Peritendinous adhesion: Therapeutic targets and progress of drug therapy

Abstract

Peritendinous adhesion (PA) is one of the most common complications following hand surgery and characterized with abnormal hyperplasia of connective tissue and excessive deposition of extracellular matrix. Subsequently, various clinical symptoms such as chronic pain, limb dyskinesia and even joint stiffness occur and patients are always involved in the vicious cycle of "adhesion - release - re-adhesion", which seriously compromise the quality of life. Until present, the underlying mechanism remains controversial and lack of specific treatment, with symptomatic treatment being the only option to relieve symptoms, but not contributing no more to the fundamentally rehabilitation of basic structure and function. Recently, novel strategies have been proposed to inhibit the formation of adhesion tissues including implantation of anti-adhesion barriers, anti-inflammation, restraint of myofibroblast transformation and regulation of collagen overproduction. Furthermore, gene therapy has also been considered as a promising anti-adhesion treatment. In this review, we provide an overview of anti-adhesion targets and relevant drugs to summarize the potential pharmacological roles and present subsequent challenges and prospects of anti-adhesion drugs.

Keywords: Adhesion formation; Anti-adhesion drugs; Collagen deposition; Peritendinous adhesion.

Graphical abstract

Fig. 1

Schematic diagram of therapeutic targets and drug therapy of PA. It exhibited the therapeutic biomarkers, drug therapy, gene therapy and drug delivery of PA.

Fig. 2

Schematic diagram showing the pathologic process of PA and molecular mechanism of intrinsic and extrinsic healing of tendon.

Fig. 3

The crystal structures of TGF-β1 (UniProt number: P01137), TGF-β2 (UniProt number: P61812) and TGF-β3 (UniProt number: P10600) were downloaded from Alphafold database.