Perifollicular Lymphocytic Inflammation and Fibrosis in Dissecting Cellulitis: Evidence of a Consistent Histopathologic Pattern.
Source: PubMed, NCBI / U.S. National Library of Medicine
Dissecting cellulitis of the scalp (DCS) is a chronic, relapsing, suppurative primary cicatricial alopecia. Perifollicular infundibulo-isthmic lymphocytic inflammation and fibrosis (PIILIF) occurs in clinically normal-appearing scalp (cNAS) in other primary cicatricial alopecias but has not been systematically evaluated in DCS. In this retrospective exploratory study, we reviewed consecutive patients with clinicopathologically concordant DCS evaluated at a single Los Angeles dermatology clinic from December 2022 to November 2024. Patients underwent trichoscopy-guided 6-mm punch biopsy of cNAS and a second biopsy of an active lesion or inactive nodule. Specimens were processed with vertical and transverse sections and independently reviewed by two blinded board-certified dermatopathologists. CD4, CD8, CD117, and, when needed, α-smooth muscle actin immunostaining supported characterization. Exact tests with false-discovery-rate adjustment were exploratory. Twelve men were included (mean age, 30 years; range, 21-46 years). PIILIF was identified in all cNAS biopsies (12/12; 100%; exact 95% CI, 73.5-100%) and all inactive nodules (3/3). Active lesions (9/9) showed suppurative inflammation and remodeling superimposed on PIILIF (infundibulo-isthmic fibrosis, 9/9; lymphocytes, 8/9), with increased neutrophilic infiltrates (9/9 vs 0/9 in matched cNAS; adjusted P<0.001), granulation tissue (5/9 vs 0/9; adjusted P=0.035), and complete sebaceous gland loss (6/9 vs 0/9; adjusted P=0
Abstract
Dissecting cellulitis of the scalp (DCS) is a chronic, relapsing, suppurative primary cicatricial alopecia. Perifollicular infundibulo-isthmic lymphocytic inflammation and fibrosis (PIILIF) occurs in clinically normal-appearing scalp (cNAS) in other primary cicatricial alopecias but has not been systematically evaluated in DCS. In this retrospective exploratory study, we reviewed consecutive patients with clinicopathologically concordant DCS evaluated at a single Los Angeles dermatology clinic from December 2022 to November 2024. Patients underwent trichoscopy-guided 6-mm punch biopsy of cNAS and a second biopsy of an active lesion or inactive nodule. Specimens were processed with vertical and transverse sections and independently reviewed by two blinded board-certified dermatopathologists. CD4, CD8, CD117, and, when needed, α-smooth muscle actin immunostaining supported characterization. Exact tests with false-discovery-rate adjustment were exploratory. Twelve men were included (mean age, 30 years; range, 21-46 years). PIILIF was identified in all cNAS biopsies (12/12; 100%; exact 95% CI, 73.5-100%) and all inactive nodules (3/3). Active lesions (9/9) showed suppurative inflammation and remodeling superimposed on PIILIF (infundibulo-isthmic fibrosis, 9/9; lymphocytes, 8/9), with increased neutrophilic infiltrates (9/9 vs 0/9 in matched cNAS; adjusted P<0.001), granulation tissue (5/9 vs 0/9; adjusted P=0.035), and complete sebaceous gland loss (6/9 vs 0/9; adjusted P=0.012). Infiltrates were CD4-predominant with prominent CD117-positive mast cells. PIILIF was observed in a sideburn biopsy in one patient, and 3 patients (25%) had concurrent histologic acne keloidalis nuchae. In this small cohort, PIILIF was consistently observed in cNAS and inactive nodules from patients with DCS, while active lesions showed additional suppurative destruction. These findings support the hypothesis that PIILIF may represent a subclinical histopathologic component of DCS. Prospective controlled studies are needed to determine specificity, temporal sequence, and prognostic significance.