If our tendons are not loaded progressively they are likely to become pathological/diseased/unhealthy. This is known as a tendinopathy. We are likely to develop a tendionpathy, which is described in the literature as a pain and impaired function to a tendon with associated swelling. This used to be described as a tendonitis, but there is a wealth of evidence to suggest the absence of inflammatory cells which is the fancy medical suffix “itis”, is not actually present.
There are number of current the theories to try and explain the pathology of a tendinopathy. Cook and Purdam describe the “tendinopathy continuum”. This involves a reactive, disrepair and degenerative phase of the injury. Fu has described a “failed healing theory” with Abate taking this one step further and coining “the iceberg theory”. This theory involves a tendinonic healing process with failed healing. Pain in this case is the tip of the iceburg and occurs when the degeneration outweighs its ability to self heal.A healthy tendon subjected to exercise will undergo some degradation and synthesis, with synthesis prevailing and the tendon becoming stronger.
However, when damage develops 2 phases are recognised:
(i) asymptomatic and;
(ii) symptomatic phase.
If recovery is too short and the blood supply is inadequate the repetitive strain loads will cause micro damage inside the tendon. The iceberg theory explains the frequent relapses of a profession athlete when rehab periods are too short but pain has diminished but the neo-angiogenesis (growing of new blood vessels) and neural in growth (growing of new nerve cells) can still cause the tendon to be pathological.
Overuse is the initial disease factor with micro-disruption of the tendon fibers. From their research they believe that noxious mechanisms are activated with increased expressions of inflammatory mediators. This then stimulates the synthesis of MMP’s and enzymes that increase the degradation of the extra cellular matrix and promotes neo-angiogenesis. This results in degeneration and weakening of the normal tendon structure. Neural in-growth accompanies the neo-vessels which leads to over expression of glutamate and other chemicals which explain the occurrence of pain and possibly triggers neurogenic mediated inflammation.
In my next blog 2 blogs I will describe the Cook and Purdam “continuum model” and the Fu “failed healing” response.