Keloids are common in the skin types most Indian dermatologists see, recur after almost every intervention, and have no drug developed specifically for them. This review pulls together what multiomic work has added to the picture.
The familiar description — fibroblast overproduction, excess extracellular matrix, persistent inflammation and growth beyond the original wound — now has cell populations and signalling networks attached to it. Three strands are highlighted as newer: adipocyte lipolysis as a modulator of repair, epigenetic regulation by microRNAs, and disrupted vitamin D signalling. Genetic studies continue to implicate heritable risk, consistent with the familial clustering seen in clinic.
No clinical data, no numbers, no treatment recommendation — it is an orientation to a field rather than a result. Its usefulness for a practising dermatologist is limited but real: it explains why single-modality treatment keeps failing, and why the disrupted vitamin D signalling strand is worth watching in a population where deficiency is widespread. Management today remains what it was: intralesional triamcinolone with or without 5-fluorouracil, silicone, pressure, and surgery only with adjuvant therapy planned in advance.
- Nothing here changes treatment: intralesional steroid with or without 5-fluorouracil remains first line
- Never excise a keloid without an adjuvant plan agreed before the operation
- Take a family history — heritable risk is consistently implicated
- Counsel prevention in high-risk patients: avoid elective piercings and non-essential procedures on chest and shoulders
- Watch the vitamin D signalling strand, but do not treat keloids with vitamin D on this basis
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