Acne Scars - Mixed Atrophic and Hypertrophic Clinical Trial
Official title:
The Role of Topical Timolol 0.5% in Wound Healing and Scar Improvement Following Atrophic Acne Scar Microneedling
The aim of the study is to evaluate the efficacy and safety of microneedling combined with topical timolol 0.5% in the treatment of atrophic acne scars.
Acne vulgaris (AV) is a common chronic inflammatory disease of skin that develops from sebaceous glands associated with hair follicles. Typically AV begins at puberty and may continue through adulthood affecting the comedogenic areas of face, back and chest (Mazzetti et al., 2019). One of the undesirable outcomes of acne is acne scars that are divided into two main types based on a loss (atrophic) or gain (hypertrophic) of collagen. Atrophic type is the most common type, further subdivided into three subtypes: icepick, boxcar and rolling scar (Bahl et al., 2020). Post acne scars occur in nearly 75% of patients with acne affecting both male and female equally (Khunger and Kumar, 2012). Acne scars impair quality of life and may be a risk factor for depression, suicide, low academic performance and unemployment (Sood et al., 2020). There are different therapeutic modalities for atrophic acne scars including microneedling, chemical peeling, laser, filler, surgical procedures (punch excision, punch grafts) and fat transfer (Pavlidis and Katsambus, 2017). Microneedling is considered safe for all skin types. It is performed by dermapen or dermaroller to induce new collagen formation that remains for a few months after the procedure (Cohen and Elbuluk, 2016). Microneedling enhances the effect of topical preparations when used combined with them due to increasing their absorption by creating small channels through the epidermis to the dermis (Jaffe, 1981). Ghassemi et al. (2021) observed that application of 0.5% timolol after TCA-CROSS caused a slight increase in scar improvement with more physician and patients' satisfaction. Timolol, a beta-adrenergic receptor blocker, improves healing of skin wounds by increasing the phosphorylation of extracellular signal regulated kinases (ERK) leading to keratinocyte migration (Zeigler et al., 1999). Also, ERK initiate signaling cascades leading to fibroblast mitosis and proliferation with regulation of fibroblast functions in replacement of disorganized collagen and the reposition of the extracellular matrix (de Araújo et al., 2019). ;
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