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As the outermost layer of the epidermis, the stratum corneum is the first line of defense for the body, serving an essential role as a protective skin barrier against the external environment. The stratum corneum aids in hydration and water retention, which prevents skin cracking, and is made up of corneocytes, which are anucleated keratinocytes that have reached the final stage of keratinocyte differentiation. Corneocytes retain keratin filaments within a filaggrin matrix, and the cornified lipid envelope replaces the keratinocyte plasma membrane. These flat cells organize in a brick-and-mortar formation within a lipid-rich extracellular matrix. Pathophysiology of the stratum corneum is typically secondary to either protein or lipid defects (see Image. Cells of the Epidermis). Other clinically significant signs include parakeratosis, which is the incomplete maturation of keratinocytes, and the morphological retention of nuclei in the stratum corneum. Abnormal parakeratosis of the stratum corneum can appear in patients with psoriasis, chronic eczema, and squamous cell carcinoma.[1] Scaling, or visible peeling and flaking of the skin, furthermore is a salient manifestation of diseases of the stratum corneum.[2][3][4]

Defects in the stratum corneum may occur secondary to lipid or protein dysfunction. Lipid abnormalities may stem from a variety of causes and generally result in defective barrier function, resulting in increased transepidermal water loss and desquamation. An acute loss of lipids from the stratum corneum may occur secondary to the topical application of organic solvents or detergents, which extract lipids and allow the passive loss of extracellular calcium and potassium. Deficiency in essential fatty acids also results in lipid abnormalities and manifests as increased transepidermal water loss, scaling, and alopecia. Lipid abnormalities can also occur secondary to genetic disorders, such as deficiency in steroid sulfatase leading to recessive X-linked ichthyosis. In addition to pathologies secondary to lipid abnormalities, stratum corneum protein abnormalities can also result in defects in the stratum corneum layer of the epidermis. Defects in corneodesmosomes, the junctional proteins that connect corneocytes, result in diseases such as peeling skin disease. Defects in the profilaggrin and filaggrin proteins cause significant damage to the stratum corneum, and profilaggrin defects are associated with both ichthyosis vulgaris and harlequin ichthyosis. Defects in the cornified envelopes of the stratum corneum cells can also result in pathologies such as keratosis follicularis and psoriasis. Finally, parakeratosis refers to corneocytes in the stratum corneum with retained nuclei. While retention of nuclei in stratum corneum cells is normal in mucosal surfaces, parakeratosis in other skin is abnormal. Parakeratosis typically signifies increased cell turnover, which can be secondary to inflammatory or neoplastic processes. Additionally, when corneocytes retain their nuclei, there is associated thinning and eventual loss of the granular layer.