Tendon Pathophysiology: Difference between revisions

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== Overview  ==
== Overview  ==
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== Current Thinking&nbsp;  ==
== Current Thinking&nbsp;  ==


The current term that is recommended to describe this cohort of patients is ‘tendinopathy’. Cook and Purdum (2015) have proposed a new strategy when approaching tendon pain, and this is called the tendon continuum. They propose there are 3 stages to this continuum. The Reactive tendinopathy, the tendon disrepair and the degenerative tendinopathy. They suggest that the tendon can move up and down this continuum and this can be achieved through adding or removing load to the tendon especially in the early stages of a tendinopathy. They suggest that by reducing the load it may allow the tendon to return to the previous stage on the continuum.<ref name="Khan K">Khan K 2007. New Laboratory Insights into the pathogenesis in tendinopathy  https://docs.google.com/viewer?a=v&amp;pid=sites&amp;srcid=ZGVmYXVsdGRvbWFpbnxhZmFwdWt8Z3g6M2U2YTRjZDkxZjRiODQ2MQ (accessed 19/12/15)</ref>  
The current term that is recommended to describe this cohort of patients is ‘tendinopathy’. Cook and Purdum (2015) have proposed a new strategy when approaching tendon pain, and this is called the tendon continuum. They propose there are 3 stages to this continuum. The Reactive tendinopathy, the tendon disrepair and the degenerative tendinopathy. They suggest that the tendon can move up and down this continuum and this can be achieved through adding or removing load to the tendon especially in the early stages of a tendinopathy. They suggest that by reducing the load it may allow the tendon to return to the previous stage on the continuum.<ref name="Khan K">Khan K 2007. New Laboratory Insights into the pathogenesis in tendinopathy  https://docs.google.com/viewer?a=v&amp;amp;pid=sites&amp;amp;srcid=ZGVmYXVsdGRvbWFpbnxhZmFwdWt8Z3g6M2U2YTRjZDkxZjRiODQ2MQ (accessed 19/12/15)</ref>  


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== Reactive Tendinopathy  ==
== Reactive Tendinopathy  ==

Revision as of 16:16, 30 January 2016

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Tendon continuum.jpg

Overview[edit | edit source]

Overuse can occur in any tendon throughout the body and this usually occurs at the boney attachment, but can also occur in the mid-portion of the tendon, most commonly seen in the Achilles tendon. The cause of tendinopathy has been linked to the repetitive energy storage and release with excessive compression. The quantity, intensity and frequency of this load is unknown, as it can differ from person to person. This component is considered to be 1 factor (extrinsic), another is the intrinsic factors which can include a person's’ biomechanics, body composition, age, gender etc. Previous theories have thought that tendinopathy develops through inflammation via the collagen fibre separation and degeneration through repetitive overload causing microtrauma but studies have shown that in chronic Achilles tendon pain there is an absence of inflammation. The term tendinosis has also been given to patients who have tendon pain. This implies a disorganised healing response is occurring. It has been recommended that these terms should only be used after histopathological examination, which would nott seem appropriate for all patient suffering from tendon pain. So this has led to further research and theories. [1]


Current Thinking [edit | edit source]

The current term that is recommended to describe this cohort of patients is ‘tendinopathy’. Cook and Purdum (2015) have proposed a new strategy when approaching tendon pain, and this is called the tendon continuum. They propose there are 3 stages to this continuum. The Reactive tendinopathy, the tendon disrepair and the degenerative tendinopathy. They suggest that the tendon can move up and down this continuum and this can be achieved through adding or removing load to the tendon especially in the early stages of a tendinopathy. They suggest that by reducing the load it may allow the tendon to return to the previous stage on the continuum.[2]


Reactive Tendinopathy[edit | edit source]

A reactive tendon is the 1st stage on the tendon continuum and is a non-inflammatory proliferative response in the cell matrix. This is as a result of compressive or tensile overload. The cells change shape and have more cytoplasmic organelles for increased protein production (proteogycans and collagen). During this process the collagen integrity are usually maintained although some elongation separation has been shown previously. This phase is a relatively short term adaptation, this process thickens the tendon to reduce stress and increases the stiffness. On imaging the tendon does appear to be thickened and swollen due to the changes in the proteogycans. This can occur after a sudden increase stress or direct impact to the tendon. At this stage of tendon has the potential to revert back to the normal tendon.[3]


Tendon Dysrepair[edit | edit source]

The progression of the reactive tendinopathy can occur if the tendon is not offloaded and allowed to regress back to the normal state. During this phase there is the continuation of increased protein production which has been shown to result in separation of the collagen and disorgansiation within the cell matrix. This is the attempt of tendon healing as with the 1st phase but with greater involvement and breakdown physiologically. This is now visible on MRI and ultrasound scans. Also there may be evidence of increased vascularity and neural ingrowth within the tendon. This phase has been said to be a difficult one to diagnose so history taking is essential, the most accurate method to diagnose this stage is through imaging. This phase of tendinopathy can be developed by frequently overloading the tendon in phase 1 of the continuum. This phase can be developed much more quickly in the older stiffer tendon as there is less flexibility and adaptivity readily available in the tissues. [3]

Degenerative Tendinopathy[edit | edit source]

This is the final stage on the continuum and is suggested that at this stage there is a poor prognosis for the tendon and changes are now irreversible. It has been documented that there areas of cell death, trauma and tenocyte exhaustion and general disorganisation of the cell matrix. On imaging there are areas of this degeneration scattered throughout the tendon and interspersed with normal sections of tendon and parts of the tendon that are in the dysrepair phase. The tendon can be thickened and present with nodular sections on palpations. Clinically this tendon is present in the older individual who has had ongoing problems with tendinopathy, or the younger individual who has continued to overload the tendon.[3]

References[edit | edit source]

  1. Maffulli N, Sharma P, Luscombe KL. Achilles tendinopathy: aetiology and management. Journal of The Royal Society of medicine 2004;97:472–476
  2. Khan K 2007. New Laboratory Insights into the pathogenesis in tendinopathy https://docs.google.com/viewer?a=v&amp;pid=sites&amp;srcid=ZGVmYXVsdGRvbWFpbnxhZmFwdWt8Z3g6M2U2YTRjZDkxZjRiODQ2MQ (accessed 19/12/15)
  3. 3.0 3.1 3.2 Cook JL, Purdam CR. Is tendon pathology a continuum? A pathology model to explain the clinical presentation of load-induced tendinopathy. British Journal of Sports Medicine 2009;43:409–416