Tendonitis or Tendinopathy? Classifying Tendon Pain

Tendon pain that has a slow onset as opposed to an acute or traumatic onset is one of the most common types of injury we treat.

It may be an upper limb tendon problem such as a rotator cuff tendon, or a lower limb tendon such as an Achilles or patellar tendon.

Over the last few decades the mechanism for what causes tendon pain has been a changing ‘landscape’. Two key models of tendon pain have been prevalent. One the ‘tendonitis’ model is now outdated, while the ‘tendinopathy continuum’ model is now in vogue.

Let’s take a look at each:

The ‘tendonitis’ model

Tendon pain of an overuse origin amongst runners has historically been diagnosed as being ‘tendinitis’. The suffix ‘itis’ denotes inflammation. Hence a runner suffering from Achilles tendinitis, was thought to be experiencing pain due to inflammation of their Achilles tendon. However, this widely accepted (and still espoused) mechanism and model for tendon pain is now defunct. The inflammatory model is void of scientific evidence and therefore clinically inaccurate as a diagnosis of Achilles tendon pain.

Contemporary medical practitioners share the understanding that at a cellular level the tendon cells of a pathological Achilles tendon are actually not ‘inflammed’ per se. Histological (cell analysis) samples of chronically painful tendons were actually found to not have inflammatory cells present (1).

Additionally, prostaglandins (markers of the inflammation process in our bodies) were found to be in no greater concentration in patients suffering from Achilles tendon pain, than people without Achilles tendon pain (2). As a result of these findings (and many more research papers) over the last decade medical practitioners began to drop tendonitis as a valid diagnosis for not just Achilles tendon injuries and pain, but for all tendon conditions that frequently occur.

Following the cessation of an inflammatory tendon pathology model, tendon pain was considered to occur on a ‘degenerative’ continuum.

The degenerative model

At a molecular level pathology of the tendon is consistent with several cell changes. The very ‘materials’ or ‘building blocks’ of the tendon themselves, when tendon pain is present, begin to change.

In chronically painful tendons degenerative cell changes can occur. For example, the collagen fibres of the tendons which provide tensile strength to the tendon, can with overload occurring over time begin to become ‘disorganized’. Rather than being tightly packed parallel bundles, the fibres can become criss-crossed, and aligned in an ad-hoc fashion.

Furthermore, the ground substance (think of a bath) that bathes the collagen fibres of the tendon, can begin to house a greater concentration of proteins (proteoglycans such as gylcosaminogylcan-GAG). These proteoglycans are the proteins needed for tendon cell integrity.

Additional cell changes can also include calcification, and lipid (fat) accumulation.

Chronic tendon pain at a cellular level is often characterized by an increase in vascularity and accompanying proliferation of nerve endings. This progressive indwelling of nerves and blood vessels into a chronically sore tendon is termed ‘neo-vascularisation’ of the tendon.

Overall these characteristic changes in tendon structure result in the tendon being less capable of sustaining repetitive tensile (think stretch) loading. At this point the tendon had lost some of its ability to store and release energy, and with continued loading cycles the runner’s Achilles tendon will become progressively more painful.

A model of degenerative tendon pathology: the continuum model

In 2008 researchers (3) developed a framework to classify the continuum of tendon structural changes that can occur. The framework reflects the degree of tissue changes present in pathological tendons.

In contemporary sports medicine circles this continuum degenerative model has become the standard for classifying tendon pain, and then prescribing an appropriate course of treatment.

In this 3 stage continuum model the first stage is a ‘reactive’ tendinopathy, second ‘dysrepair’ tendinopathy, and third ‘degenerative’ tendinopathy. The stages are not mutually exclusive stages, rather a runner may have a reactive on dysrepair tendon, or recative on degenerative presentation.

Source: Br J Sports Med 2009;43:409–416, Cook & Purdam.

If you are suffering from a tendon condition, and perhaps a little confused with why some people refer to your condition as a tendinitis while others call it a tendinopathy I hope that this article will help clarify things for you.

I hope that this gives you a little bit more understanding into the term ‘tendinopathy’ and what it actually means. If you are suffering with a tendon injury, be patient as rehabilitating tendinopathies will typically take time.

All the best with your recovery.

In the next blog I will share with you my clinical approach to classifying tendons that allows for optimal rehabilitation to occur.

Physio With A Finish Line,

Brad Beer (APAM)

Physiotherapist (APAM)
Author ‘You CAN Run Pain Free!’
Founder POGO Physio

References

(1) Khan KM, Cook JL, Bonar F, et al. Histopathology of common overuse tendon conditions: update and implications for clinical management. Sports Med1999;27:393–408.[CrossRef][Medline][Web of Science]

(2) Alfredson H. In situ microdialysis in tendon tissue: high levels of glutamate, but not prostaglandin E2 in chronic achilles tendon pain. Knee Surg Sports Traumatol Arthrosc1999;7:378–81. [CrossRef][Medline][Web of Science]

(3) Br J Sports Med 2009;43:409-416 doi:10.1136/bjsm.2008.051193
Review: Is tendon pathology a continuum? A pathology model to explain the clinical presentation of load-induced tendinopathy

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