Early Dissecting Cellulitis of the Scalp Following Repeated Microinfusion of Medication Into the Skin in a Patient With Androgenetic Alopecia and Long-Term Exogenous Testosterone Use: A Case Report.

Dissecting cellulitis of the scalp is an uncommon chronic inflammatory disorder within the follicular occlusion spectrum and may progress to permanent cicatricial alopecia if not recognized early. We report a case of a 34-year-old male with androgenetic alopecia, two years of exogenous testosterone use, and a recent history of six-monthly sessions of scalp microinfusion of medication into the skin, who developed painful and pruritic inflammatory scalp nodules approximately 45 days after the last procedure. The procedure was performed using a Cheyenne Unlimited 4 dermograph fitted with a 2710MG cartridge, corresponding to a 27-needle magnum configuration with 0.30 mm diameter needles, operating at 6.1 V, with the needle depth set to 1.2 mm. Clinical examination showed focal inflammatory alopecic nodules over a background of patterned hair thinning. Trichoscopy demonstrated perifollicular erythema, reduced follicular density, broken hairs, black dots, white structureless areas, and partial preservation of follicular openings, without classic features of alopecia areata. Histopathology showed hypodermal granulation tissue, intense mixed leukocytic inflammation composed of lymphocytes, plasma cells, neutrophils, macrophages, and foreign body-type multinucleated giant cells, follicular involvement with miniaturization, negative periodic acid-Schiff staining for fungi, and bacterial colonization in the infundibular and isthmic portions of hair follicles. These findings were consistent with dissecting folliculitis of the scalp. The patient was treated with oral antibiotics, intralesional corticosteroid, and high-potency topical corticosteroid, with partial inflammatory improvement and stabilization. This case highlights the value of clinicotrichoscopic-pathologic correlation in early dissecting cellulitis and raises the possibility that repeated procedural microtrauma, barrier disruption, follicular injury, or secondary bacterial colonization may act as a local trigger in a predisposed patient. The long-term exogenous testosterone exposure should be interpreted as a possible modifying factor rather than proof of causality.