Differential cell composition and split epidermal differentiation in human palm, sole, and hip skin

Effects of a leave‐on product on the strength of the dermoepidermal junction: An exploratory, intraindividual, randomized controlled trial in older adults with dry skin

“…37 Previous reports on relative gene expression in the suction blister roof showed that application of urea containing formulation resulted in upregulation of genes like loricrin (LOR) and FLG, which are involved in skin cell differentiation and barrier function. 55,58 LOR was found to be enriched in skin areas where the interdigitation of the epidermis and dermis are more prominent 59 which is a characteristic of healthy DEJ. However, because the difference in time to blistering was observed previously by treating with petrolatum only, the overall physiological and structural changes caused by application of leave-on products may also induce changes in the underlying epidermal tissue and the DEJ, hence improving the resistance against mechanical loads.…”

Acquired diffuse palmoplantar erythema with keratoderma in Chinese patients with pustular psoriasis: A predictor for IL36 receptor antagonist c.115+6T>C mutation?

“…In murine models, transgenic IL36α expression resulted in epidermal hyperplasia and hyperkeratosis, 35 which were further aggravated in Il36rn −/− mice, an established animal model of DITRA 36,37 . Furthermore, markedly elevated IL36G and IL36RN gene expression are found in palmoplantar skin compared to non‐palmoplantar skin in healthy individuals 38 . Overall, it seems that disturbed IL36 signalling homeostasis, shaped by both external factors and genetic predisposition, might be involved in the development of PPK among pustular psoriasis patients with DITRA.…”

“…36,37 Furthermore, markedly elevated IL36G and IL36RN gene expression are found in palmoplantar skin compared to nonpalmoplantar skin in healthy individuals. 38 Overall, it seems that disturbed IL36 signalling homeostasis, shaped by both external factors and genetic predisposition, might be involved in the development of PPK among pustular psoriasis patients with DITRA.…”

The case for considering volar skin in a “separate status” for wound healing

“…A key feature of the immune system is its high degree of specialization in different tissue sites ( 55 ), and there is evidence that innate and adaptive immunity both vary considerably between different skin areas ( 56 ). One of the main findings of a recent study utilizing bulk and single-cell RNA sequencing to compare human palm, sole, and hip skin was a broadly diminished immunological presence in palmoplantar skin, with reduced immune cell populations and downregulation of immunological processes ( 10 ). This is consistent with the reported 2–3 fold reduction in the density of Langerhans cells (LCs, specialized epidermal dendritic cells that serve as our foremost immunological barrier against the outside world) in normal, uninjured volar skin, compared to other non-volar skin areas ( 13 , 57 ).…”

“…Many of these are reasonable practices, especially in light of constraints associated with animal/human studies (e.g., animals' trunk/back skin offers logistical benefits such as a large area and relatively flat contour, while requiring control wounds on the plantar skin in clinical studies is likely to be both impractical and ethically dubious), but they do carry the implicit, and largely unvalidated, assumption that results and conclusions drawn from wounds on any one part of the body are necessarily applicable to wounds occurring everywhere else. The body of data showing skin site-specific variations in cell populations (8)(9)(10) and wound healing (11) should cast doubt on this assumption, but it is especially questionable in palmoplantar skin, also known as volar skin, which has long been known for its highly specialized nature. This review aims to summarize the key volar-specific specializations that are likely to affect wound healing, and to make the case that these specializations should be taken into consideration both in our understanding of DFU's pathophysiology, and in efforts to develop treatment options for DFU.…”