Mycosis Fungoides Scalp: Clinical and Trichoscopic Findings

Mycosis fungoides is the most common form of cutaneous T-cell lymphoma, often presenting with skin lesions that mimic other dermatologic conditions. While it primarily affects the trunk and extremities, scalp involvement can pose diagnostic challenges due to its variable presentation. Recognizing the distinct clinical and trichoscopic features of mycosis fungoides on the scalp is essential for early diagnosis and effective management.

Clinical Scalp Manifestations

Scalp involvement in mycosis fungoides presents with a range of dermatologic changes that complicate early recognition. Unlike the classic patch, plaque, and tumor stages seen on the trunk and extremities, scalp lesions often exhibit subtle erythema, fine scaling, and atrophic changes, resembling seborrheic dermatitis or psoriasis. In some cases, affected areas show diffuse hair thinning due to folliculotropic infiltration. This variant, known as folliculotropic mycosis fungoides, tends to be more resistant to conventional therapies and has different prognostic implications.

Lesions on the scalp often appear asymmetrically, with patches of alopecia interspersed with erythematous or hyperpigmented skin. In darker skin tones, lesions may have a violaceous hue, making differentiation from other inflammatory scalp disorders more difficult. Pruritus is common but varies in intensity, and some cases remain asymptomatic until advanced stages. The presence of follicular papules or keratotic plugs suggests deeper follicular involvement, distinguishing mycosis fungoides from other scalp conditions.

Over time, lesions may progress to infiltrative plaques, leading to scarring alopecia. This scarring is subtle early on but becomes more apparent as the disease advances, with follicular dropout and dermal fibrosis contributing to permanent hair loss. Unlike alopecia areata, which presents as sharply demarcated, non-inflammatory patches of hair loss, mycosis fungoides-associated alopecia is accompanied by epidermal atrophy and fine scaling. Telangiectasia within affected areas further supports the diagnosis, as vascular changes are common in cutaneous T-cell lymphomas.

Histopathological Presentation

Microscopic examination of scalp lesions in mycosis fungoides reveals distinct epidermal and dermal alterations that reflect disease progression and folliculotropic involvement. A hallmark feature is the presence of epidermotropic atypical lymphocytes—small to medium-sized cells with hyperchromatic nuclei and irregular contours. These lymphocytes often cluster within the epidermis, forming Pautrier microabscesses, though this is less consistent in folliculotropic variants. Epidermal involvement varies, with some cases showing mild spongiosis and basal layer vacuolization, while others exhibit epidermal atrophy.

In folliculotropic cases, histopathological findings extend beyond the epidermis to involve follicular structures and the perifollicular dermis. Dense lymphocytic infiltrates surrounding and invading follicles often lead to follicular mucinosis—marked by mucin accumulation within follicular epithelium. This contributes to follicular dropout and alopecia. Unlike classic mycosis fungoides, where epidermotropism is a defining feature, folliculotropic forms show a greater affinity for adnexal structures, sometimes with minimal epidermal involvement, making histopathological assessment crucial.

The dermis frequently contains a band-like or lichenoid lymphocytic infiltrate interspersed with histiocytes and rare eosinophils. Fibrosis in the deeper dermis contributes to subtle scarring in advanced lesions. Immunohistochemical staining aids in diagnosis, with atypical lymphocytes typically expressing CD3 and CD4 while showing loss of CD7. CD8-positive variants, though less common, have been reported. Ki-67 proliferation indices provide insight into disease activity, particularly in progressive or treatment-resistant cases.

Trichoscopic Findings

Trichoscopy of mycosis fungoides on the scalp reveals vascular, follicular, and structural abnormalities reflecting lymphocytic infiltration and epidermal changes. Short, broken hairs and scalp scaling are common findings, often mistaken for other inflammatory dermatoses. Perifollicular scaling suggests follicular epithelium disruption due to lymphocytic infiltration. Scaling is fine and diffuse in early stages but can become more pronounced, sometimes forming adherent white scales that obscure follicular openings.

Vascular patterns offer additional diagnostic clues, with dotted and linear vessels interspersed within lesions. Unlike the arborizing vessels of basal cell carcinoma or the regular dotted vessels of psoriasis, mycosis fungoides exhibits irregularly distributed tortuous and glomerular patterns. These vessels may be more prominent in erythematous areas, reinforcing the inflammatory nature of the condition. In darker skin tones, vascular findings may be less conspicuous, but faint telangiectasia can still be detected under polarized light trichoscopy.

Alopecia in affected areas presents with a patchy distribution and loss of follicular openings, a hallmark of folliculotropic involvement. Black dots—representing fractured hairs—may be visible in regions with active follicular destruction. Yellowish-white globules within hair follicles suggest follicular plugging, a feature more commonly associated with folliculotropic variants. These plugs can be distinguished from those in lichen planopilaris by their irregular shape and distribution.

Approaches To Diagnosis

Diagnosing mycosis fungoides involving the scalp requires clinical evaluation, histopathological assessment, and specialized diagnostic techniques. Given its resemblance to common inflammatory scalp disorders, a thorough patient history is essential to identify chronicity, treatment resistance, and prior skin manifestations suggestive of cutaneous T-cell lymphoma. Patients often report slowly evolving scalp lesions that fail to respond to treatments for seborrheic dermatitis or psoriasis, raising suspicion for an alternative etiology.

Scalp biopsies confirm the diagnosis, with deep punch biopsies preferred in suspected folliculotropic cases to capture follicular involvement. Immunohistochemical staining enhances accuracy, with atypical lymphocytes typically expressing CD3 and CD4 while showing reduced or absent CD7 expression. Clonality studies using T-cell receptor gene rearrangement analysis can further support the diagnosis by detecting monoclonal T-cell populations, distinguishing malignant infiltration from reactive inflammatory processes.

Distinguishing From Other Conditions

The clinical and trichoscopic variability of mycosis fungoides on the scalp makes differentiation from other dermatologic conditions challenging. Several inflammatory, autoimmune, and neoplastic disorders share overlapping features, necessitating careful evaluation of lesion morphology, disease progression, and histopathologic characteristics.

Alopecia areata, a common cause of non-scarring hair loss, can mimic early mycosis fungoides when presenting with patchy alopecia. However, alopecia areata lacks epidermal involvement and typically exhibits exclamation mark hairs and yellow dots on trichoscopy. Lichen planopilaris, another inflammatory condition causing scarring alopecia, may present with perifollicular erythema and scaling similar to folliculotropic mycosis fungoides. The distinction lies in histopathology, where lichen planopilaris demonstrates an interface lymphocytic infiltrate targeting the follicular epithelium rather than the atypical lymphocytes of mycosis fungoides.

Psoriasis, often considered in the differential, manifests with well-demarcated erythematous plaques and silvery scale but lacks the folliculotropic infiltration seen in scalp mycosis fungoides. Seborrheic dermatitis, another frequently confused condition, presents with diffuse erythema and greasy scaling, often responding to antifungal or steroid therapy. In contrast, mycosis fungoides follows a chronic and progressive course with therapy-resistant lesions.

Cutaneous B-cell lymphomas can also involve the scalp, presenting with nodular or infiltrative plaques. Immunohistochemical staining is essential in these cases, as B-cell lymphomas express CD20 and CD79a, distinguishing them from the T-cell phenotype of mycosis fungoides. By integrating clinical features with histopathologic and immunophenotypic analyses, clinicians can refine the diagnostic process and ensure appropriate management.