Send to

Choose Destination
See comment in PubMed Commons below
Med Hypotheses. 2008 Oct;71(4):493-500. doi: 10.1016/j.mehy.2008.05.020. Epub 2008 Jul 9.

Keloid and hypertrophic scarring may result from a mechanoreceptor or mechanosensitive nociceptor disorder.

Author information

  • 1Department of Plastic, Reconstructive and Aesthetic Surgery, Nippon Medical School, 1-1-5 Sendagi Bunyko-ku, Tokyo 113-8603, Japan.


Keloid and hypertrophic scars (HSs) are fibroproliferative diseases (FPDs) of the skin. It is well known that stretching tension of skin, in other words mechanical force (mechanical loading, mechanical stress) on the skin, is an important factor that promotes their growth. Currently, the widely held view is that while mechanical force is a factor that aggravates keloid/HS growth after their induction, it is not a causative factor. However, there is no evidence that supports this view and recent observations from studies of keloids/HSs suggest that mechanical force in fact not only promotes the growth of such scars, it also drives their generation. Here, I hypothesize that FPDs of the skin, including keloids and HSs, are the result of an excessive responsiveness or functional failure of either dermal cell mechanoreceptors (mechanosensors) or mechanosensitive nociceptors of sensory fibers in the skin. In other words, FPDs of the skin are mechanoreceptor/mechanosensor or mechanosensitive nociceptor (mechanosensory) disorders, respectively. Moreover, by examining the site specificity of keloids, I show that stretching tension may be a major mechanical force that drives their generation. While further experimental studies of signaling pathways related to mechanotransduction, mechanosensitive (MS) channels, cell adhesion molecules, and cytoskeleton dynamics are needed, this hypothesis may provide new insights into the etiology and pathology of FPDs of the skin such as keloids and HSs.

[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Support Center