Literature Review (2)

Summary and Perspective of Recent Literature

Cook JL, Rio E, Purdam CR, Docking SI. (2016). Revisiting the continuum model of tendon pathology: what is its merit in clinical practice and research? British Journal of Sports Medicine; 50:1187-1191

In 2009, Cook and Purdam presented a model of load-induced tendinopathy with an emphasis on encouraging clinicians not to treat all tendon problems in the same way. The authors stated that both overloading and unloading can produce the same degenerative changes and there are various hypotheses that try to explain the process of tendon pathology. They asked the question of whether the various pathologies that have been described could be seen to be on one continuum. The authors presented a new model of tendon pathology which proposed three stages:

  1. Reactive tendinopathy
  2. Tendon disrepair
  3. Degenerative Tendinopathy

It was suggested, based on the available evidence at the time, that these changes form a continuum of tendon pathologies (Figure 1) and that these changes are reversible as long as the tendon is not in the degenerative tendinopathy stage, even though they still acknowledge the possibility of healing at this stage. The authors note that if degeneration is extensive or loads sufficiently high, rupture can occur.

literature table 3

The clinicians are then guided in clinical decision making by dividing the continuum model into two clear groups with implications for management (Figure 1):

  1. Reactive/early tendon disrepair
    Management entails identifying the ‘abusive load’ and then focusing on load reduction and modification, allowing the tendon to normalize and become less reactive.
  2. Late tendon disrepair/degenerative tendinopathy
    Progressively loading the tendon positively stimulates cell activity and matrix restructuring and offers pain relief. Eccentric exercise is especially “beneficial for pain, function and return to activity.”

This brings us to the 2016 “revisit” by Jill Cook et al. “Revisiting the Continuum Model of Tendon Pathology: What is its Merit in Clinical Practice and Research?” They reflect on the original model and its relevance to sports medicine and attempt to answer some of the questions that have been raised in the literature since.     

First of all, the authors summarise the main categories of tendon pathology models, of which the continuum model is one:

  1. Collagendisruption/tearing hypothesis
    This model is challenged as a primary event of disruption. Normal tendon cannot tear as a result of day to day loading unless there has already been changes in the collagen matrix.
  2. Inflammation
    Although changes in the level of inflammatory markers occur in response to cyclic load, there is not the support that inflammation is the primary event or ‘key driver’ of tendon pathology. So, this model is also challenged.
  3. Tendon cell response
    This model suggests that loading (sensed by the tendon call) is the key factor affecting the collagen fibers and adaptation that occur.

The authors state that “It is unlikely that any one model fully explains all aspects of the pathoaetiology of tendon pathology”. It is a complex process, especially in regards to the relationship between structure, pain and function.

In revisiting the Continuum Model, the authors propose a hybrid of reactive and degenerative pathology, which is ‘reactive-on-degenerative tendinopathy’.

Where pain fits into the continuum is discussed. It falls into two categories in the revised Continuum Model:

  1. Reactive tendon with first presentation of tendon pain following acute overload
  2. Reactive-on-late disrepair/degenerative tendon pathology

The authors ‘strongly’ suggest that there is a local nociceptive driven pain, hypothesizing that either of the above situations may “increase expression of nociceptive substances and their receptors, stimulating the peripheral nerve and be interpreted as pain”. They acknowledge a potential role for the central nervous system in influencing the pain experience, but suggest that local nociceptive driven pain is critical.

This figure adapted from the paper summarises the complex interplay between structure, function and pain.  

literature table 4

What is most valuable for clinicians is the analysis by the authors on how to optimise treatment by ‘tailoring’ it to the stage of tendon pathology. Exercise and ‘load management’ are at the core of treatment. Authors discuss those interventions in three ways:

  1. Interventions treating pain.
    Pharmaceutical and modality interventions can reduce pain in the short-term, but without addressing tissue capacity this may result in recurrence. Isometric exercises have a potential to reduce pain and improve strength. Loading programmes are deemed to have broader structural, cortical and functional benefits that may lead to a better outcome.
  2. Interventions addressing function and load capacity.
    This aspect has had little research to guide the clinician and it is acknowledged that it is difficult to quantify function and for the clinician to get a clear sense of the tendon load capacity. Hopefully, further research will elucidate on these issues.
  3. Interventions targeting structure.
    This is where the Continuum Model can provide a framework to understand the potential of the tendon to regain normal structure. It is important to understand that in the reactive stage, heavy loading with eccentric exercises may be highly provocative. At this stage, unloading is the key in order to allow the tendon to regain its normal structure. In the degenerative stage, interventions to change structure are not necessarily successful. Treatment should be aimed at building loading capacity and ‘optimizing adaptation’ in the healthy or in the reactive stage tissue rather than the degenerated portion of the tissue i.e. ‘treat the donut, not the hole’. However, for long term tendon health and outcomes, treatment must progress to improve load capacity of the degenerated portion through progressive loading rehab.

In summary, it looks like we are far from having all the answers to the questions surrounding our understanding and management of tendon injury and pathology. It is not likely that any one model will be entirely comprehensive in accounting for all the complex changes that occur, especially in relation to pain and the implications for rehabilitation. For now, the paper’s elucidation of these two overlapping phases and the need to manage these phases very differently gives us some guidance to target our interventions. To complete the picture as MDT clinicians, we are always looking towards the patient, their environment and tissue demands, their needs, their expectations and goals in order to tailor our management to achieve the best outcomes we can, putting the patient first.