WHAT IS ECZEMA / DERMATITIS?

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Skin inflammation and rashes are often used interchangeably. Not all cases of dermatitis are classified as eczema, although all cases of eczema are considered a kind of dermatitis. Eczema, also known as dermatitis, refers to a collection of skin conditions that involve inflammation of the skin. It is considered a skin reaction that occurs as a result of some underlying mechanism, such as immunological reactions (Mitamura et al., 2018; Zaniboni et al., 2016). There are many types of dermatitis. Atopic dermatitis is the most common eczema with symptoms such as redness, rashes, scaling, and occasionally small blisters (Szilveszter & Mocsai, 2019).

 

WHAT CAUSES  ECZEMA / DERMATITIS?

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Histologically, serous exudate (spongiosis) between epidermal cells and an underlying dermal perivascular lymphoid infiltration are the hallmarks of all eczematous eruptions and exocytosis (lymphocytes present individually or in clusters in the epidermis covering it). In most cases, spongiosis is excessive compared to the lymphoid cells in the epidermis (Murphey et al., 2022). 

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Eczema and dermatitis strongly related with the impaired of skin barrier function. The upper layer of the epidermis called the stratum corneum, the corneocytes have lost their nuclei and cytoplasmic organelles. They release their fatty substances into the space between cells, which is crucial for maintaining the barrier function and cohesiveness between cells. Therefore, in functional skin, the stratum corneum is rich in ceramides, free sterols and free fatty acids. Linoleate appears to be essential for proper barrier function as an ester-linked residue in acyl ceramides; thus, in essential fatty acid deficiency, substitution of this linoleate by oleate causes a defect in barrier function. The skin is an active lipid-synthesizing tissue, with a daily production rate of 100 mg/day (Li et al., 2020).
Filaggrin, the protein component of the keratohyalin granule responsible for keratin filament aggregation, causes the cells to flatten and the keratin filaments to align into disulphide cross-linked macrofibers. Loss-of-function mutations in the filaggrin gene have been linked to the genetic disorder ichthyosis vulgaris, as well as atopic dermatitis, asthma, and systemic allergies (Zaniboni et al., 2016).

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WHAT ARE THE TYPES OR DERMATITIS?

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There are two major types of dermatitis:

EXOGENOUS DERMATITIS - External factors or insult from outside the body which induces skin inflammation. Common cause are: 

• Allergic contact dermatitis: due to individual immune's response to an allergen such as nickel, hair dye, perfume, or rubber and can identified by patch test. 

• Irritant contact dermatitis: occur in anyone when exposed to an irritant at sufficient concencentration in a long period of length. These irritants can be soaps, detergents, solvents, abrasives, dust, degreasing agents, urine and even water.

• Photosensitive dermatitis: occur when exposed to light or UV radiation

• Drug-induced dermatitis

• Dermatitis induced by local skin infections: from bacterial, fungal and viral exposure (DermNet, 2024).

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ENDOGENOUS DERMATITIS - Often occur from underlying health-related internal factors. Common types include:

• Atopic dermatitis: this is the most common type of dermatitis in children and adults with commonly from families have history of hay fever and asthma. 

• Seborrheic Dermatitis: due to a reaction to a yeasts that colonise the skin. This is a common chronic eczema affecting scalp, face, ears and major flexures such as under the breasts, armpits, groin and behind the knees (DermNet, 2024).

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WHAT TREATMENTS FOR THIS CONDITION?

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The major goal would be on to repair the impaired skin function at first to rebuild and strengthening the stratum corneum (Piipponen & Landen, 2020) as the skin's first line defense. And also to introduce active ingredients gradually until skin itself climatised (Zhou et al., 2021).

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At Skinderm Aesthetics, there are ranges of treatments to repair and rebuild the skin barrier function such as:

• Ultrasound dermal delivery

• Clinical peels

• Perfect Pair

• Exfol & Hydrate

• Bright & Clear

 

Recommend treatment intervals are vary between weekly and fortnightly to ensure the efficacy of these treatments. It also including education for homecare routines and in many cases referral to see medical practitioners such as GPs or dermatologists to reach maximum results while meet our patients goals. 

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REFERENCES

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DermNet (2024). Retrieved from https://dermnetnz.org/topics

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Li, Q., Fang , H., & Dang, E. G. (2020). The role of ceramides in skin homeostasis and inflammatory skin diseases. Journal of dermatological science, 97(1), 2-8. doi:https://doi.org/10.1016/j.jdermsci.2019.12.002

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Mitamura, Y., Nunomura, S., Nanri, Y., Ogawa, M., Yoshihara, T., Masuoka, M., . . . Izuhara, K. (2018). The IL-13/periostin/IL-24 pathway causes epidermal barrier dysfunction in allergic skin inflammation. Allergy, 73(9), 1881-1891. doi:https://doi.org/10.1111/all.13437

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Murphrey, M. B., Miao, J. H., & Zito, P. M. (2022). Histology, Stratum Corneum (In StatPearls ed.). StatPearls. Retrieved from https://pubmed.ncbi.nlm.nih.gov/30020671/

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Piipponen, M., Li, D., & Landen, N. X. (2020). The Immune Functions of Keratinocytes in Skin Wound Healing. International journal of molecular sciences, 21(22), 8790. doi:https://doi.org/10.3390/ijms21228790

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Szilveszter, K. P., Nemeth, T., & Mocsai, A. (2019). Tyrosine Kinases in Autoimmune and Inflammatory Skin Diseases. Frontiers in immunology, 10, 1862. doi:https://doi.org/10.3389/fimmu.2019.01862

 

Zaniboni, M. C., Samorano, L. P., Orfali, R. L., & Aoki, V. (2016). Skin barrier in atopic dermatitis: beyond filaggrin. Anais brasileiros de dermatologia, 91(4), 472-478. doi:https://doi.org/10.1590/abd1806-4841.20164412

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Zhou, S., Wang, Q., Huang, A., Fan, H., Yan, S., & Zhang, Q. (2021). Advances in Skin Wound and Scar Repair by Polymer Scaffolds. Molecules (Basel, Switzerland), 26(20), 6110. doi:https://doi.org/10.3390/molecules26206110

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