What is the pathophysiology of Riehl melanosis (pigmented contact dermatitis)?

Updated: May 27, 2021
  • Author: Elizabeth K Satter, MD, MPH; Chief Editor: William D James, MD  more...
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The hyperpigmentation in pigmented contact dermatitis is postulated to be caused by frequent and repeated contact with small amounts of sensitizing allergens primarily in cosmetic and textile materials. Nakayama hypothesized that allergens used in commercial products were too low in concentration to produce typical eczematous dermatitis, but rather accumulation of these allergens resulted allergic contact dermatitis, a type IV cytolytic reaction. [13, 14] This later reaction is characterized by vacuolar degeneration of the basal layer of the epidermis associated with pigment incontinence in the superficial dermis. The melanin pigment is slowly engulfed by macrophages; therefore, resolution of the hyperpigmentation is a prolonged process. Because most cases of pigmented contact dermatitis occur in patients with a darker completion, one hypothesis is that various pigment-genetic interactions contribute to the development of this condition. [7] Furthermore, Imokawa and Kawai have provided clinical evidence that various allergens implicated in allergic contact dermatitis can stimulate melanogenesis. [15]

In 2020, Woo et al evaluated biopsies obtained from 12 patients with Riehl melanosis that showed increased dermal expression of stem cell factor (SCF) and c-kit, along with increased expression of epidermal and dermal endothelin-1 in the lesional skin of Riehl melanosis. [16] These authors concluded that their findings support the role of these paracrine melanogenic molecules in the pathogenesis of Riehl melanosis. [16] In 2021, Woo et al also showed that that lesional skin of patients with Riehl melanosis exhibited increased epidermal and dermal expression of estrogen receptor (ER)β and progesterone receptor (PR) mRNAs and concluded that these hormone receptors may play a role in the pathogenesis of Riehl melanosis. [17]

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