Tendon healing is adversely affected by low-grade inflammation

Emanuele Chisari,Laura Rehak,Nicola Maffulli,Wasim S Khan

doi:10.1186/s13018-021-02811-w

Abstract

BackgroundTendinopathy is common, presents with pain and activity limitation, and is associated with a high risk of recurrence of the injury. Tendinopathy usually occurs as a results of a disrupted healing response to a primary injury where cellular and molecular pathways lead to low grade chronic inflammation.Main findingsThere has been a renewed interest in investigating the role of Inflammation in the pathogenesis of tendinopathy, in particular during the initial phases of the condition where it may not be clinically evident. Understanding the early and late stages of tendon injury pathogenesis would help develop new and effective treatments addressed at targeting the inflammatory pathways.ConclusionThis review outlines the role of low-grade Inflammation in the pathogenesis of tendinopathy, stressing the role of proinflammatory cytokines, proteolytic enzymes and growth factors, and explores how Inflammation exerts a negative influence on the process of tendon healing.

Highlights

Tendons are well recognized essential structure of the musculoskeletal system [1, 2]
This review outlines the role of low-grade Inflammation in the pathogenesis of tendinopathy, stressing the role of proinflammatory cytokines, proteolytic enzymes and growth factors, and explores how Inflammation exerts a negative influence on the process of tendon healing
While their microscopical and macroscopic structure is still debated, it is well recognized that tendons are basically made by an abundant extracellular matrix made of elongated type I collagen (70–80%) and elastic fibres, and a less predominant cellular component made by tenoblasts and tenocytes

Summary

Conclusion

The prolonged state of low-grade Inflammation seen in chronic tendinopathy may act as a risk factor after an acute tendon injury, predisposing to a failed healing response that may persist despite surgery. Further studies on inflammation pathways and antiinflammatory therapies directed at specific chronic inflammation molecular targets are necessary to investigate the topic further. Active control of the immune system is a very plausible therapeutic strategy to induce tissue regeneration. One of the main challenges is to target the right immune cell populations and pathways for the tissue that need to be regenerated

Introduction

Findings