Tendon Paradigms

 

Tendinosis Paradigm (1990’s)

Prior to the 1990’s tendon pain was referred to tendinitis, which reflected the belief that inflammation was the primary driver of the pathological process (Rees et al 2013). This view was ingrained deeply in the medical literature of the time and, as a result of this belief, the primary treatment for this condition was non-steroidal anti-inflammatories and corticosteroids (Rees et al 2013).

 

In the 1990’s there was a shift in the literature away from this inflammatory model of tendon disorder. This shift was in light of studies being published at the time which failed to demonstrate the presence of any acute inflammatory cells in the load bearing areas of tendons. Other studies began describing symptomatic tendons which displayed collagen thinning and separation without any inflammatory infiltrate (Rees et al 2013). With this evidence there was a strong push for the tendinosis model describing tendon pain arising completely without the presence of any inflammation.

 

 

 

 

 

 

Tendinosis Paradigm (2000’s)

This shift towards a non-inflammatory based model of tendon disorder has continued into the 21st century with a new “Degenerative” model being established. This umbrella term includes the cumulative damage, vascular insufficiency modes and failed healing response; all of which are commonly associated with the modern thinking around tendinopathy. Ironically the tendinosis model has now become as deeply ingrained in the medical literature as tendinitis had been previously. This puts our understanding of the pathological process at risk of being oversimplified and result in potentially effective treatments being ignored (Rees et al 2013). Recent improvements in immunohistochemistry and gene expression analysis have enabled a more accurate understanding of the underlying pathophysiology at work within tendinopathy.