Keratosis Pilaris and its Subtypes

Associations, New Molecular and Pharmacologic Etiologies, and Therapeutic Options

Jason F. Wang; Seth J. Orlow

Disclosures

Am J Clin Dermatol. 2018;19(5):733-757. 

In This Article

Cellular and Biochemical Characterization

The epidermal permeability barrier consists of corneocytes and the extracellular, hydrophobic lamellar bilayers of the stratum corneum (SC), formed from the secretions of the lamellar bodies (LBs).[24] This is aided by tight junctions in the underlying granular layer and by corneodesmosomes.[24,73,74] These structures protect against the inward entry of pathogens and the outward loss of water and electrolytes.[24,75] Although skin surface pH is normal in KP, baseline transepidermal water loss is increased in patients with KP (p < 0.01).[24] The follicular and interfollicular SC appears to have an abnormal permeability barrier in KP lesions. In KP lesional skin, non-lamellar domains disrupt lamellar membrane arrays. Lipid processing in the upper parts of hair follicles and in the interfollicular epidermis may be delayed. LB internal structures are abnormal, which can affect loading into organelles.

A few groups have attempted to characterize KP and its subtypes on a molecular level. Trichohyalin is weakly expressed in lesional KP.[76] In a flow-cytometric investigation, both KP- and KFSD-affected skin had lower proportions of cells positive for involucrin and higher proportions of cells positive for keratin 4 than normal skin.[77] Elevated levels of cellular retinoic acid-binding protein have also been found in lesions of KFSD, which may account in part for the responsiveness of KP (at least in some individuals) to retinoid therapy.[78]

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