Friction removes nascent epithelium

In aging human skin, a proposed mechanism asks why superficial injuries can remain slow to close after maintenance gaps even when sweating and uninterrupted repair appear normal. The idea is that ordinary friction may repeatedly strip away newly formed epithelium, the thin cell layer rebuilding the wound surface, before it anchors firmly. Each interruption could erase some repair progress and force the surface to start again. A future comparison would match heat exposure, friction dose, sweat chemistry and systemic support. It would contrast frequent interruptions with the same friction dose outside one protected repair interval. Longer recovery plus serial images showing lost new coverage would support the hypothesis.