The Molecular Pathogenesis of Dupuytren Disease Review of the Literature and Suggested New Approaches to Treatment

被引:7
作者
Sayadi, Lohrasb R. [1 ]
Alhunayan, Danah [1 ]
Sarantopoulos, Nikolaos [1 ]
Kong, Christina [1 ]
Condamoor, Shreya [1 ]
Sayadi, Jamasb [2 ]
Banyard, Derek A. [1 ]
Shaterian, Ashkaun [1 ]
Leis, Amber [1 ]
Evans, Gregory R. D. [1 ]
Widgerow, Alan D. [1 ]
机构
[1] Univ Calif Irvine, Dept Plast Surg, Ctr Tissue Engn, Orange, CA 92868 USA
[2] Stanford Univ, Sch Med, Stanford, CA 94305 USA
关键词
Dupuytren disease; Pathophysiology; Hand; BONE MORPHOGENETIC PROTEINS; SMOOTH MUSCLE ACTIN; GROWTH-FACTOR; TGF-BETA; EXTRACELLULAR-MATRIX; MYOFIBROBLAST; EXPRESSION; CONTRACTURE; CELLS; FIBROBLASTS;
D O I
10.1097/SAP.0000000000001918
中图分类号
R61 [外科手术学];
学科分类号
摘要
Background Ever since the classification of Dupuytren disease into the proliferative, involutional, and residual stages, extensive research has been performed to uncover the molecular underpinnings of the disease and develop better treatment modalities for patients. The aim of this article is to systematically review the basic science literature pertaining to Dupuytren disease and suggest a new approach to treatment. Methods Following Preferred Reporting Items for Systematic Reviews and Meta-Analysis guidelines, a systematic review was conducted using the MEDLINE database to identify basic science literature on Dupuytren pathophysiology falling under 1 or more of the following categories: (1) Molecular alterations, (2) Structural alterations, and (3) Genetic predisposition. Results A total of 177 articles were reviewed of which 77 studies met inclusion criteria. Articles were categorized into respective sections outlined in the study methods. Conclusion The pathophysiological changes involved in Dupuytren's disease can be divided into a number of molecular and structural alterations with genetic predisposition playing a contributory role. Understanding these changes can allow for the development of biologics which may disrupt and halt the disease process.
引用
收藏
页码:594 / 600
页数:7
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