How Inflammation Affects Hair
Inflammation directly damages hair follicles through three distinct mechanisms: it triggers immune-mediated destruction of follicular structures, disrupts the normal hair growth cycle by pushing follicles prematurely into the shedding phase, and impairs nutrient delivery to hair follicles through systemic metabolic effects. 1, 2, 3
Mechanism 1: Direct Follicular Damage Through Immune Attack
Inflammation weakens hair follicles by causing lymphocytic infiltration that targets critical follicular structures, particularly the bulge epithelium and infundibulum. 4, 5
T-lymphocytes directly attack hair follicles in inflammatory conditions like alopecia areata, creating perifollicular inflammatory infiltrates composed of lymphocytes and histiocytes that physically damage the follicular architecture. 2, 4
Early inflammatory changes show epithelial cell damage in the hair follicle infundibulum (just above the sebaceous gland), with liquefaction and disarrangement of peripheral infundibular epithelial cells occurring alongside T-lymphocytic invasion. 5
The inflammatory infiltrate specifically targets the bulge epithelium, which houses hair follicle stem cells essential for regeneration, thereby compromising the follicle's ability to produce healthy hair shafts. 4
Inflammatory genes including CASP7 and TNF are upregulated in pattern hair loss, contributing to follicular miniaturization and progressive weakening of hair production. 2
Mechanism 2: Disrupted Nutrient Absorption and Metabolic Effects
Systemic inflammation impairs nutrient availability to hair follicles through redistribution of essential micronutrients and altered metabolic pathways. 6
Zinc concentrations in serum decrease rapidly during the acute phase inflammatory response, with plasma zinc falling significantly whenever CRP exceeds 20 mg/L due to redistribution from plasma albumin to the liver where it binds to metallothionein. 6
This inflammation-induced zinc redistribution occurs very quickly (demonstrated in perioperative studies) and normalizes only with clinical improvement, creating a functional deficiency state even when total body zinc stores may be adequate. 6
Reduced circulating zinc correlates with increased inflammatory cytokines (IL-6, IL-8, and TNF-α), creating a vicious cycle where inflammation depletes zinc and zinc deficiency perpetuates inflammation. 6
Chronic zinc deficiency specifically increases inflammation while acute deficiency decreases both innate and adaptive immunity, affecting T-cell functions that are particularly susceptible to zinc status changes. 6
Severe zinc deficiency manifests clinically with alopecia as a cardinal feature, alongside skin rash, growth retardation, and impaired immune function. 6
Mechanism 3: Premature Transition to Telogen (Shedding Phase)
Inflammation accelerates the anagen-to-telogen transition, forcing actively growing hair follicles prematurely into the resting and shedding phases. 3, 7
Multiple inflammatory triggers—including systemic inflammation, hormonal changes, stress, and nutritional deficiencies—promote the transition from anagen (growth phase) to telogen (resting phase), with 9% of follicles normally in telogen but this percentage dramatically increasing under inflammatory conditions. 3
Inflammation fundamentally disrupts normal hair biology by altering the delicate balance between growth and rest phases, with the relative contributions varying between individuals and over time. 7
Perivascular mononuclear cell infiltration in the upper dermis correlates with regression of the lower follicle, demonstrating how upper dermal inflammation translates to disrupted hair cycling. 5
Eosinophilic infiltration (present in 40% of early alopecia areata cases) correlates with more severe perivascular lymphocytic inflammation and prominent peri-follicular infiltration, amplifying the telogen-promoting effects. 5
Clinical Implications and Common Pitfalls
The inflammatory component of hair loss is often underrecognized in common conditions like androgenetic alopecia, where significant perifollicular inflammatory infiltrates are present alongside the hormonal component. 2, 4
Measuring serum zinc during active inflammation is problematic because CRP >20 mg/L causes artifactually low zinc values through redistribution rather than true deficiency, requiring simultaneous CRP and albumin measurement for proper interpretation. 6
Cases showing positive immunoreactant profiles (IgM deposits in epidermal basement membrane zone with complement activation) respond better to combined anti-inflammatory therapy with minocycline and topical steroids compared to those with negative immunoreactant profiles. 4
Inflammation in the upper dermis with damage to the hair follicle infundibulum may be an important early component of hair loss pathogenesis, possibly involving both hypersensitivity and autoimmune mechanisms. 5