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Stratum corneum corneocyte–corneocyte cohesion refers to the physiological and structural forces that bind the flattened, keratinized cells (corneocytes) of the outermost skin layer together to form a resilient physical barrier. This cohesion is primarily mediated by specialized protein junctions called corneodesmosomes—which contain proteins such as corneodesmosin, desmoglein 1, and desmocollin 1—and a surrounding lipid-rich extracellular matrix [1][4]. The strength of this cohesion is tightly regulated by a balance of protease activity (e.g., kallikrein-related peptidases) and protease inhibitors, which ensures that the outermost cells are shed at the same rate new ones are produced, a process known as desquamation [2][3]. In pathological states like ichthyosis or xerosis, excessive cohesion prevents normal shedding, leading to the accumulation of thick, scaly skin. Conversely, weakened cohesion can compromise the skin's barrier integrity, contributing to inflammatory conditions like atopic dermatitis. Therapeutic strategies often involve the use of keratolytics, such as alpha-hydroxy acids or salicylic acid, which weaken these intercellular bonds to promote desquamation and restore skin smoothness [3][5]. Sources: [1] Milstone, L. M. (2004). Journal of Dermatological Science; [2] Rawlings, A. V., et al. (1995). Journal of the American Academy of Dermatology; [3] StatPearls: Physiology, Stratum Corneum; [4] Haftek, M. (2015). Corneodesmosomes; [5] PubChem: Salicylic Acid.
Keratolytic agents reduce cohesion by disrupting the intercellular cement, solubilizing desmosomal proteins, or lowering the pH to activate endogenous proteases that degrade corneodesmosomes [1][3].
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