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唇裂术后瘢痕的现有及新兴治疗方法:疗效与机制

Current and Emerging Treatments for Postsurgical Cleft Lip Scarring: Effectiveness and Mechanisms.

作者信息

Papathanasiou E, Trotman C A, Scott A R, Van Dyke T E

机构信息

1 Center for Clinical and Translational Research, Forsyth Institute, Cambridge, MA, USA.

2 Department of Periodontology, Tufts University School of Dental Medicine, Boston, MA, USA.

出版信息

J Dent Res. 2017 Nov;96(12):1370-1377. doi: 10.1177/0022034517717261. Epub 2017 Jun 26.

Abstract

Cleft lip with or without cleft palate is the most common congenital malformation of the head and the third-most common birth defect. Surgical repair of the lip is the only treatment and is usually performed during the first year of life. Hypertrophic scar (HTS) formation is a frequent postoperative complication that impairs soft tissue form, function, or movement. Multiple lip revision operations are often required throughout childhood, attempting to optimize aesthetics and function. The mechanisms guiding HTS formation are multifactorial and complex. HTS is the result of dysregulated wound healing, where excessive collagen and extracellular matrix proteins are deposited within the wound area, resulting in persistent inflammation and resultant fibrosis. Many studies support the contribution of dysregulated, exaggerated inflammation in scar formation. Fibrosis and scarring result from chronic inflammation that interrupts tissue remodeling in normal wound healing. Failure of active resolution of inflammation pathways has been implicated. The management of HTS has been challenging for clinicians, since current therapies are minimally effective. Emerging evidence that specialized proresolving mediators of inflammation accelerate wound healing by preventing chronic inflammation and allowing natural uninterrupted tissue remodeling suggests new therapeutic opportunities in the prevention and management of HTS.

摘要

唇裂伴或不伴腭裂是最常见的头部先天性畸形,也是第三常见的出生缺陷。唇裂手术修复是唯一的治疗方法,通常在出生后第一年进行。肥厚性瘢痕(HTS)形成是一种常见的术后并发症,会损害软组织的形态、功能或运动。在整个儿童期通常需要多次唇部修复手术,以优化美观和功能。导致HTS形成的机制是多因素且复杂的。HTS是伤口愈合失调的结果,伤口区域会沉积过多的胶原蛋白和细胞外基质蛋白,导致持续炎症和纤维化。许多研究支持炎症失调、过度在瘢痕形成中的作用。纤维化和瘢痕形成源于慢性炎症,它会中断正常伤口愈合中的组织重塑。炎症途径未能有效主动消退也与此有关。HTS的治疗一直是临床医生面临的挑战,因为目前的治疗效果甚微。新出现的证据表明,专门的促炎症消退介质可通过预防慢性炎症并允许自然的不间断组织重塑来加速伤口愈合,这为HTS的预防和治疗提供了新的治疗机会。

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