Striae distensae (SD), commonly known as stretch marks, are visible linear scars that develop in areas of dermal damage as a result of excessive stretching of the skin.
Striae generally develop in various physiological states such as pregnancy, growth spurts during puberty, or a rapid change in the proportion of specific body regions such as can be seen in weight lifters, those who are obese, or with substantial weight loss [1]. They are also seen in pathological conditions with hypercortisolism, such as Cushing’s syndrome [2] and genetic disorders.
The primary pathology lies in an altered dermal connective tissue framework involving components of the extracellular matrix (ECM) namely, fibrillin, elastin, fibronectin, and collagen. In the initial stages, elastic fibres undergo elastolysis and degranulation of mast cells [3]. Affected tissue may also show low expression of collagen and fibronectin genes or a high proportion of rigid cross-linked collagen, which makes the connective tissue prone to stress rupture [4]. However, despite several advances, no fully effective treatment has emerged. Unfortunately, there is a lack of strong evidence in the literature for the effective treatment of striae. Although SD is common among females between 10 and 50 years old, a growing percentage of males are now affected by SD.
Case report
A 35-year-old male attended my private practice with SD on his buttocks. He requested to improve the appearance and the texture of the area. Clinically SD appear as multiple, symmetric, irregularly linear, atrophic scars that follow the lines of cleavage and lie parallel to the skin surface [5]. The patient reported that the blemish appeared during puberty. Before coming to my clinic, he had never undergone any treatment. The treatment plan was to biostimulate SD tissue with Revypeel High by MBE, a chemical peeling composed of Trichloroacetic Acid (20%), Kojic Acid (5–7%), Mandelic Acid (5–7%), which is pH 0.2–1%, and is suitable for all phototypes (I–VI) and skin types. Before treatment, we prepared the skin with a pre-peeling solution rich in ascorbic acid, citric acid, and lactic acid.
The application time of the product for each session carried out was approximately three to five minutes. In this case, we carried out three sessions, one every seven days. After every session, we used a neutralising gel of sodium bicarbonate to buffer the pH of peeling. At the end of every session, we applied a post-peeling cream (SPF 50+) composed of shea butter, argan oil, hyaluronic acid, panthenol, and vitamin E. We suggested the patient apply post-peeling cream also at home every day until the next session. The patient was advised to avoid sun exposure. No complications were observed, just a local redness after the topic application of acids, solved with post-peeling cream. We observed the improvement of SD from the first application. The marks appeared less grooved and more vascularised. We observed an increasing texture after the third session. The patient was very satisfied; he obtained a better result than he expected without the use of needles, and without pain or discomfort.
Discussion
Trichloroacetic acid produces excellent improvement in the tonicity, the gloss, and the smoothness of the skin, a great action on cutaneous dyschromia. It has strong smoothing power on scar tissue and produces deep fibroblast stimulation. The action, combined with kojic acid and mandelic acid, penetrates the superficial dermis without generating a ‘frost’ effect and it induces a ‘controlled damage’ and a regenerative and revitalising stimulus that induces tissue self-repair and remodelling. In three weeks of treatment, we can observe the effect on the remodelling of the subcutaneous matrix and the stimulus on the vascular pattern. This result allows us to conclude that using Revypeel High alone achieves excellent results. Revypeel can also be used as a basis for combination with other devices to treat SD, such as oxyneedling, radiofrequency, and lasers.
References
1. Ammar NM, Rao B, Schwartz RA, Janniger CK. Adolescent striae. Cutis 2000;65:69–70.
2. Shuster S. The cause of striae distensae. Acta Derm Venereol Suppl (Stockh) 1979;59:161–9.
3. Sheu HM, Yu HS, Chang CH. Mast cell degranulation and elastolysis in the early stage of striae distensae. J Cutan Pathol 1991;18:410–6.
4. Lovell CR. Acquired Disorders of Dermal Connective Tissue – Striae. In: Griffiths C, Barker J, Bleiker T, et al. (Eds). Rook’s Textbook of Dermatology 9th Edition. Chichester, UK; John Wiley & Sons; 2016:96.9–10.
5. Lokhande AJ, Mysore V. Strie distensae treatment review and update. Indian Dermatol Online J 2019;10(4):380–95.
Declaration of competing interests: None declared.
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