Cook and Purdum have the most widely appreciated theory of tendinopathy pathology, their model is based on a 3 stage continuum, a reactive, disrepair and degenerative stage.
The reactive phase is a non-inflammatory proliferative response, which generally follows a period of single incidence of overload/un-accustomed activity as previously mentioned. It is essentially the tendon trying to protect itself by thickening, this occurs as prostaglandins are produced which have a high affinity for water and thus the tendon swells. There is no change in collagen integrity at this point, it is felt that the reactive stage occurs prior to changes in structure or mechanical properties can occur. The tendon can easily revert back to its normal state if the load is reduced and the tendon is rested. Imaging will show swelling in a fusiform manner with increased diameter on both US and MRI. Ultrasound will show hypoechogic areas due to the increase in water molecules, MRI will show minimal or no increased signal at this stage.
In the dysrepair(failed healing stage) there is disorganization in the matrix with neovasculrisation and neural in-growth. This is similar to the reactive stage, however there is greater matrix breakdown. There is an increase in cells which are many condroyctic as well as some myofribrolblasts. The increase in prostogldins causes separation of the collagen and disorganization of the matrix. Some reversibility of the pathology is still possible with load management and exercise to stimulate matrix structure. Imaging will show hypoechoic areas once more but also neovasulrisation on Doppler. On MRI the tendon in swollen and there is increased signal.
In the degenerative stage there a progression of the cell and matrix changes. There are areas of cell death due to apoptosis, trauma or tenocyte exhaustion. This causes areas of acellularity and large areas of the matrix become disorganized and filled with neovasculraisation and neural in-growth. Once things have progressed to this stage, there is little or no chance to reverse these changes. The matrix at this stage displays areas of heterogeneity due to areas of degeneration mixed with areas of normal unpathological tendon interspersed together. Imaging will show extensive vascular changes with few reflections from collagen fascicles. MRI will once more show increased signal but this will be focal in nature.
Like all theories, Fu, abate and cook and Purdam have presented their thoughts based upon current evidence. However they are just that, theories. Therefore all theories should be considered when assessing, treating and managing tendinopathies.