Hameedi Sophia G, Saulsbery Angela, Olutoye Oluyinka O
Center for Regenerative Medicine, Nationwide Children's Hospital, Columbus, Ohio, USA.
Department of Surgery, The Ohio State University, Columbus, Ohio, USA.
Adv Wound Care (New Rochelle). 2025 Jan;14(1):48-64. doi: 10.1089/wound.2023.0185. Epub 2024 Apr 25.
Pathologic scarring occurs secondary to imbalances in the cellular mechanisms of wound healing and affects millions of people annually. This review article aims to provide a concise overview of the pathophysiology and management of pathologic scarring for clinicians and scientists alike. Contemporary research in the field has identified aberrations in transforming growth factor-β/small mothers against decapentaplegic (TGF-β/SMAD) signaling pathways as key drivers of pathologic scar formation; indeed, this pathway is targeted by many treatment modalities and translational investigations currently underway. Although intralesional injection of corticosteroids has been the gold standard in the treatment of pathologic scarring, studies show greater treatment efficacy with the use of combination injections such as triamcinolone/5-fluorouracil and triamcinolone/botulinum toxin. Adjunctive therapies including ablative fractional carbon dioxide/erbium-doped yttrium aluminum garnet and non-ablative pulsed-dye lasers, microneedling, and carboxytherapy have shown encouraging results in small cohort studies. Translational investigations involving the use of nanogels, RNA interference, and small molecules targeting TGF-β/SMAD pathways are also currently underway and hold promise for the future. The heterogeneous nature of hypertrophic scars and keloids poses significant challenges in formulating standardized treatment and assessment protocols, thereby limiting the conclusions that can be drawn. Rigorous clinical trials into the individual and synergistic effects of these therapies would be ideal before any definitive conclusions or evidence-based treatment recommendations can be made. Owing to the heterogeneity of the pathology and patient population, well-conducted cohort studies may be the next best option.
病理性瘢痕继发于伤口愈合细胞机制失衡,每年影响数百万人。本文综述旨在为临床医生和科研人员简要概述病理性瘢痕的病理生理学及治疗方法。该领域的当代研究已确定转化生长因子-β/抗五聚体蛋白母系小型蛋白(TGF-β/SMAD)信号通路异常是病理性瘢痕形成的关键驱动因素;事实上,该通路是目前许多治疗方式及转化研究的靶点。虽然病灶内注射皮质类固醇一直是治疗病理性瘢痕的金标准,但研究表明,使用曲安奈德/5-氟尿嘧啶和曲安奈德/肉毒杆菌毒素等联合注射治疗效果更佳。包括剥脱性分次二氧化碳/掺铒钇铝石榴石激光和非剥脱性脉冲染料激光、微针疗法和羧基疗法在内的辅助治疗在小型队列研究中显示出令人鼓舞的结果。目前也正在进行涉及使用纳米凝胶、RNA干扰和靶向TGF-β/SMAD通路的小分子的转化研究,有望取得未来进展。增生性瘢痕和瘢痕疙瘩的异质性给制定标准化治疗和评估方案带来了重大挑战,从而限制了可得出的结论。在得出任何明确结论或提出循证治疗建议之前,对这些疗法的个体和协同效应进行严格的临床试验将是理想的。由于病理和患者群体的异质性,开展良好的队列研究可能是次优选择。