Advances in tendinopathy

Previously I have touched on my summer research project on tendinopathy but today I thought I would share a bit of what I have done with you all, enjoy!

The driving force behind my research was due to the fact that soft tissue disorders represent the third most common musculoskeletal condition in the UK with 18 cases per 1000. These primarily affect tendons, accounting for 30% of all rheumatological consultations with a general practitioner. Causes are multifactorial but with an ever increasing number of professional athletes and also an ageing population whose tendons decrease in elasticity; there is an annual estimated cost to the NHS of £250 million. Though molecular pathophysiology of tendinopathy remains incompletely understood key inflammatory mediators such as proinflammatory cytokines are found to play a vital role.

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This little fella is tenascin-C

The extracellular matrix molecule tenascin-C is highly expressed during embryonic development, in pathological situations such as chronic inflammation, cancer. By this report it is found to be at significantly higher levels during diseased tendon tissue repair as compared to healthy tendons to carry out its role as an inflammatory mediator and induce inflammation in attempts to repair the diseased tendon. Tenascin-C prolongs inflammation at site of trauma and leads to further tendon damage. These results provide useful insight into the complex cross-regulation of inflammation and tissue remodelling mediated by tenascin-C.

Some background information

Tendons are a band of flexible fibrous connective tissue which connects muscle to bone. They are present in joints and largely inelastic to conserve energy whilst transmitting the contractile movement of muscle to move bone. Despite the frequent mention of tendinopathy, tendons are in fact extremely tough it is found that collagen fibrillogenesis begins as an assembly of collagen molecules in a series of extracellular compartments, progressing through post-depositional maturation leading to thicker and longer fibrils and ending in their coalescence in the final stages of fibre production.

 

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Figure 1Various tendons on the body which are affected by tendinopathy especially the Achilles tendon and rotator cuff

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