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Stratum corneum cohesion structures are the specialized intercellular components of the skin's outermost layer that maintain structural integrity and regulate the permeability barrier (Neubert, 2024). These structures primarily comprise corneodesmosomes—modified desmosomes containing proteins such as corneodesmosin (CDSN), desmoglein 1 (DSG1), and desmocollin 1 (DSC1)—and an intercellular lipid matrix rich in ceramides, cholesterol, and free fatty acids (Haftek, 2015). Their biological function is to provide mechanical cohesion between corneocytes while facilitating the orderly process of desquamation through enzymatic degradation by kallikrein-related peptidases, such as KLK5 and KLK7 (Simon et al., 2001). In pathological conditions like psoriasis and ichthyosis, excessive cohesion leads to hyperkeratosis and scaling, whereas in atopic dermatitis, structural defects contribute to barrier failure and inflammation (Haftek, 2015). Therapeutic agents such as keratolytics, including salicylic acid, urea, and alpha-hydroxy acids, target these structures by promoting the breakdown of protein junctions or disrupting the lipid matrix to alleviate scaling (StatPearls, 2023). Conversely, barrier-repair therapies utilize physiological lipids to reinforce these structures and restore skin health (Neubert, 2024).
Keratolysis via chemical or enzymatic degradation of corneodesmosomal proteins and disruption of the intercellular lipid matrix; restoration of barrier function through lipid replenishment (StatPearls, 2023; Neubert, 2024).
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