When there is a reduction in joint capacity, i.e. amount of useable range of motion, movement exploration becomes confined and variability in movement is restricted. Continually using the same confined range of motion leads to the same tissues becoming repetitively overloaded. Acute and chronic overloading of tendinous tissue can lead to tendon pathology – TENDINOPATHY.
Tendinopathy occurs along a continuum:
Normal Tendon ←→ Reactive Tendon ←→ Tendon Dysrepair ←→Reactive Tendon
Reactive Tendinopathy – This is a response to acute overload or direct trauma. It is a non-inflammatory proliferative response in the cell matrix due to acute tensile or compressive overload. Collagen integrity is mostly maintained. The short-term adaptive response is thickening of a portion of the tendon, which will either reduce stress (force/area) by increasing cross-sectional area or allowing adaptation to compression.
Tendon Dysrepair – This is the tendon’s attempt at healing, similar to reactive tendinopathy but with greater cell matrix breakdown. There is an overall increase in number of cells (chondrocytes and myofibroblasts), resulting in increased protein production (proteoglycans and collagen). This results in separation of the collagen and disorganization of the cell matrix. These changes are more focal, and there may be an increase in vascularity and associated neuronal ingrowth. This often occurs in chronically overloaded tendon in younger individuals but may appear across a spectrum of ages and loading environments. Older individuals with reduced viscoelastic tendons that have less adaptive ability may develop this stage of tendinopathy with relatively lower loads.
Degenerative Tendinopathy – There is a progression of both matrix and cell changes. Areas of cell death due to apoptosis, trauma or tenocyte exhaustion appear. This results in areas of acellularity, with large areas of matrix disordered and filled with vessels, matrix breakdown products and little collagen. This stage is primarily seen in older individuals, but also seen in younger persons or elite athletes with chronically overloaded tendon. The classic presentation is middle-aged, recreational athlete with focal achilles tendon swelling and pain. These people commonly have a history of repeated bouts of tendon pain, often resolving but returning as the tendon load changes. Degenerative tendinopathy can rupture under high load – 97% of tendons that rupture have degenerative changes.
Let’s backtrack and remind ourselves what a “continuum” is:
“A continuous sequence in which adjacent elements are not perceptibly different from each other, although the extremes are quite distinct.”
The exact transition points between phases of the tendinopathy continuum cannot be identified. The histological findings and clinical presentations vary and may fall on multiple points along the continuum. As well, there is no precise transition from health to unhealthy tissue. Thus, we must keep in mind that a patient may present with findings indicative of more than one phase, or tendinous tissue in multiple pathological phases. We must also consider the general health and age of a patient, as this may provide clues to the underlying viscoelastic properties of the tendon.
Adding or removing load is the primary stimulus that drives the tendon forward or backward along the tendinopathy continuum. The further to the right along the continuum, the smaller the capacity to reverse pathological changes. The earlier along the continuum we can intervene, the better the prognosis. Along this continuum, the pathological tendon can accept different magnitudes of load. For optimal exercise prescription, the tissue capacity should be taken into careful consideration.
Research on tendon rehab greatly supports eccentric muscle contraction having the most beneficial effect on both tendon structure and pain levels. Applying the general research of eccentric tendon training to what we now know about the tendon pathology continuum, we can prescribe with more precision. Tendons at the reactive end of the continuum can accept greater intensities of load than tendons at the degenerative end. The intensi2ty can be modified to accommodate the tendon’s capacity as it moves along the pathological tendon during your plan of management. Other parameters such as frequency and duration should also be prescribed in a similar way.
On a final note – The tendinopathy continuum model is strikingly similar to what is seen is articular cartilage pathology, such as osteoarthritis. Can we apply the same thought process to managing joint health and osteoarthritis?
Written By: Dr. Mitch Broser
@mbroser
Reference:
1. Cook JL,. Purdam CR. Is tendon pathology a continuum? A pathology model to explain the clinical presentation of load-induced tendinopathy. BR J Sports med. 43:409-416. 2009.