory erythema and oedema, not the firm fibrous overgrowth described here, and it resolves within ten to fourteen days.
- B. Scurvy produces swollen, spongy, haemorrhagic gingiva from defective collagen cross-linking. It is soft and bleeds readily rather than firm, but it belongs in the differential of an enlarged gingiva.
- C. Hereditary gingival fibromatosis gives generalized, firm, pale, dense fibrous enlargement that may bury the crowns entirely. It appears around the time of eruption and is the non-drug mimic of this presentation.
- D. Leukaemia, particularly acute myelomonocytic leukaemia, produces gingival enlargement by direct infiltration with leukaemic cells. It is boggy, bluish-red and bleeds easily, and it is the diagnosis you must not miss.
Note: Sort the differential by CONSISTENCY. FIRM and fibrous: drug-influenced enlargement, hereditary gingival fibromatosis. SOFT and haemorrhagic: scurvy, leukaemic infiltration, pregnancy-associated enlargement. ACUTE and ulcerated: herpetic gingivostomatitis, necrotizing gingivitis — these are not enlargements at all.
Question 3
What is the appropriate FIRST step in managing this enlargement?
Show answer and explanation
Correct answer: B. Rigorous plaque control with scaling and root planing, alongside liaison with his physicians about substituting the causative drugs
- A. Gingivectomy performed while plaque control remains poor and the drugs continue unchanged has a high recurrence rate. Surgery may still be needed, but it is the SECOND step, not the first.
- B. CORRECT. PLAQUE IS THE MODIFYING FACTOR. The drug creates susceptibility, but the degree of enlargement tracks the inflammatory burden — which is why meticulous scaling, root planing and oral hygiene instruction produce genuine reduction on their own. In parallel, consult the prescribing physicians: valproate or levetiracetam can replace phenytoin, a non-dihydropyridine antihypertensive can replace amlodipine, and tacrolimus causes far less enlargement than ciclosporin. Re-evaluate after resolution of inflammation and only then decide whether residual fibrous tissue needs excision.
- C. Apically positioned flap surgery with osseous recontouring addresses pocket elimination in periodontitis with bony defects. This patient has pseudopockets from enlarged tissue, not intrabony defects.
- D. Metronidazole treats anaerobic infection. Some studies report modest reduction in ciclosporin-associated enlargement, but it is adjunctive at best and is not the first step.
Note: Sequence: plaque control and drug substitution first; re-evaluate at six to eight weeks; then excise residual fibrous tissue by gingivectomy for accessible enlargement, or by an internal-bevel flap where attached gingiva is limited or bone must be exposed. Without ongoing plaque control after surgery, it recurs.