Molecular mechanisms and treatment strategies for Dupuytren's disease

Abstract

Dupuytren's disease (DD) is a common disease of the hand and is characterized by thickening of the palmar fascia and formation of tight collagenous disease cords. At present, the disease is incurable and the molecular pathophysiology of DD is unknown. Surgery remains the most commonly used treatment for DD, but this requires extensive postoperative therapy and is associated with high rates of recurrence. Over the past decades, more indepth exploration of the molecular basis of DD has raised the hopes of developing new treatment modalities. This paper reviews the clinical presentation and molecular pathophysiology of this disease, as well as current and emerging treatment. It also explores the implications of new findings in the laboratory for future treatment.

Keywords: Dupuytren’s contracture; Dupuytren’s disease; fibrosis.

Figure 1

Proposed scheme in which TGF-β signalling, ECM stress tension, and/or other ECM-associated factors may lead to dysregulation of myofibroblast differentiation. These pathways seem to be involved in the molecular pathogenesis of Dupuytren’s disease and targeted interruption of abnormal signalling components may lead to future treatment approaches. Abbreviations: ECM, extracellular matrix; TGF-β, transforming growth factor-beta.