The mechanisms and treatments of muscular pathological changes in immobilization-induced joint contracture: A literature review

Chin J Traumatol. 2019 Apr;22(2):93-98. doi: 10.1016/j.cjtee.2019.02.001. Epub 2019 Mar 11.

Abstract

The clinical treatment of joint contracture due to immobilization remains difficult. The pathological changes of muscle tissue caused by immobilization-induced joint contracture include disuse skeletal muscle atrophy and skeletal muscle tissue fibrosis. The proteolytic pathways involved in disuse muscle atrophy include the ubiquitin-proteasome-dependent pathway, caspase system pathway, matrix metalloproteinase pathway, Ca2+-dependent pathway and autophagy-lysosomal pathway. The important biological processes involved in skeletal muscle fibrosis include intermuscular connective tissue thickening caused by transforming growth factor-β1 and an anaerobic environment within the skeletal muscle leading to the induction of hypoxia-inducible factor-1α. This article reviews the progress made in understanding the pathological processes involved in immobilization-induced muscle contracture and the currently available treatments. Understanding the mechanisms involved in immobilization-induced contracture of muscle tissue should facilitate the development of more effective treatment measures for the different mechanisms in the future.

Keywords: Disuse skeletal muscle atrophy; Immobilization-induced joint contracture; Skeletal muscle fibrosis; Treatment.

Publication types

  • Systematic Review

MeSH terms

  • Atrophy
  • Autophagy
  • Calcium / metabolism
  • Caspases / metabolism
  • Connective Tissue / metabolism
  • Connective Tissue / pathology
  • Contracture / etiology*
  • Contracture / metabolism
  • Contracture / pathology
  • Contracture / therapy
  • Fibrosis
  • Humans
  • Immobilization / adverse effects*
  • Joints*
  • Lysosomes / metabolism
  • Matrix Metalloproteinases / metabolism
  • Muscle, Skeletal* / metabolism
  • Muscle, Skeletal* / pathology
  • Proteasome Endopeptidase Complex / metabolism
  • Proteolysis
  • Signal Transduction / physiology*
  • Transforming Growth Factor beta1 / metabolism
  • Ubiquitin / metabolism

Substances

  • Transforming Growth Factor beta1
  • Ubiquitin
  • Caspases
  • Matrix Metalloproteinases
  • Proteasome Endopeptidase Complex
  • Calcium