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Is tendon pathology a continuum? A pathology model to explain the clinical presentation of load-induced tendinopathy
Cook, J.L. and 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), pp.409-416.
In todayโs letter
Overview of the Jill Cooks brilliant paper looking at 3 phases of tendinoapthy
Rapid Results = 3 distinctive phases
(1) Reactive tendinopathy = Reversible and usually seen in younger active individuals.
(2) Tendon disrepair (failed healing) = Somewhat reversible. Itโs characterised by non-inflammatory cell and matrix proliferation, due to overload.
(3) Degenerative tendinopathy = Mostly irreversible. Tendon dysrepair is similar to reactive tendinopathy but with heightened matrix degradation
Top 3 reads to check out: To further your knowledge about:
Tendons
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Deeper look
Aim of study
This paper analysed current tendinopathy concepts and propose a comprehensive model for tendon pathology, supported by evidence from human clinical studies.
Did you Know?
Overuse tendon injury (tendinopathy) happens in loaded tendons of upper and lower limbs, leading to pain, reduced exercise tolerance, and diminished function.
Tendon injury can occur mid-tendon or at the tendon attachment to bone, such as in the Achilles tendon, patellar tendon, medial and lateral elbow tendons, and groin tendons.
Although morphologically different in their healthy state, both mid-tendon and insertion sites show similar cell matrix changes when pathology sets in.
Load can have both building up (anabolic) and breaking down (catabolic) effects on tendons.
Repetitive energy storage and release, along with excessive compression, are significant factors triggering tendinopathy.
The precise amount of load (volume, intensity, frequency) that causes pathology remains unclear, but allowing sufficient time between loadings seems crucial for tendon adaptation.
Existing tendon pathology concepts
The authors suggest a continuum of tendon pathology with three stages:
(1) Reactive tendinopathy
(2) Tendon disrepair (failed healing)
(3) Degenerative tendinopathy.
Modifying load serves as the main trigger shifting the tendon along this continuum, particularly in the initial phases.
Within the recovery framework outlined in the model, decreasing load could facilitate the tendon's regression to a previous state of structure and capacity within the continuum
What are the pathological, imaging and clinical manifestations at each stage?
Reactive Tendinopathy
Reactive tendinopathy is characterised by non-inflammatory cell and matrix proliferation, coming from sudden overload.
This leads to short-term adaptive thickening of the tendon, to either avoid stress or to adapt to compression.
Clinically, reactive tendinopathy results from sudden overload, often due to a burst of physical activity.
It can also occur prominently after direct impact, such as falling directly onto the patellar tendon.
The cell response to load in reactive tendinopathy is non-inflammatory, triggering metaplastic changes and cell proliferation.
Initial alterations in ground substance occur as a rapid adaptation until longer-term structural or mechanical changes (true adaptation) take place.
This reactive response serves as a short-term adaptation, thickening the tendon, reducing stress, and enhancing stiffness.
Given adequate reduction in overload or sufficient time between loading sessions, the tendon may potentially return to normal.
Imaging
The tendon shows fusiform swelling, with enlarged diameter visible on both MRI and ultrasound scans.
MRI typically reveals minimal or absent signal increase during this stage.
The altered imaging appearance primarily results from heightened bound water content within the proteoglycan
Clinical signs
As mentioned, it typically comes after an increase in load (intensity, volume, frequency) and is seen in younger active individuals
For instance, a young athlete increasing the frequency of jumping/landing repetitions per week dramatically may experience swelling and pain in the patellar tendon.
Tendons accustomed to low levels of load, such as in detrained athletes recovering from illness or injury, or sedentary individuals, may also be susceptible to this stage of tendinopathy when subjected to a moderate increase in load.
Additionally, direct trauma to the tendon, particularly affecting the Achilles, patellar, and elbow tendons, can induce reactive tendinopathy
Tendon Disrepair
Tendon disrepair (failed healing) is also characterised by non-inflammatory cell and matrix proliferation, due to overload.
This phase brings about a notable rise in cell count, primarily chondrocytic, alongside some myofibroblasts, leading to a significant upsurge in protein synthesis.
The augmented presence of proteoglycans causes collagen separation and matrix disarray, with changes being more localixed and matrix alterations more diverse compared to the reactive stage.
Increased vascularity and nerve ending sensitivity may also occur during this stage
Imaging
The imaging changes reflect increased matrix disorganisation, and these tendons are swollen, with increasing evidence of collagen disorganisation
On MRI the tendon is swollen and there is increased signal within the tendon
Clinical signs
This condition has been observed in tendons subjected to chronic overload, primarily in younger individuals, but its occurrence spans various age groups and loading conditions.
Clinically it may difficult to distinguish reactive & disrepair tendinopathy
Affected tendons typically show increased thickness
Factors such as the frequency, volume, or duration of load application (e.g., months or years of overload) play significant roles.
Older individuals with less flexible tendons and reduced adaptive capacity may develop this stage of tendinopathy.
Despite its progression, some degree of reversibility in the pathology is possible through load management and targeted exercise aimed at promoting matrix retructuring (heavy slow or eccentric)
Degenerative tendinopathy
The literature provides a clear description of this stage, highlighting an increase in both matrix and cell alterations.
Evidence of cell death from apoptosis, trauma, or tenocyte depletion is notable, leading to acellular zones and widespread matrix disarray filled with vessels and breakdown products.
Pathological changes at this stage show minimal potential for reversal
Imaging
The compromised matrix and the vascular changes can be large
MRI demonstrates increased tendon size and intra-tendinous signals (typically refers to abnormalities or changes detected within the structure of a tendon itself)
Clinical signs
This stage is predominantly observed in older individuals but may also come about in younger individuals or elite athletes with chronically overloaded tendons.
Typically involves middle-aged recreational athletes experiencing localised swelling and pain in the Achilles tendon.
Those with degenerative changes frequently report recurrent episodes of tendon pain, often subsiding temporarily but resurfacing with changes in tendon loading.
Extensive degenerative tendinopathy or high tendon loading can lead to ruptures, with approximately 97% of tendon ruptures associated with degenerative alterations
๐ Top 3 reads ๐
That will further your knowledge about tendons
How to train a tendon for peformance - https://www.sportsmith.co/articles/how-to-maximise-tendon-adaptation-for-sports-performance/
A quick summary of Tendon load in clinic
A revisited (and shorter) look into tendon pathology continuum
Credit: IG @Physiodrkaren
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