Erosive Pustular Dermatosis of the Scalp

Clinicopathological Correlation Leading to a Definition of Diagnostic Criteria

Robin Reschke, MD; Sonja Grunewald, MD; Uwe Paasch, MD; Marco Averbeck, MD; Jan C. Simon, MD; Tino Wetzig, MD

Disclosures

Wounds. 2021;33(6):143-146. 

In This Article

Discussion

Erosive pustular dermatosis of the scalp can clinically imitate other diseases, such as cutaneous squamous cell carcinoma, basal cell carcinoma, Brunsting-Perry cicatricial pemphigoid, bacterial or mycotic infections, and folliculitis decalvans. After the exclusion of epithelial tumor growth, EPDS is thought to be a nonspecific wound healing disorder,[6] and clear diagnostic criteria for EPDS are lacking. For this reason, in-depth clinicopathological correlations were performed in this study to review the criteria defining this disease.

Erosive pustular dermatosis of the scalp usually develops on previously damaged skin of the scalp in elderly persons. Most often, patients have previously undergone treatment for actinic keratosis or field cancerization using methods that have a proinflammatory effect or that traumatize the epidermis and superficial dermis, such as PDT or surgery. Elderly patients tend to frequently scratch preexisting lesions on their scalp, which could in turn further aggravate inflammatory processes.[7] In some cases, the resulting EPDS remains itchy.[8] These inflammatory or traumatic insults trigger the accumulation of inflammatory cells, such as lymphocytes and plasma cells, which further contribute to this wound healing disorder. The literature indicates that both women and men are affected.[8–10] In the present study, there were more male patients than female patients, most likely owing to the higher frequency of androgenetic alopecia and subsequently actinic keratosis in this sun-exposed area. One side effect of EPDS is secondary alopecia owing to the destruction of hair follicles by chronic inflammation. The authors of this study hypothesize that missing or destructed hair follicles delay the re-epithelialization process. This has already been shown in experimental models, in which half of the keratinocytes involved in wound healing are derived from adnexal structures.[11]

Hence, the healing process is slowed because it must be initiated from the marginal areas of the lesion. The epidermis is easily detachable in the marginal area, which could result in increased size of the lesion. However, the detachable epidermis could be used as an additional clinical sign of EPDS.

In patients with normal C-reactive protein values, the increased ESR might reflect the autoinflammatory nature of the disease. Larger trials are necessary to determine whether ESR monitoring might be useful as a parameter for disease activity and the treatment response. In addition to the existing literature concerning histopathologic evaluation of EPDS, the authors of the present study postulate that the occurrence of plasma cells in the dermis is the most characteristic histological criterion of EPDS (Figure 2, Figure 5). In patients with EPDS, tissue biopsies of the scalp show the occurrence of plasma cells to be significantly more extensive than in patients who do not exhibit EPDS. Other authors also describe dermal plasma cells but characterize neutrophils as the predominant histopathological feature.[12] Similarities with other neutrophilic dermatoses, such as pustular pyoderma gangrenosum, have been proposed. The authors of the present study observed neutrophils mostly located around ulcerations. Thus, neutrophils can be interpreted as part of the acute inflammation.[13] Plasma cells and lymphocytes prevail in the chronic status of EPDS, however. Clinically, EPDS is easy to distinguish from other dermatoses with prominent plasma cells, such as lues, Lyme disease, or erythema elevatum diutinum. Infiltrates of lymphocytes and plasma cells can also occur in actinic keratoses. However, lymphoplasmacytic infiltrates of EPDS are much more pronounced and affect deeper dermal layers. There is reason to believe that the peritumoral inflammation remains and even intensifies after healing of the precancerous lesion being triggered by external stimuli (eg, surgery, cryotherapy). The exact and early diagnosis of EPDS prevents futile treatments with expensive wound care products. Instead, patients are sufficiently treated with topical steroids. Other topical therapies, such as 5% dapsone gel or tacrolimus, have shown positive effects in smaller case series.[10,14] Erosive pustular dermatosis of the scalp relapse occurs but responds well to repeated treatment with topical steroids.

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