Oily skin, Skin lipids dysregulation

Skin surface Lipid dysregulation in oily skin, what causes acne with a focus on role of topical linoleate

Introduction

skin surface lipids and how they change to produce oily skin
Considering essential fatty acids in acne treatments has not been standardized yet. However, there are many studies which bring up a possible role for essential fatty acids in treatment of acne and oily skin. Rising antibiotic drug resistance consequent to the widespread use of topical antibiotics and failure of many other topical/systemic treatments in maintenance treatments is causing concern and call for new modalites. Acne is a multifactorial disease and pathologically characterized by increased sebum production which results in an oil forming skin, sebaceous gland hypertrophy, abnormal follicular keratinization and inflammation. Hyperactivity of sebaceous glands may be associated with change in lipid composition of the sebum [1]. This hyperactivity is also a marker of severity of the disease so there is a linear relationship between acne severity and over-secretion of sebaceous glands [2].

There is evidence of association between sebum linoleate concentration and comedo formation. Essential fatty acids deficiency contributes to sebaceous gland hypertrophy and hyperkeratinization of the ducts. Linolenic acid level in the stratum corneum has been reported to be much higher in normal subjects than that in the comedones in particular linoleate content of wax esters. Oily skin and hypersecretion of sebaceous glands is well known as one of four major players in pathogenesis of acne [1] [3]. However, change in composition of the secreted oils during acne has been less studied. Studies by Stewart ME, et al suggest that skin’s fatty acid composition may change with changes in sebaceous gland activity, and that sebum fatty acids can enter the epidermis and be incorporated into epidermal lipids [4]. In this article we are going to examine how different composition of oily secretions in acne patients is from those of normal subjects. We have attempted to look across multiple studies reported in dermatology literature to determine if correction of skin surface lipids can control sebaceous gland overactivity which, in turn, may improve acne.

Change in quantity as well as quality of skin lipids in acne vulgaris

Studies by Downing et al indicates that differrentiating sebaceous cells implement sebaleic acid instead of linoleic acid in wax esters if the later fatty acid is not available [5]. Sebum fatty acid composition is not fixed but changes in relation to sebum secretion rates. Specifically, with increasing sebum secretion, changes appear to occur both in the lipid class composition (more wax esters compared with cholestrol esters [6] and in the fatty acid composition of the ester lipids [7].

Linoleic acid-defeicient Ceramides lead to dysfunctional keratinocyctes

Another aspect of alteration of skin surface lipids and linoleate deficiency is impact of this change on skin’s sphingolipids in particular acylceramides. Acylceramides are a component of the membranous extracellular matrix in the startum conrneum that constitutues the epidermal water barrier [8]. Downing, et al [5] also suggest that the presence of linoleic acid-deficient sebum in the follicle may cause substitution of sebaceous fatty acids for linoleic acid in the normally rich acylceramides. These altered ceramides might be dysfunctional, resulting in hyperkeratotic follicular epithelium with an incompetent water barrier and possibly other functional defects favorable to the formation of acne and oily skin [4]. Lower amount of sphingolipids and ceramides in keratinocytes of acne subjects of various level of oily skin has been shown [9]. This would be associated in decrease in ability of keratinocytes’ walls to hold water, one possible mechanism that can explain how hyperkeratinization starts in comdeones since impaired water barrier function is concurrently seen in hyperkeratosis. In addition ceramides can trigger nuclear factor-kappa B (NF-kB), leading to induction of human beta defensin-2 (hBD-2) expression, enhancing the skin’s innate antibacterial defense [10].

Squalene peroxidation, a by-product of sebum hypersecretion, triggers an inflammatory response

Change in lipid composition can contribute in a quite different way to invoke an oily skin. Study by Summerly R, et al [11] propose that the larger sebaceous glands of acne patients elaborate sebum which has an enhanced potential for inducing comedo formation by virtue of an increased concentration of squalene. Following UV exposure squalene undergoes massive oxidation. Upon oxidative challenge, squalene is readily oxidized giving rise to different squalene peroxidation by-products (some are comedogenic [12] ), exerting harmful activities in skin cell cultures and in vivo including keratinocyte cytotoxicity and immunosuppression [13].

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