Tendinopathy Models

 

 

Degenerative Model

The most prevalent model in the research which outlines the stages of tendinopathy is the “Three Stage Continuum Model” put forward by Cook and Purdam (2009).  These stages include some of the histological information outlined previously however, as part of the continuum model, it enables to structure when these changes occur. These stages of tendinopathy are outlined as follows:

 

Reactive Tendinopathy:

This occurs as the tendon attempts to adapt to acute overload. In this stage the tendon thickens due to increased cellular activity, proliferation and permeability along with the presence of aggrecan which binds to water. This response results in pushing of the collagen fibres apart and the overall swollen appearance of the tendon. Tenocyte shape distortion likely occurs due to surrounding pressure, impacting upon the function of the tendon cells. The tendon is attempting to buffer the overload by increasing stiffness while also attempting to reduce the stress by increasing volume.  Importantly however during this stage fibre integrity is maintained, which influences the reversibility of this stage of tendinopathy. While this can be a painful stage of tendinopathy, full repair is achievable.

 

Dysrepair:

The tendon reaches this stage if persistent overload continues. Increased protein production continues however the tendon enters the phase of failed healing. Structural changes occur, such as the increased production of weaker Type III collagen, neovascularisation and neural ingrowth. As outlined previously, it is unlikely that neovessels and sprouting nerve fibres are involved in pain in tendinopathy. However they may provide a sign-post informing when the tendon has transitioned from reactive to late dysrepair. Clinically this stage often presents with ongoing intermittent symptoms however the structural changes which have occurred during this phase resulting in a limited capacity of full repair.

 

Degenerative:

This is the final stage of the tendinopathy continuum. Within this stage there are widespread structural changes. Type III collagen continues to replace Type I, while areas of reduced cellularity exist among a normally hyper cellular matrix. The thinner and irregular fibres reduce the tendons ability to absorb load, placing the tendon at risk of rupture. 97% of spontaneous ruptures display degenerative changes which undoubtedly pre-date the rupture. The capacity for recovery from this stage is poor and it is very unlikely that the tendon will be able to transition backwards through the stages to full repair. However the tendon should still be able to adapt and tolerate functional loading.

 

A pictorial representation of this continuum can be seen in Fig 1.8

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Fig 1.8: Pathology of load-induced tendinopathy (Cook and Purdam 2009)

 

 

The Iceberg Theory

 

Another theory put forward which attempts to rationalise the events occurring within the tendon and the occurrence of pain is the “Iceberg Theory”, which was first proposed by Abate et al (2009).

 

To understand this theory one must first acknowledge the natural events that occur during loading within a physiological range deemed tolerable by the tendon. In this range, load does not damage the tendon but instead reinforces it as it stimulates the production of new collagen fibres (Abate et al 2009). Various forms of exercise which load tendons (e.g. eccentric, eccentric-concentric) have been shown to demonstrate, via microdialysis techniques, up-regulation of both the synthesis and degradation of collagen within the tendon. However, collagen synthesis not only outmatches collagen degradation; it also occurs for longer (Langberg et al 2007, Olesen et al 2007). The overall result of this synthesis and degradation is that the tissue within the tendon becomes stronger, more resistant to injury and demonstrates increased tensile strength and elastic stiffness (Corps et al 2008).

 

When tendons are pushed outside the normal physiological range of loading is when tendinopathy can occur (Abate et al 2009). Overload and repetitive strain results in collagen fibres sliding past each other, causing cross-link breaking and tissue denaturation (Abate et al 2009). Strenuous exercise also may result in high temperatures developing within the tendon itself. When poorly controlled this can result in cell death, namely fibroblasts which cannot sustain temperatures greater than 42.50C (Temperature of 43-45oC have been demonstrated in tendons). In hypo-vascular areas of tendons, where homeostasis and temperature regulation can be limited, the tissue may be at greatest risk of degeneration (Li et al 2004).

 

Tendons, as mentioned previously, have low metabolic rates therefore optimal conditions for healing are: sufficient recovery time void of further overloading and with suitable blood supply (Abate et al 2009).  Extrinsic factors, such as excessive sporting participation and training errors, along with intrinsic factors, such as osteoarticular pathologies and diseases impacting collagen metabolism, both may play a role in optimal healing conditions being achieved (Abate et al 2009). Considering these potential variables, healing potential may vary between individuals (Abate et al 2009).

 

The iceberg theory attempts to explain the differences between the extent of tissue degeneration and clinical presentation of pain. It propagates the idea that the events that occur within the tendon (i.e. collagen thinning etc.) lay hidden under the surface and only when a certain threshold of degeneration results in pain being registered (i.e. the tip of the iceberg). This theory acknowledges that there is two phases in tendon damage; the asymptomatic and symptomatic phases.  It also acknowledges the potential relapse of symptoms which can be seen in some patients. Primarily, however, it explains how extensive tendon degeneration, enough to result in full rupture, can be painless prior to injury (Chester et al 2007).

 

 

 

 

Key References

• 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, 43:409–416.

• Abate, M., Silbernagel, K. G., Siljeholm, C., Di Iorio, A., De Amicis, D., Salini, V., Werner, S. and Paganelli, R. (2009) ‘Pathogenesis of Tendinopathies: Inflammation or Degeneration’, Arthritis Research and Therapy, 11: 235.