Tendinopathy General Principles

Tendinopathy is persistent tendon pain and loss of function related to mechanical loading, understood as a failed healing response rather than an acute inflammatory 'tendinitis'.

Common sites are the Achilles, patellar tendon, lateral elbow, rotator cuff, gluteal tendons, proximal hamstring and tibialis posterior. Progressive loading is first-line at every site; injections and shockwave have different evidence at each tendon and are judged site by site.

Tendon is mainly type I collagen in parallel bundles, with relatively few tenocytes that remodel the matrix in response to load. Blood supply is poor, with vulnerable zones such as the Achilles mid-portion and the supraspinatus near its insertion.

The enthesis is a distinct site: overuse enthesopathy is mechanical, while enthesitis in spondyloarthritis is inflammatory and systemic.

The Cook and Purdam continuum describes 3 stages. Tendons can move back and forth between them, and different regions of one tendon can sit at different stages:

• •Reactive: a non-inflammatory response to a sudden load increase, with swelling as proteoglycan draws water into the tendon. Largely reversible with load management
• •Dysrepair: failed healing with disorganised collagen, increased ground substance and new blood vessels, often with new nerve ingrowth. Still able to improve with loading
• •Degenerative: matrix breakdown and cell death, with limited structural reversal and a higher rupture risk. Pain and function can still improve by loading the healthier tendon around it

Most ruptures occur in degenerate tendons, often without previous symptoms.

Risk factors:

• •Load (the most important): a sudden rise in training, unaccustomed activity or a change of surface or footwear
• •Intrinsic: older age, obesity, diabetes, hypercholesterolaemia and menopause
• •Drugs: fluoroquinolones and corticosteroids
• •Biomechanical: muscle weakness and kinetic chain deficits