Rodent Ulcers

UVB radiation carries enough energy to fuse adjacent pyrimidine bases in a DNA strand, creating cyclobutane pyrimidine dimers that the cell’s repair machinery must correct. If repair fails, mutations accumulate, most critically in PTCH1, the gatekeeper gene for the Hedgehog signalling pathway. Without functional PTCH1, the pathway runs unchecked, driving basal keratinocytes into uncontrolled proliferation.

BCC grows slowly, often presenting for years as nothing more than a small pearly nodule with fine surface vessels. As the tumour expands, its centre outgrows its blood supply, ischaemic necrosis sets in, and the surface breaks down into the classic ulcer – rolled edges, crusting, intermittent bleeding. The historical term “rodent ulcer” captures it well: a wound that gnaws quietly through tissue without much outward drama.

Neglected or mismanaged, the ulcer deepens into subcutaneous tissue, cartilage, or bone, secondary infection takes hold, and well-intentioned interventions accelerate the deterioration. Topical steroids thin the surrounding skin and suppress immune surveillance; Betadine, despite its antiseptic rationale, is cytotoxic to the fibroblasts and keratinocytes that might otherwise support any residual healing.

By the time surgical intervention arrives, what could have been a straightforward excision has become a reconstruction problem.