Scalp inflammation

Scalp inflammation refers to a pathological state involving the activation of immune pathways, infiltration of immune cells, and/or the upregulation of pro-inflammatory cytokines within the scalp skin and hair follicles. It is not a molecule or receptor but a clinical descriptor that encompasses diverse etiologies including autoimmune attack (as in alopecia areata), microbial imbalance (dysbiosis), neurogenic inflammation (as in stress-induced hair loss), and chronic skin diseases such as psoriasis or seborrheic dermatitis. Cellular mediators involved include T cells, cytokines (such as IL-6, TNF-α, TGF-β), and neuropeptides (substance P). The pathophysiology is heterogeneous and can involve disruption of local hair follicle immune privilege, dysregulated growth factor signaling, and impaired skin barrier function. Many therapeutic approaches for scalp conditions with inflammatory components (e.g., alopecia areata, scarring alopecia, seborrheic dermatitis) target upstream mediators like cytokines, the JAK-STAT pathway (e.g., JAK inhibitors), androgen receptor signaling (e.g., 5α-reductase inhibitors, anti-androgens), or immune cell infiltration. Drugs used in treatment include corticosteroids, immunomodulators (such as JAK inhibitors or cyclosporine), antiandrogens (finasteride), antibiotics or antifungals (when microbial dysbiosis is a component), minoxidil, biologics (in severe cases of psoriasis), and platelet-rich plasma (PRP). These drugs do not act on a single canonical "scalp inflammation" molecular target but on diverse pathways or effector molecules underlying the inflammatory response. In summary, "scalp inflammation" is not a druggable molecular target, but rather a clinical condition arising from the dysregulation of multiple molecular pathways; it is scientifically incorrect to list it as a discrete target like a receptor or enzyme.

Other names

Scalp dermatitisScalp inflammatory diseaseInflammatory scalp alopecia