Tendons are connective structures that connect muscle to bone and are under great tensile force when loaded. Tendon injuries can occur at many different areas of the body, most commonly the Achilles tendon, the patella tendon, rotator cuff tendons, hamstring tendons; but are not limited to these specific tendons.
Tendon injuries are usually the result of increased load, overuse and or direct trauma. Injuries are most commonly insertional (where the tendon attaches to the bone) but can also occur mid belly. When injury occurs in then tendon there are pathological changes within the tendon resulting in pain, decreased exercise tolerance and a reduction in function (Cook and Purdam 2009). Consequently the tendon is now less able to sustain repeated tensile load.
Extensive research has been conducted in the pathogenesis of tendon injuries and subsequently there has been a change in terminology from tendonitis to tendinopathy – whereby there are pathological changes in the tendons and it can be a progressive and degenerative injury if not accurately diagnosed and or staged. The move away from the term tendonitis has resulted from randomized controlled trials concluding that little to no inflammation occurs within a tendon when exposed to overuse (Andres and Murrell 2008).
The pathology of tendon injury varies between acute, dysrepair and chronic degenerative presentations and so does tendon response to treatment. Consequently, interventions should be tailored to the specific stage of a tendon injury (Cook and Purdam 2009).
There is the notion now that there is a continuum of tendon pathology and it comprises of three stages: reactive tendinopathy, tendon dysrepair and degenerative tendinopathy (Cook and Purdam 2009). Load is the stimulus that drives tendon pathology thereby by adding load can advance the tendon injury and removing load can return the tendon back along the continuum.
image: (Cook and Purdam 2009)
Reactive Tendinopathy:
This is a non-inflammatory proliferative response in the cell and matrix, which is a short-term adaptive thickening of the tendon in attempt to reduce stresses (Cook and Purdam 2009) and can result in increased stiffness. This takes place in the short term to allow the tendon to cope with increased loads. The tendon can return to normal structure if the overload is reduced or time is given between loading. Reactive tendinopathies tend to follow a period of acute overload or unaccustomed load and can also result from a direct trauma to the tendon (e.g a hockey ball to the Achilles).
Tendon Dysrepair:
In the stage of tendon dysrepair there is an attempt at tendon healing, similar to reactive tendinopathy but with greater matrix breakdown (Cook and Purdam 2009). There is an increase in cells within the tendon leading to separation of the collagen and disorganization of the matrix. These tendons tend to be thick with more localized changes in one area of the tendon and are often associated with neuronal ingrowth (often picked up on ultrasound and MRI imaging). Often older people, with stiffer tendons that have less adaptive ability, may develop this stage of tendinopathy with relatively low loads. Reversibility of tendon disrepair is possible with load management and exercise to stimulate matrix structure. This stage of tendon injury is often reported in chronically overloaded tendons.
Degenerative tendinopathy:
Degenerative tendinopathy is the final stage of the continuum and is associated by the progression of both matrix and cell changes (Cook and Purdam 2009), There are areas of cell death resulting in large areas of disorganization in the matrix filled with vessels, matrix breakdown and less collagen. Once a tendon reaches this stage of injury there is little reversibility of pathological stages at this stage and intervention focuses on management to prevent tendon rupture which is at a greater risk in this stage (Cook and Purdam 2009).
Pain and the tendon:
Tendinopathic pain is induced by load and has two key features (Cook and Purdam 2009): (1) dose-dependent pain in relation to singular or cumulative load, and (2) pain that is well localised to the tendon or enthesis (point of attachment). Therefore by increasing load on the tendon there will usually be an increase pain (Cook and Purdam 2009). The source of pain has been associated with cellular changes as well as neurovascular ingrowth as seen in the tendon dysrepair/ degenerative phase. However, changes in the tendons can also be pain-free.
Treatment of Tendinopathy:
Pain is often the overarching clinical feature of tendinopathy in all stages. Therefore, interventions aiding pain management as well as tendon repair are an important feature to address without compromising the stage of the tendon injury along the continuum.
Reactive Tendinopathy:
- Load management will usually allow time for the tendon adapt and the cells to become less reactive and the matrix to resume normal structure (Cook and Purdam 2009).
- Allowing a day or two days in between bouts of loading in conjunction with modification of intensity, frequency and duration and the type of load.
- Identify any biomechanical abnormalities which may be adversely contributing to tendon loading (Cook and Purdam 2009).
- Despite the lack of inflammation, often Non-Steroidal Anti-inflammatory (NDAIDS), medications such as Ibruprofen, Ibruprofen inhibits the production of proteins responsible for tendon swelling (Cook and Purdam 2009).
- Graded increase in return to sport without re-loading the tendon too soon.
Tendon Dysrepair and Degenerative Tendinopathy:
- Treatments that stimulate cell activity, increase protein production (collagen or ground substance) and restructure the matrix.
- Physiotherapy
- Identify any biomechanical abnormalities which may be adversely contributing to tendon loading (Cook and Purdam 2009).
- Eccentric exercise has been shown to increase collagen production in abnormal tendon (and decrease tendon vessels (Cook and Purdam 2009)
- Prolotheapy (Blood injections) stimulates cell proliferation and production of vascular endothelial growth factor (Cook and Purdam)
References:
Cook J Purdam C (2009) Is tendon pathology a continuum? A pathology model to explain the clinical presentation of load-induced tendinopathy. British Journal of Sports Medicine;43:409–416.
Andres B and Murrel G (2008) Treatment of Tendinopathy: What Works, What Does Not, and What is on the Horizon. Clinical Orthopaedics and Related Research ; 466 (7) :1539–1554
Penny Stern
Range of Motion Physiotherapist
BSc Physiotherapy.
Australian Physiotherapy Association Member (APAM).
Musculoskeletal Physiotherapy Association Member (MPA).
Sports Physiotherapy Association Member (SPA).
