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Wound Closure in Older Adults Delayed by Sweat Glands


Annals of Long-Term Care: Clinical Care and Aging. 2016;24(6):36.


ALTC Editors

A group of scientists and dermatologists have, for the first time, identified the cellular mechanisms of altered skin wound repair in elderly patients. The findings of their research was recently published online in Aging Cell (doi: 10.1111/acel.12493).

The researchers had already determined that eccrine sweat glands (ESGs), which are located throughout the body, are important for wound closure; they are major contributors of new cells to replace cells that are lost due to injury. Thus, for this study, researchers concentrated on the healing function of sweat glands in older adults.

Researchers, led by senior author Gary Fisher, PhD, pro- fessor of molecular dermatology at the University of Michi- gan, compared 18 elderly subjects’ (> 70 years old) skin to 18 young adults’ (< 40 years old) skin to see how each group healed from small skin lesions.

Researchers developed a human wound healing model that utilizes a CO2 laser to generate partial-thickness wounds. Wounds created by this procedure are highly reproducible and heal according to a typical repair process that can be read- ily studied. The skin was considered healed when the new growths merged together and the scab fell off the surface.

In young people, they discovered sweat glands contributed more cells to wound closure than in aged adults. Strikingly, in aged skin, although ESG density is unaltered, less than

50% of the ESGs generate epithelial outgrowths during re- pair (vs. 100% in young). Surprisingly, aging does not alter the wound-induced proliferation response in hair follicles or ESGs. Instead, there is an overall reduced cohesiveness of keratinocytes in aged skin. Fewer cells participating, spaced further apart, means a delay in wound closure and a thinner repaired epidermis in aged versus young skin.

In summary, it wasn’t that the sweat glands were less ac- tive in older people, rather, that the environment in the aging skin had been slowly degraded, making the skin structures less able to support the new cells that were generated. By dem- onstrating that reduced ESG outgrowth results from impair- ment of keratinocyte cohesive organization, likely mediated by age-related damage to the underlying ECM, our results highlight the critical importance of the wound environment. Dr Fisher noted: “These important findings could not have been revealed in animal studies because laboratory animals don’t have sweat glands, they don’t sweat like we do.”

These findings provide a framework to better understand the mediators of delayed re-epithelialization in aging and fur- ther support the importance of ESGs for the repair of human wounds. The research team plans to continue investigations in this area with the target of improving aging skin healing. —Amanda Del Signore

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