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Follicular keratinized material refers to the accumulation of keratin proteins and desquamated corneocytes within the follicular infundibulum, the upper segment of the hair follicle [1]. Under normal physiological conditions, these cells are shed and cleared from the pore; however, in conditions such as acne vulgaris, abnormal keratinocyte cohesive forces and hyperkeratosis lead to the formation of a dense keratinous plug known as a microcomedo [1][2]. This plug acts as a physical barrier that traps sebum and creates an anaerobic environment, facilitating the colonization of Cutibacterium acnes and subsequent inflammation [1]. Therapeutic agents target this material through two primary mechanisms: chemical keratolysis and the normalization of follicular keratinization [3]. Keratolytic drugs, such as salicylic acid and benzoyl peroxide, work by breaking down the structural integrity of keratin filaments and intercellular cements to dissolve the plug [3]. Topical retinoids, including tretinoin and adapalene, interact with retinoic acid receptors to modulate gene expression, thereby reducing the stickiness of keratinocytes and promoting the expulsion of existing plugs while preventing new ones from forming [2].
Keratolysis and comedolysis through the disruption of desmosomal adhesion between corneocytes and the chemical breakdown of keratin filaments, alongside the normalization of keratinocyte differentiation to prevent plug formation.
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