This high-yield revision note on Gingival Enlargement: Drug-Induced vs Inflammatory vs Neoplastic covers everything examiners typically test under Periodontics — structured as quick-reference tables, clinical correlations, mnemonics and previous-year-style high-yield points. It's built for last-mile revision before NEET MDS, INI-CET MDS and INBDE, so you can scan it in minutes instead of re-reading a whole textbook chapter.
| Type | Cause | Feature |
|---|---|---|
| Inflammatory (chronic) | Chronic plaque-induced gingivitis progressing to fibrotic enlargement | Bleeds easily, soft/edematous initially, becomes fibrotic if long-standing |
| Drug-induced | Phenytoin (anticonvulsant, roughly 50% incidence in long-term users), Cyclosporine (immunosuppressant), Nifedipine and other calcium channel blockers | Begins at the interdental papilla; combines fibrous and vascular components; worsened by poor oral hygiene |
| Hormonal | Pregnancy (pregnancy tumor/pyogenic granuloma - vascular, typically regresses postpartum), Puberty gingivitis | Represents an EXAGGERATED inflammatory response to existing plaque due to hormonal influence, not hormones causing enlargement alone |
| Hereditary gingival fibromatosis | Genetic, autosomal dominant inheritance (commonly linked to the SOS1 gene) | Dense fibrous enlargement that can cover the crowns of teeth; often requires surgical excision (gingivectomy), with a tendency to recur |
| Leukemic gingival enlargement | Especially the AML M4/M5 (monocytic/myelomonocytic) subtypes | Diffuse, boggy, hemorrhagic enlargement representing direct leukemic cell infiltration |
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