Introduction
Irritant contact dermatitis results from the exposure of the skin to irritants. The function of the skin is to protect an individual from dehydration, irradiation, mechanical trauma and direct exposure to harmful sensitizing irritant chemicals (Johansen, Frosch and Lepoittevin, 2010). Perturbation of the skin barrier may lead to development of irritant contact dermatitis. Jack’s line of work, which deals with using abrasive solvents and chemical are a cause of the irritation he is experiencing. A small perturbation of the skin might have resulted to an entry of an irritant, which further impaired the skin causing an increase in irritation on Jack’s hand.
The outer layer of the skin consists of several layers of keratin discs referred to as corneocytes, which are enclosed by a small layer of cholesterol and free fatty acids produced by the epidermal cells known as keratinocytes (Kutzscher, 2012). The corneocytes and the keratinocytes ensure that the skin performs its function of defense and reducing water loss. The introduction of an irritant causes alteration of the skin barrier. According to Johansen, Frosch and Lepoittevin (2010), the penetration of the irritant through the stratum corneum causes the development of cytotoxic effects on the keratinocytes and triggers the keratinocytes to discharge alarm signals in the form of cytokines and chemokines. This results to the initiation of irritant contact dermatitis. The pathophysiology normally occurs in three stages involving skin barrier penetration (breaking down of the lipid layer), epidermal cellular changes and cytokine activation.
Skin Barrier Interruptions
According to Rycroft (2001), the skin barrier is composed of a layer of epidermis referred to as stratum corneum, which consists of protein rich cells (corneocytes) that are part of the rich lipid matrix. The likelihood of a potential irritant to cause an irritant reaction mainly depends on the ability of the irritant to penetrate the stratum corneum (Johansen, Frosch and Lepoittevin, 2010). Introducing the skin irritant results in the breaking down of the lipid layer, and this facilitates the penetration of the irritant itself (Rycroft, 2001). Haur, Stieger, Yawalkar and Masato (2013) indicate that, the mechanisms leading to the injuring of the skin barrier depend on the nature of the irritant. For instance, an organic solvent like acetone has the capability to remove lipids from the stratum corneum, which results to the disturbance of the epidermal barrier. Additionally, anionic surfactants like the sodium lauryl sulphate (SLS) damages the protein structures such as the keratin and profilaggrin, which results to exposure of the water binding sites and leads to water loss resulting to dehydration of the stratum corneum. Additionally, the SLS has the ability to alter the synthesis of new lipids, which cause a disturbance in the lamellar body lipid intrusion (Smith, Basketter and McFadden, 2002). An acetone causes increased proliferation in the basal cell layer (Smith, Basketter and McFadden, 2002). With the barrier disrupted, some cytokines such as (IL)-1 alpha, IL-1 beta and the tumor necrosis factor (TNF) alpha are released (Smith, Basketter and McFadden, 2002). Skin barrier impairment will lead to increased entry of irritants into the epidermis, which increases the release of cytokines.
Cellular Immunological Changes
According to Rycroft (2001), the cellular infiltrate in irritant contact dermatitis is characterized by the presence of mononuclear cells especially the T lymphocytes belonging to the CD4+ subset. Cellular immunological changes are based on the necrosis of the keratinocytes, which can be caused by exposure to strong acids or alkalis (Rycroft, 2001). According to Smith, Basketter and McFadden (2002), irritants have the ability to disrupt the functional activity of the keratinocytes. Structurally different irritants will cause varying cellular changes. According to Smith, Basketter and McFadden (2002), keratinocytes normally undergo structural changes based on the irritant used. For instance, nonionic acid induces eosinophilic degeneration of keratinocytes, with nuclear degeneration and only minimal spongiosis. Additionally, the use of a dithranol irritant result to development of marked swellings of the keratinocytes in the upper epidermis. SLS causes the development of upper epidermal parakeratotic cells (Smith, Basketter and McFadden, 2002). The presence of irritants also causes morphological changes in the skin by causing up-regulation of the cell surface molecules on epidermal cells.
The presence of the cellular inflammatory infiltrate causes the langerhans cells to migrate. Furthermore, these cells can be activated causing the development of Birbeck granules (Smith, Basketter and McFadden, 2002). The cellular changes involving keratinocytes result in the release of epidermal cytokines.
Release of Cytokines
SLS, dimethylsulphoxide and phorbol myristate exposure leads to the up-regulation of TNF-alpha (Smith, Basketter and McFadden, 2002). Cytokines released by the skin during response to an irritant indicate that the irritants are heterogeneous (Smith, Basketter and McFadden, 2002). A known cytokine inducer is croton oil. The SLS is relatively a weak cytokine inducer. Most of the cytokines released are normally proinflammatory. TNF-alpha is a major cytokine, which cause an increase in MHC class II expression and intracellular adhesion molecule 1 expression on keratinocytes. This indicates that the TNF-alpha helps in the maintenance of the inflammatory process.
References
Johansen, J. D., Frosch, P. J., & Lepoittevin, J.-P. (2011). Contact dermatitis. Heidelberg: Springer.
Haur Yueh, L., Stieger, M., Yawalkar, N., & Masato, K. (2013). Cytokines and Chemokines in Irritant Contact Dermatitis. Mediators of Inflammation, 1-7
Kutzscher, L. (2012). Management of Irritant Contact Dermatitis and Peripherally Inserted Central Catheters. Clinical Journal Of Oncology Nursing, 16(2), E48-E55
Rycroft, R. J. G. (2001). Textbook of contact dermatitis. Berlin: Springer.
Smith, H., Basketter, D., & McFadden, J. (2002). Irritant dermatitis, irritancy and its role in allergic contact dermatitis. Clinical & Experimental Dermatology, 27(2), 138-146.
