An evidence-based, peer-reviewed journal for practicing clinicians in the field of dermatology
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U nderstanding the Epidermal Barrier in Healthy and Compromised Skin: Clinically Relevant Information for the Dermatology Practitioner [APRIL 2016 • VOLUME 9 • NUMBER 4 • SUPPLEMENT 1] SUPPLEMENT TO THE JOURNAL OF CLINICAL AND AESTHETIC DERMATOLOGY S5 and flaking; loss of elasticity and increased rigidity leads to microfissuring and macrofissuring; and epidermal proliferation can lead to hyperkeratosis. 3 The stepwise progression of changes secondary to c ontinued SC permeability barrier damage are demonstrated in Figure 4, depicting alterations induced by increased TEWL over time within visibly normal skin, xerotic skin, and eczematous skin. What are the Physiologic Stratum Corneum Self-repair Mechanisms? As skin is exposed to multiple exogenous factors that may lead to EB impairments, the SC is continuously active in maintaining a functional physiologic state by utilizing a variety of self-repair mechanisms. Once TEWL is increased beyond the normal homeostatic level, multiple self-repair mechanisms are induced within the SC and at the granular zone transition layer of the epidermis. 3,8,10,19,20–22 These self-mechanisms are: • Immediate release of precursor lipids into the SC from lamellar bodies within the granular layer that are immediately converted to physiologic lipids (such as ceramides), providing recovery of approximately 20 percent of overall permeability barrier function. • Increase in synthesis of physiologic lipid precursors and conversion to SC lipids for replenishment of the intercellular lipid membrane. • Increased conversion of prefilaggrin to fillagrin with degradation of filaggrin to several NMFs. These NMFs, primarily amino acids, maintain humectancy within the SC, which decreases TEWL by inhibiting loss into the ambient atmosphere. • Increased TEWL initiates an inflammatory cascade through release of tumor necrosis factor (TNF), interleukin (IL)-1, and IL-6. This cascade promotes keratinocyte hyperproliferation as increasing epidermal thickness serves to decrease TEWL. • When microbial organisms gain access to the SC, specific antimicrobial peptides may be activated by certain microbes, thus providing an innate immune response to deter the development of infection. On a daily basis, the SC is dynamic and utilizes self-repair mechanisms to maintain a normal physiologic balance within skin, and to contribute to overall homeostatic water balance. When exogeneous and/or exogenous factors create EB impairment that is not correctable by self-repair alone (overstressed SC), visible xerotic, eczematous, and specific disease state manifestations emerge. 1,3,8 This underscores the need to incorporate proper daily skin care utilizing a gentle cleanser and well-formulated moisturizer to assist the SC in maintaining EB integrity. The use of gentle skin cleansing and moisturization/barrier repair becomes more evident clinically in patients with underlying disease states that are characterized by asteatotic skin changes and/or sensitive skin due to the disease state itself and/or topical therapies used for treatment. 1,4,23–30 Are there Differences in the Epidermal Barrier Related to Race or Ethnicity? Although the structural and functional components of the SC and EB barrier have been reasonably defined, there is more recent interest in ethnic and racial differences that may translate to differences in clinical presentations of xerotic skin changes and skin sensitivity. 31–34 Although conflicting evidence exists in some areas, some observations have been made that may assist in targeting certain groups with specific skin care formulations. 31–37 The following observations have been gleaned from studies assessing potential differences in SC/EB barrier structure and functions among different races and ethnicities: Figure 3. Physiological adaptions of the stratum corneum in response to factors promoting desiccation (e.g., increase in transepidermal water loss, decrease in natural moisturizing factor, damage or reduction in stratum corneum lipids, damage to stratum corneum proteins). Reprinted with permission from: Del Rosso JQ, Levin J. J Clin Aesthet Dermatol. 2011;4(9): 22–42. © 2011 Matrix Medical Communications.