
Study Highlights Hidden Inflammation Beyond Visible Lesions in Dissecting Cellulitis of the Scalp
Key Takeaways
- Trichoscopy-guided biopsies 2–3 cm from visible DCS lesions demonstrated PIILIF in 12/12 clinically normal-appearing scalp samples, indicating subclinical perifollicular inflammation and fibrosis beyond overt disease.
- Active DCS lesions layered destructive pathology onto PIILIF, including universal neutrophilic inflammation, plus granulation tissue, sebaceous gland loss, extravasated hair shafts, and follicular rupture in substantial subsets.
New biopsies reveal hidden scalp inflammation in dissecting cellulitis, even in normal-looking skin, hinting at a field effect behind stubborn recurrences.
A small retrospective study suggests that dissecting cellulitis of the scalp (DCS) may involve a broader inflammatory process than is apparent from clinically visible lesions.1 Researchers found perifollicular infundibulo-isthmic lymphocytic inflammation and fibrosis (PIILIF) in the scalp that appeared clinically normal, as well as in clinically inactive nodules, while active DCS lesions demonstrated additional suppurative inflammation and tissue destruction.
The findings, published in Clinical, Cosmetic and Investigational Dermatology, may provide a potential explanation for the recurrent and progressive nature of DCS.2 However, the authors emphasized that the results are preliminary and do not establish whether PIILIF precedes active disease, predicts recurrence, or contributes directly to disease progression.
"Dissecting cellulitis is usually recognized after it becomes painful, drains pus or forms tunnels," said Sanusi Umar, MD, FAAD, board-certified dermatologist at Dr. U Hair and Skin Clinic in Manhattan Beach, California, and lead author of the study. "Our findings suggest these visible flares may sit on top of a quieter, wider inflammatory process involving normal-looking scalp. That changes where we look, when we biopsy and what future treatment studies need to address."1
Study Design
The retrospective study included 12 men with clinicopathologically confirmed DCS who were evaluated at a single Los Angeles dermatology clinic between December 2022 and November 2024. The patients had a mean age of 30 years, with ages ranging from 21 to 46 years.
Each patient underwent trichoscopy-guided 6-mm punch biopsy of clinically normal-appearing scalp (cNAS), generally located approximately 2 to 3 cm from the nearest clinically evident lesion. A second biopsy was obtained from either an active lesion or, when active lesions were absent, a clinically inactive nodule. Specimens were evaluated using vertical and transverse sections by 2 blinded board-certified dermatopathologists.
Results
PIILIF was identified in all 12 cNAS biopsies. It was also present in all 3 clinically inactive nodules. These findings indicate that the lymphocytic inflammation and associated fibrosis around the upper portion of the hair follicle were present even when the scalp did not show obvious DCS activity.
The 9 active lesions showed the same upper-follicle PIILIF pattern, but with additional findings associated with active, destructive disease. All 9 active lesions demonstrated neutrophilic inflammation, compared with none of the matched cNAS biopsies. Granulation tissue was identified in 5 of 9 active lesions, and complete sebaceous gland loss occurred in 6 of 9. Follicular destruction or rupture and extravasated hair shafts were each observed in 6 of 9 active lesions.
In contrast, the upper-follicle features associated with PIILIF were largely shared between active lesions and cNAS. Infundibulo-isthmic fibrosis was present in all 9 active lesions and all 9 matched cNAS samples, while infundibulo-isthmic lymphocytes were identified in 8 active lesions and all 9 cNAS samples.
Immunohistochemical analysis was available for 8 active lesion/cNAS pairs. The inflammatory infiltrates were consistently CD4-predominant, and CD117-positive mast cells were prominent in both sampling sites. The study also identified histologic acne keloidalis nuchae in 3 patients, or 25% of the cohort, suggesting that overlapping folliculocentric pathology may occur in some individuals with DCS. PIILIF was also observed in a sideburn biopsy from 1 patient.
Potential Clinical Implications
Three patients had previously been treated for presumed seborrheic dermatitis, although none of the study biopsies showed histopathologic features supporting that diagnosis. The authors noted that subtle perifollicular changes could potentially be mistaken for dandruff, but they cautioned that prior treatment could have altered histopathologic findings.
The researchers stressed that the study was limited by its small sample size, single-center design, retrospective and cross-sectional approach, heterogeneous treatment exposure, and lack of healthy controls. Larger prospective controlled studies are needed to determine whether PIILIF is specific to DCS and whether it predicts new lesions, disease extension, relapse, progression, or treatment response.
The authors propose that the findings support a “field-effect” hypothesis in DCS, in which a low-grade inflammatory and fibrotic process may extend beyond clinically apparent lesions. This could potentially help explain why disease can recur after appearing clinically quiet or extend into nearby scalp.
"The recurring pattern raises the possibility that PIILIF is a foundational inflammatory component shared across several difficult hair-loss conditions," Umar said. "That remains a hypothesis, but it creates a focused research path: determining whether addressing PIILIF alongside active inflammation improves long-term control."1
References
1. New Study Finds Hidden Scalp Inflammation That May Help Explain Why Dissecting Cellulitis Returns and Spreads. News release. PR Newswire. Published August 4, 2026. Accessed August 13, 2026.
2. Umar S, Ogah O, Yang J, Tan BH, Aiead N, Shitabata PK. Perifollicular Lymphocytic Inflammation and Fibrosis in Dissecting Cellulitis: Evidence of a Consistent Histopathologic Pattern. Clin Cosmet Investig Dermatol. 2026;19:614816. Published 2026 Jul 17. doi:10.2147/CCID.S614816








