Inflammation's Role in AGA: Microinflammation Beyond Just Hormones

Histological studies of AGA scalp consistently show lymphocytic infiltrates around miniaturised follicles. The DHT narrative is incomplete — inflammation is an active participant, not a bystander.

The androgenetic alopecia narrative — DHT acts on genetically sensitive follicles via androgen receptors, causing progressive miniaturisation — is accurate but incomplete. Histological studies have consistently documented a microinflammatory component that contributes to the AGA process and may help explain why DHT suppression alone does not produce complete recovery in many patients.

The histological evidence

Scalp biopsies from men with AGA, when processed with appropriate horizontal sectioning and immune staining, reveal perifollicular lymphocytic infiltrates — clusters of CD4+ T cells, mast cells, and dendritic cells surrounding follicular infundibula — in a significant proportion of cases. These infiltrates are not a universal finding (approximately 10–40% of biopsies in various series) but are consistently more common and more severe in biopsies from actively miniaturising and advanced AGA scalp than in non-balding scalp.

The inflammatory infiltrates are located specifically around the upper follicle — the infundibulum and isthmus — rather than the follicle bulb, distinguishing them from the follicle-destructive inflammation of alopecia areata (where the attack targets the bulb). Their anatomical position around the permanent portion of the follicle, including the vicinity of the bulge, suggests that chronic inflammation may compromise bulge stem cell niche integrity over time.

What triggers the microinflammation

The inflammatory trigger in AGA scalp is likely multifactorial:

Malassezia: The commensal scalp yeast produces lipases that metabolise sebum, generating free fatty acids that penetrate into the follicle and trigger keratinocyte inflammatory signalling. Malassezia colonisation is heavier in sebaceous-rich AGA scalp.

Sebum components: Oxidised squalene and other sebum degradation products have direct proinflammatory effects on follicular keratinocytes.

Physical trauma: The mechanical stress on the follicle infundibulum from repeat brushing, styling, and daily physical impact may chronically stress the follicle wall.

The microinflammation-fibrosis link

Perifollicular lymphocytes and mast cells secrete profibrotic mediators — TGF-beta1 in particular — that activate perifollicular fibroblasts to deposit excess collagen. The microinflammatory infiltrates are therefore not merely coincidental to AGA progression; they may be the proximal trigger for the perifollicular fibrosis that limits recovery in advanced disease. Treating the microinflammatory component may thus provide an anti-fibrotic benefit independent of DHT suppression.