Gingival Enlargement: Dental Case #56

The finding that gives this away is the gap. His teeth are not getting shorter — the tissue around them is getting taller — and the distribution of that tissue is the whole answer. Everywhere he has teeth, the gum is grossly enlarged; in the edentulous span in his lower left, where two teeth came out years ago, the ridge is flat and completely healthy, sitting between two badly affected segments. This condition is not observed in edentulous areas and disappears when teeth are extracted, so a span that is spared while its neighbours are not tells you the process depends on the presence of teeth. Two further features locate it precisely. It began at the interdental papillae and spread outwards to the facial and lingual margins, and it stops at the boundary of the keratinised attached gum without crossing onto the looser lining mucosa. The anterior segments are worse than the posterior, which is also characteristic. And the tissue is firm and pale rather than red and friable, because the pathology is in connective tissue rather than epithelium — an excessive accumulation of extracellular matrix-like collagen, which is why the old name "hyperplasia" is a misnomer and why this does not look like inflammation even when inflammation is layered on top. The cause is on his repeat prescription. Three drug classes are responsible with different frequencies: anticonvulsants, where 50% of adults treated with phenytoin develop it; immunosuppressants, at 30% with cyclosporine; and calcium channel blockers, at 20% with nifedipine, with amlodipine the other primary agent of that class. He started amlodipine five months ago, and onset typically follows 1 to 3 months after the responsible drug is begun, with amlodipine reported within two months — which matches his four-month history exactly. The radiographs earn their place by excluding the diagnosis everyone reaches for first: crestal bone is at normal height with an intact lamina dura, so this is soft tissue piled on top of healthy bone rather than tissue collapsing around bone that has been destroyed. Management has two halves and he has been quietly sabotaging one of them. Severity is directly proportional to the degree of plaque build-up, and he has been avoiding brushing the area precisely because it bleeds — so the first step is plaque control, uncomfortable though it is. The second is substituting the responsible drug where the prescriber can: phenytoin for carbamazepine or valproic acid, nifedipine for diltiazem or verapamil, cyclosporine for tacrolimus, with an azithromycin combination shown to reduce severity. If surgery is eventually needed, the result typically lasts at least 12 months — and lasts longer if the drug and the plaque have both been dealt with first.