Welcome to tendinopathy blog 6. I was inspired this week by a recent review entitled ‘Hormones and tendinopathies’ to ponder the link between these two. As always, have tried to think of an applicable angle for clinicians (to help in our mission of joining the clinical dots), so have included ‘The worlds shortest guide to considering risk of tendon pain in your patients’.
The blog is a bit of a clinical tip sandwich on some research bread this week! Following the clinical tip is the other study to make the blog this week - it examines proprioception changes in patellar tendinopathy, with interesting findings.
Until next time, keep joining the dots
Oliva et al. have explored the link between hormonal disease and tendinopathy in this review. They argue that ‘we know that the genetic background of the affected individuals can affect their susceptibility to tendon injury’. Furthermore, hormone imbalance can alter biological pathways and cellular homeostasis. They found evidence from animal and human studies that diabetes (a disease of the hormone insulin or its receptors), thyroid disease and reduced estrogen (i.e. menopause) were associated with tendon pathology. The mechanism may relate to a change in cell signalling and tendon metabolism, although this is not clear.
‘The worlds shortest review of factors that may increase an individual’s risk of tendon pain’
There are what you might call ‘classic’ risk factors for tendinopathy. These include the following key groups…
1) Increased load – as we know often it is a sudden change in load that is the issue – it could be an increase in volume or intensity (for example, an extra run per week or starting to run up hills). Specific activities that are thought to lead to injury involve fast or stretch shorten cycle loading of the tendon (particularly true for the lower limb) and compression of the tendon.
2) Biomechanics – physios and other movement clinicians live mainly in this area – we feel at home here. We like to think that there are relevant muscle function or flexibility or other biomechanics (e.g. foot posture) issues that relate to a person’s tendon load and therefore to tendon pain. Sometimes this is true, sometimes it is not. An example is reduced range of ankle dorsiflexion which may be related to increased Achilles insertion compression or change how load is distributed in the lower limb during function (e.g. lead to greater hip adduction in landing from a jump). The premise is that these factors somehow increase tissue load – and this often depends on an interaction between how severe these biomechanical factors are and an individual’s habitual activities.
3) Systemic factors – common ones linked to tendon injury include age, genes, hormones, lipid levels, obesity, autoimmune diseases (e.g. rheumatoid arthritis and Crohn’s disease), etc. The mechanisms, that is, how they relate to tendon injury are not clear, but prevailing thought is that these factors reduce TENDON CAPACITY – i.e. the tissue is less able to cope with loads – as is the main argument in the Oliva paper above.
It is important to remember that other factors may increase the risk of developing pain and the risk of persistent pain, in some individuals. Cognitive-emotional factors are often associated with persistent pain, including chronic tendon pain. These factors include beliefs, fear avoidance, hypervigilance, catastrophizing, maladaptive coping, stress etc.
We also know that the neuroimmune, endocrine and autonomic body systems may be involved in chronic pain states (see figure below, from Chapman 2008), which may explain the links between chronic pain and obesity, poor sleep, IBS, autoimmune disorders etc. So it is possible that some of the systemic factors that are classically thought of as reducing TENDON CAPACITY, may actually influence pain sensitivity, eg menopause, obesity, even lipid levels.
Key take home message is: classic tendon risk factors are focused on tendon load/capacity which is important for tendon pathology mainly, and no doubt also for pain, to some extent. BUT, many other factors influence development and persistence of pain (even some classic systemic tendon risk factors). A thorough physical-cognitive-emotional assessment is important, and physical includes classic risk factors and signs of involvement of stress, immune and endocrine systems in the pain experience. So if you’re not dealing with the individual, ie thoughts/beliefs, load modification, exercise and movement, general health, aerobic health, stress management, diet, etc, etc – then you may be missing a key part, that in combination with other relevant parts, may mean the best rehab in the world is ineffective. Nothing wrong with focusing treatments to the tendon, but remember, a tendon is part of a person, which may be a more important consideration than the tendon itself!
I have purposefully steered clear of discussion of what is ‘typical’ tendon pain and whether it is nociceptive or central, or both (i.e. trying to label or put in a basket). That is not the point. The point is that right now it is not clear how much central factors contribute to emergence, modulation or persistence of pain in tendinopathy – so keep an open mind!
Torres et al. have investigated proprioception in patellar tendinopathy. Proprioception is defined as afferent information that contributes to balance and motor control. They argue that golgi tendon organ receptors that are involved in proprioception may be damaged if the tendon is pathological. They included 21 male and female athletes with patellar tendinopathy and 21 matched controls. They assessed 2 aspects of proprioception - joint position sense (trying to reproduce a knee angle without visual input) and weight discrimination (detecting small increases in load of 0.2, 0.25, 0.3, 0.35kg from a baseline load of 2.5kg on a leg extension machine). They found that joint position sense is not affected but weight discrimination was (see figure below which shows percentage correct discrimination on the Y axis – the tendinoapthy group were significantly worse at detecting an increase load of 0.25kg (figure shows grams but it is kg in the methods). The main explanations put forward is potential damage to golgi tendon organ mechanoreceptors related to tendon pathology, which is plausible. Because the muscle spindle is a strong contributor to joint position sense this aspect of proprioception may not affected. Another possible explanation is change motor cortex control (most likely related to pain) in patellar tendinopathy patients (as shown by Rio et al.). The clinical message is to consider interventions that restore normal motor cortex and proprioception function.
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