I attended my first lecture held by Jill Cook in September 2013, when Jill presented to our masters class on about current trends in tendon management. To say that Jill Cook is at the forefront of the best tendon research in the world would be an understatement. What an incredible impact Jill has already made and such a contribution to Physiotherapy internationally. There are many great ideas that I learnt from this master class, one of which is the continuum of tendon pathology. Before we can understand how to treat tendons we need to first understand the pathological process that occurs. The aim of this blog is to explore one landmark article published in 2009 titled "Is tendon pathology a continuum? A pathology model to explain the clinical presentation of load-induced tendinopathy" which describes the pathological process as a continuum and not an absolute. Cook proposes that from the new research on tendon pathology there are three main phases of the process; reactive tendinopathy, tendon dysrepair, and degenerative tendinopathy. It is an excellent article which presents these ideas in such a clear manner. I couldn't stress more highly the importance of reading the original paper.
Tendinopathy is a process which describes injury to the tendon that is a result of overload beyond the capacity of that tendon.
Yes a vague sentence but very important one to understand. Tendon pathology only occurs with overload. How much load you might wonder? Each individual will vary in terms of their gender, age, percentage visceral fat, history of physical activity through puberty, current physical activity, medication use, medical history and lifestyle, therefore the tendon's capacity for load is specifically and uniquely related to the individual's make up. More importantly, what activity leads to overload will vary enormously too.
I remember asking Jill why it has been found that volleyball players in lower divisions are more susceptible to developing patella tendinopathy. My thought process was that if the honours level played and trained more frequently then surely the rate of injury would be higher? As Jill explained, it doesn't matter about the level of difficultly of training in more elite levels, it comes purely down to capacity and load. Yes, the elite players have more load placed on them but their capacity to tolerate load is far greater too.
Over time our understanding of tendon pathology has changed significantly. The term tendinitis is no longer used because studies show that there is no inflammatory process occurring in the tendons. Unfortunately this belief is deeply entrenched in many health practitioners and people are still being prescribed anti-inflammatories for tendinopathies. It is time for us to move forward and accept that this is not the process occurring within the tendon cells and the term tendinitis needs to be abandoned from our description of the problem (Khan, et al., 2002).
The key factors in the onset of tendinopathy appear to be repetitive energy storage and release, and excessive compression. The key word here is compression, not tearing in the collagen. Compression is thought to create the cell-induced tendinopathic process within the tissues (Cook & Purdam., 2012).
Compressive overload can occur in three ways: rapid overload, repetitive overload or abusive overload (from blunt trauma).
The amount of load (volume, intensity, frequency) required to induce tendon pathology is not currently known and varies considerably between individuals for reasons mentioned above (Cook & Purdam, 2009). Adequate time between loading is important to allow a tendon to respond, therefore volume (hours) and frequency (number of sessions per day/week) of intense load is likely critical in the capacity of tendons to endure load (Cook & Purdam, 2009). Tendinopathy has been described as a continuum of pathology that has three distinct stages and is presented below. It is described with distinct stages for convenience, however being a continuum, there is continuity between stages.
Reactive tendinopathy is a non-inflammatory proliferative response in the tendon cell and matrix which occurs after acute overload from tensile or compressive forces (Cook & Purdam, 2009). In this proliferative response there is increase protein production, mainly proteoglycans, and water becomes bound to the proteoglycan. This causes changes in the matrix of the tendon, making the tendon cells become more chondroid in shape (Scott et al., 2007). The collagen however, is intact and not torn, and the neurovascular structures remain unchanged too.
Clinically, reactive tendinopathy occurs from acute overload or acute blunt trauma to the tendon. The changes described above result in adaptive thickening of the tendon, increasing the cross sectional area and assists to reduce stress (force/unit area) or allows adaption to compressive load (Cook & Purdam, 2009). The process of reactive tendinopathy differs to the normal adaptive response of tendons to load, in which the tendons stiffen but there is minimal change in thickness (Magnusson, Narici, Maganaris, & Kjaer, 2008). For tendons to become stronger they require load. If the tendon load is reduced and the tendon has time to recover this process is reversible (and a normal adaptive response). If there isn't sufficient adaptation to the load, the reactive tendinopathy process occurs. Looking at the image below you will see on the left (red) showing the process of excessive load compared to the right (green) showing how adaptation to load occurs.
The next phase is called tendon dysrepair. This phase is categorized by the tendon's attempt at healing much like reactive tendinopathy however with greater matrix degradation. There is an increase in total number of cells (mainly chondrocytic as well as myofibroblasts) resulting in a significant increase in proteoglycan and collagen production. The increase in proteoglycans causes disorganization of the matrix and separation of the collagen, which alters the loading capacity of the tendon (Cook & Purdam, 2009; Cook et al., 2002; Magnusson et al., 2008).
The final phase in this continuum is degenerative tendinopathy. Further progression of both matrix and cell changes with areas of cell death from apoptosis and trauma (Cook & Purdam, 2009; Magnusson et al., 2008). Areas of acellularity may exist and large proportions of the matrix are disordered and filled with vessels, breakdown products and minimal collagen. At this stage of pathology there is little capacity for reversibility of pathological changes (Cook & Purdam, 2009).
While our understanding of the changes that occur within the tendon cells has improved to propose the continuum model above it is still unclear as to how pain occurs within the tendon (Rio, et al., 2014). Pain can occur at any stage during the continuum and therefore it is important to try establish which phase the tendon is in so that treatment can be targeted at both pain reduction and the stage of pathology (Cook & Purdam, 2009). There is current evidence suggesting that tendon pain can have both local nociceptive contributions and CNS-driven contributions and therefore clinical reasoning and thorough examination is paramount (Rio, et al., 2014).
Before we can begin to treat tendinopathies you need to take a thorough subjective examination with the primary purpose of determining:
- When the change of load occurred.
- Tendinopathy does not exist without overload. This overload can come from past seasons, current training, shoes and running distances. If you can't find the change in load then you need to rethink your diagnosis.
- The effect of activity on pain.
- Pain is normally proportionate to load. Tendons are stiff to warm up, then ease and then worse post activity and can take days to settle. The effect of activity on pain is a key indicator for treatment direction and how much load you will choose during treatment.
- The location of the pain.
- Tendons don't refer pain. Patients should be able to pin point their pain within 1-2 cm of the location. If pain is diffuse you again need to consider what might be contributing to their pain.
- Night pain.
- Tendons aren't generally painful at night. If they are you need to consider if there are any other red flags. If tendons are painful at night, it is a bad indicator of prognosis. The pain is not an inflammatory marker, it is a sign that even when unloaded the tendon is still painful, which makes it hard to begin loading.
- What past treatment has been done including rehabilitation, medication and other therapies.
- What functionally they want to be able to do? What makes them a good athlete? What are the requirements of their position in the team?
- Aggravating and easing factors.
Although each tendon should be treated individually, some generalisations can be make to help guide us with pattern recognition and differential diagnosis based on the region in the body where the tendon is located. Tendons have different functions and depending where they are in the body, they may be exposed to tensile, compression, friction, or a combination of these loads.
- Gluteal tendons are subject to compression as they pass over the greater trochanter. Gluteal tendinopathy is more common in middle ages women, and often more in women with increased fat deposition over the hips. Their pain is increased by compressive loads, for example, walking with a Trendelenburg gait, sleeping in side lying, and often from a direct blow to the hip during a fall.
- Adductor tendons are subject to load during sports which require change of direction and kicking movement, hence we see them in footballers and soccer players.
- Hamstring tendons are subject to compression in activities that require sustained hip flexion such as hockey.
- Patella tendons are spring loading and power tendons, most prevalent in jumpers (like volleyball).
- Achilles tendons are also spring loading and energy storing tendons which can present in a number of sports such as, running, gymnastics and can present in both younger and older people.
One key message that this research points to is that prolonged periods of rest are contraindicated (Cook & Purdam, 2012). Prolonged unloading of a tendon which is painful results in a reduction in the load capacity of that tendon and therefore make the tendon more prone to overload and injury. Tendons should not be offloaded for more that 24 hours. There will always be a way in which the tendon can be safely and effectively loaded through recovery and this is where isometrics come into play.
A second key learning point is that tendons are energy storing structures - they require rapid load - you can't overload a tendon with slow movements or static movements - tendons have to store energy to take on load. When designing a rehabilitation program keep in mind the speed and spring loading requirements of exercises.
When determining what treatment is most suitable for tendons you should consider the following:
- Medical considerations: Diabetes, Post - menopausal women, hormonal changes, medication use, visceral fat content.
- Load considerations: in season or pre season. If it is in-season you are not able to reduce load of training or games therefore management is about keeping them working and moving.
- Stage in the continuum: reactive vs degenerative
- Location: peri-tendon vs tendon
The the continuum of tendon pathology there are four stages of healing: pain, strength, power, and endurance. Let's take a closer look at these stages of treatment and current management ideas specifically around Achilles Tendinopathy and Patella Tendinopathy.
A special thanks to Grant Freckleton for contributing to this blog. Grant has recently finished his Masters in Musculoskeletal Physiotherapy at Melbourne University and too been inspired by the work of Jill Cook. Writing this blog is such a passion of mine and I'm always so appreciative for the help of others... leaves more time for exploring the world with friends :)
Cook, J., & Purdam, C. R. (2009). Is tendon pathology a continuum? A pathology model to explain the clinical presentation of load-induced tendinopathy. British journal of sports medicine, 43(6), 409-416.
Cook, J. L., & Purdam, C. (2012). Is compressive load a factor in the development of tendinopathy?. British journal of sports medicine, 46(3), 163-168.
Khan, K. M., Cook, J. L., Kannus, P., Maffulli, N., & Bonar, S. F. (2002). Time to abandon the “tendinitis” myth: Painful, overuse tendon conditions have a non-inflammatory pathology. BMJ: British Medical Journal, 324(7338), 626.
Magnusson, S. P., Narici, M. V., Maganaris, C. N., & Kjaer, M. (2008). Human tendon behaviour and adaptation, in vivo. The Journal of physiology, 586(1), 71-81.
Rio, E., Moseley, L., Purdam, C., Samiric, T., Kidgell, D., Pearce, A. J., ... & Cook, J. (2014). The pain of tendinopathy: physiological or pathophysiological?.Sports medicine, 44(1), 9-23.
Scott, A., Cook, J. L., Hart, D. A., Walker, D. C., Duronio, V., & Khan, K. M. (2007). Tenocyte responses to mechanical loading in vivo: a role for local insulin‐like growth factor 1 signaling in early tendinosis in rats. Arthritis & rheumatism, 56(3), 871-881.