Creative Touch Permanent Makeup and Aesthetics

Testosterone is the primary circulating androgen in both sexes, produced in the testes, ovaries, and adrenal cortex, and responsible for several distinctive features of male skin biology: greater dermal thickness, higher collagen density, and substantially higher sebum output. Its direct effects on skin are mediated through androgen receptor binding; many of its most clinically significant skin effects, however, are exerted not by testosterone itself but by dihydrotestosterone (DHT), the locally amplified metabolite produced when 5-alpha reductase converts testosterone within skin tissue. Testosterone’s relationship with wound healing is genuinely complex. Androgen receptor signalling promotes the inflammatory response through macrophage TNF-α activity, with evidence showing delayed healing in standard dermal wounds but enhanced collagen deposition in burn injuries, making straightforward characterisation as either beneficial or detrimental inaccurate.

Testosterone is an 19-carbon steroid hormone and the principal androgen in human physiology, produced primarily in the testes in males and in the ovaries and adrenal cortex in females, where it circulates at roughly one tenth of male concentrations but remains physiologically active. It signals through androgen receptors (AR), which are expressed in dermal fibroblasts, keratinocytes, sebocytes, and hair follicle dermal papilla cells throughout the skin. Androgen receptor binding triggers genomic signalling – transcription factor activity altering gene expression over hours, as well as faster non-genomic pathways operating through calcium mobilisation and kinase cascades. The net effect of testosterone on skin is not uniform: it promotes dermal thickness and collagen density, drives sebaceous gland activity, and modulates wound healing in ways that depend heavily on wound type and tissue context. ^[2]

Skin Thickness and Collagen

Male skin is measurably thicker than female skin by approximately 20–25%, maintaining higher collagen density across most of adult life. Testosterone is the primary hormonal driver of this difference, promoting fibroblast activity and collagen synthesis through androgen receptor signalling. Male skin thickness declines linearly from approximately the third decade onward, whilst female skin thickness remains relatively stable until the perimenopausal period, after which it decreases more rapidly in association with oestrogen and testosterone withdrawal. The practical consequence is that men accumulate dermal structural loss gradually and continuously, whilst women experience a more concentrated period of accelerated structural decline around menopause, a distinction that influences how ageing presents clinically across sexes. ^[3]

Sebaceous Gland Activity

Testosterone drives sebaceous gland proliferation and sebum production through androgen receptor activation in sebocytes. Males produce up to four times more sebum than females, accounting for characteristically larger pores, oilier surface skin, and the greater sebum-dependent surface lipid film. Male sebum output remains relatively constant throughout adult life; female sebum production varies with ovulatory cycle phases and declines after menopause. Whilst testosterone initiates this signalling, the predominant local driver of sebaceous gland activity in skin is dihydrotestosterone (DHT), the 5-alpha reduced metabolite produced within sebaceous glands by type 1 5-alpha reductase. Testosterone is the circulating precursor; DHT is the locally amplified effector. ^[4]

Wound Healing: Context-Dependent Effects

Testosterone’s relationship with cutaneous wound healing is genuinely complex and resists simple characterisation. Androgen receptor signalling in macrophages promotes TNF-α production and macrophage recruitment to wound sites, amplifying the inflammatory phase of healing. In standard dermal wound models, this elevated inflammation is associated with delayed healing – elderly males with higher systemic testosterone show slower wound closure and collagen deposition than age-matched females, a difference that correlates with tissue TNF-α expression. ^[1] In major burn injury, however, DHT treatment produced substantially greater collagen type I and III upregulation and accelerated tissue remodelling compared to control – suggesting that wound type, depth, and the inflammatory environment determine whether androgen receptor signalling is net-harmful or net-beneficial to healing. Presenting testosterone’s wound healing effects as uniformly inhibitory or uniformly beneficial misrepresents a context-dependent picture.