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The stratum corneum (SC) represents the terminal stage of epidermal differentiation, functioning as the body's primary interface with the external environment. It is structurally organized according to the "bricks and mortar" model, where keratin-filled, non-viable corneocytes are embedded within a continuous matrix of intercellular lipids, including ceramides, cholesterol, and free fatty acids [1][2]. This complex assembly provides essential barrier functions, preventing excessive transepidermal water loss and protecting against mechanical trauma, chemical irritants, and microbial invasion [4]. Keratins provide the necessary structural scaffolding, while the intercellular lipids and corneodesmosomes regulate the cohesion and eventual desquamation of the skin [2]. In diseases such as psoriasis, ichthyosis, and atopic dermatitis, the integrity of the SC is often disrupted, leading to hyperkeratosis or impaired barrier function [1]. Therapeutic strategies targeting the SC include the use of keratolytic agents like salicylic acid to reduce scaling and emollients to restore the lipid barrier [3].
Drugs targeting this complex act through keratolysis (dissolving intercellular cement), humectancy (binding water within the keratin matrix), or barrier restoration (replenishing intercellular lipids) [1][3].
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