Quemaduras solares

(Versión Completa en Inglés)

Etiology

Sunburns are caused by excessive exposure to ultraviolet radiation (from the sun or an artificial source, such as a solarium). There are several factors that contribute to the occurrence and severity of sunburn^[i]:

• Medication
  • Like tetracyclines, thiazide diuretics, sulfonamides, fluoroquinolones, non-steroidal anti-inflammatory drugs, retinoids and even St John’s wort in high doses
• Elevated UV index
  • Sun exposure between 10am and 4pm
  • High altitudes
  • Proximity to the equator
  • Cloudiness
• Ozone layer depletion
• Fitzpatrick skin phototype
  • The lighter the skin tone, the greater the likelihood of sunburn
• Tanning
  • Especially in solarium/artificial

Physiopathology

Both types of UVA and UVB radiation are directly responsible for DNA damage by introducing cyclobutane thymine dimer formation^[ii]. When these dimers are formed, the human organism generates a DNA repair response, which includes induction of apoptosis of several cells and the release of inflammatory markers, such as prostaglandins, reactive oxygen species and bradykinin^[iii]. This causes vasodilation, edema and pain, which translates into the classic presentation of sunburn: red, painful and highly reactive skin.
Additionally, skin exposure to UVB causes an increase in cytokines such as CXCL5 and activates peripheral nociceptors, leading to an over-activation of skin pain receptors^[iv].

Hystopathology

There are huge changes that occur in the skin and which characterize the histology of sunburn, especially regarding the epidermis and dermis.
In the epidermis, loss of Langerhans cells and vacuolization of keratinocytes is visible.
In the dermis, vascularization changes that occur may be visible only after 30 minutes of exposure to radiation, from an increase in endothelial cells and edema caused by mast cell degranulation.
Histamine and prostaglandin E2 levels rise, increasing by about x4, which clearly highlights the key role that histamine plays in the skin’s reaction to sunburn. Usually, this situation reverts itself back to normal after 24 hours^[v].

Differencial Diagnosis

Although these signs appear after prolonged sun exposure, it is always convenient to confirm the existence or coexistence of the following morbidities which have similar presentations:

• Autoimmune diseases such as systemic lupus erythematosus or dermatomyositis;
• Infections such as cellulitis, erysipelas or staph scalded skin syndrome;
• Idiopathic conditions such as pityriasis rubra pilaris;
• In oncological disease: Sezary syndrome and other cutaneous lymphomas;
• Common skin diseases: from rosacea, acne and stasis, to seborrheic dermatitis;
• Reactions to the sun, such as solar urticaria, phytophotodermatitis, type IV photoallergic sensitivity, and phototoxicity reactions;
• Ichthyotic congenital conditions.

Conventional Treatment

Most sunburns are self-limiting, healing on their own without the need for major interventions. However, those affected badly by sunburn are recommended the following conventional options:

• Avoidance of sun exposure to avoid further skin damage;
• Usage of non-steroidal anti-inflammatory drugs to reduce pain;
• Increase water intake to avoid dehydration;
• Application of topical creams/gels such as aloe vera or hydrocortisone and avoidance of the use of local anesthetics;
• Colloidal oatmeal baths that help soothe the skin.

Ozone Therapy

Histopathology studies have shown that the topical application of ozonated oils leads to a marked increase in the expression of fibronectins and transform growth factor β, hence proving its ability to reduce damaged and burned skin regeneration time, also being applicable to non-solar burns^[vi].
A study performed in 2017[vii]indicates which molecular and cellular mechanisms ozonated oils use in order to facilitate healing: It is by increasing fibroblast migration and the epithelial-mesenchymal transition (EMT) process through the PI3K/Akt/mTOR signaling pathway, the regulation of fibronectin, vimentin, N-cadherin, MMP-2, MMP-9, Insulin-Like Growth Factor Binding Proteins 3, 5 and 6 (IGFBP-3, IGFBP5 and IGFBP6), plus decreasing E-cadherin protein, cellular senescence and p16 marker expression.
From a mechanical point of view, ozonated oils and creams increase phosphorylation of PI3K, Akt, and mTOR, through regulation of the EMT process. With this knowledge, it becomes clear that ozonated oils significantly decrease fibroblastic infammation.

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[i] Skin Cancer Prevention; Guerra KC, Zafar N, Crane JS. Skin Cancer Prevention. 2021 Aug 14. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan–. PMID: 30137812.

[ii] Recognition and repair of the cyclobutane thymine dimer, a major cause of skin cancers, by the human excision nuclease. Reardon JT, Sancar A. Genes Dev. 2003;17(20):2539-2551. doi:10.1101/gad.1131003

[iii] Lopes DM, McMahon SB. Ultraviolet Radiation on the Skin: A Painful Experience? CNS Neurosci Ther. 2016 Feb;22(2):118-26. doi: 10.1111/cns.12444. Epub 2015 Aug 30. PMID: 26331607; PMCID: PMC4833175.

[iv] Bishop T, Marchand F, Young AR, Lewin GR, McMahon SB. Ultraviolet-B-induced mechanical hyperalgesia: A role for peripheral sensitisation. Pain. 2010 Jul;150(1):141-152. doi: 10.1016/j.pain.2010.04.018. Epub 2010 May 15. PMID: 20478657.

Dawes JM, Calvo M, Perkins JR, Paterson KJ, Kiesewetter H, Hobbs C, Kaan TK, Orengo C, Bennett DL, McMahon SB. CXCL5 mediates UVB irradiation-induced pain. Sci Transl Med. 2011 Jul 6;3(90):90ra60. doi: 10.1126/scitranslmed.3002193. PMID: 21734176; PMCID: PMC3232447.

[v] Gilchrest BA, Soter NA, Stoff JS, Mihm MC Jr. The human sunburn reaction: histologic and biochemical studies. J Am Acad Dermatol. 1981 Oct;5(4):411-22. doi: 10.1016/s0190-9622(81)70103-8. PMID: 7287956.

[vi] EL_TOBGY, Khaled. Ozone therapy in burns: our experience in Egypt [abstract]. Journal of Ozone Therapy, [S .l.] , v. 3, n. 4, p. 12, dec. 2019. ISSN 2444-9865. doi:http://dx.doi.org/10.7203/jo3t.3.4.2019.15417.

[vii] Xiao W, Tang H, Wu M, Liao Y, Li K, Li L, Xu X. Ozone oil promotes wound healing by increasing the migration of fibroblasts via PI3K/Akt/mTOR signaling pathway. Biosci Rep. 2017 Nov 9;37(6):BSR20170658. doi: 10.1042/BSR20170658. PMID: 28864782; PMCID: PMC5678031.