Systemic Inflammation and Hair Follicle Homeostasis: Implications for Scalp Health and Hair Disorders

Abstract

Low-grade systemic inflammation has been implicated in several chronic conditions and may influence peripheral tissues through circulating cytokines, metabolic mediators, oxidative stress and altered immune signalling. The hair follicle is an immunologically active mini-organ whose homeostasis depends on interactions between epithelial, mesenchymal and immune cells. This mini-review examines the evidence linking systemic inflammation, the scalp microenvironment and follicular function in alopecia areata, androgenetic alopecia, telogen effluvium, scalp psoriasis and seborrhoeic dermatitis. Ex vivo data show that pro-inflammatory cytokines can inhibit human hair follicle growth, and the efficacy of systemic Janus kinase inhibition supports a central role of immune dysregulation in alopecia areata. In androgenetic alopecia, perifollicular microinflammation, prostaglandin D2 and metabolic syndrome are associated with the disease, but the evidence does not establish systemic inflammation as a primary cause of follicular miniaturization. In telogen effluvium, systemic inflammatory events such as febrile illness and COVID-19 can act as triggers, although no specific inflammatory biomarker exists. Scalp psoriasis and seborrhoeic dermatitis illustrate the need to distinguish local scalp inflammation from concomitant systemic changes. C-reactive protein, interleukin-6 and haematological inflammation indices are of translational interest but lack the specificity required to diagnose or monitor alopecia. Because most clinical studies are cross-sectional, longitudinal studies combining standardized biomarkers with clinical and quantitative trichoscopic endpoints are needed to determine when systemic inflammation is merel