VASCULARITY AND TENDON PAIN

BLOOD VESSELS: THEIR ROLE IN TENDON PAIN AND PATHOLOGY

By Dr Jill Cook, B App Sci (Phty), Post Grad Dip Manip Physio, PhD

NORMAL TENDON Normal tendon is composed of a small number of cells, with a large extracellular matrix primarily composed of Type I collagen and a small but impor- tant amount of ground substance. This structure is supported by connective tissue, blood vessels and nerves. The vessels run along and then into the tendon with the connective tissue, extending into the tendon down to collagen fascicle level. Normal tendon has a low blood supply that is sufficient for its use, as it has low cell numbers. In addition, ten- don cells are resistant to low oxygen levels (1).

New research into tendon physiology has indicated that normal tendons have a consistent and even blood flow throughout the ten- don (2). Thus the commonly held clinical belief of an area of hypo- vascularity that predisposes to injury is not supported by research.

Blood flow is greater in women, decreases with age, and is com- promised by loading and stretching (2). Anatomically, the lowest flow is at the insertion where there are cartilaginous areas within the tendon. As cartilage has no vessels, this finding is not surpris- ing. The bone-tendon junction, where the blood flow is lowest, is where most tendon pathologies occur.

In normal tendon, peritendinous blood flow has been investigated by Michael Kjaer and his colleagues (3). His group has shown that blood flow in the peritendon is not compromised by tendon load and is increased with exercise. This is opposite to the decrease in vascularity seen in the tendon with load. It is possible that the peritendon is less sensitive to compression than the tendon itself, and that peritendinous flow may not be correlated with intratendi- nous flow. Alternately, the differing measurement tools (ultrasound Doppler in tendon and direct sampling of fluid in the peritendon) may result in these different findings. Another possibility is that the microvascular flow remains but the macrovascular flow is com- promised by load.

PATHOLOGICAL TENDON Pathological tendon is characterised by a change in cell morpholo- gy, which becomes increasingly chondrocytic. This represents an active state, allowing the tendon to produce the proteins of the extracellular matrix. Cells produce Type I collagen in normal ten- dons, in a state of pathology they produce more Type III collagen. Type III collagen is thinner and less capable of cross-linking, pro- ducing tissue with less capacity to withstand tensile load.

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Tendon injuries are common in all parts of the population, but more prevalent in the active as well as the older com- munity. Both sport and work can affect tendons, as increased load on the musculoskeletal system can provoke tendon pathology and pain. Tendons are also more vulnerable to change as a person ages, those over the age of 40 are at increased risk of tendon injury.

Our understanding of tendon injury and pain has improved over the last decade. Although it is unclear exactly what causes the pain in tendon

injury, new research into the blood vessels in the injured tendon have helped guide research into areas that may eventually answer this question. This article will detail the basic structure of normal tendons, the pathology of injured tendons and the role of blood vessels in pathology and pain.

The cells also produce ground substance, which is increased in vol- ume by about three times that in normal tendon, and there is a change from small to large proteoglycans. This in turn increases the water within the tendon. This increase in water is the reason for imaging changes seen on ultrasound and magnetic resonance imag- ing in abnormal tendon.

Blood flow in the abnormal tendon is greater than in normal tendons, but the distribution of flow is otherwise similar to normal tendons. The vessels become more numerous and prominent and they are accompanied by nerves (4).

The stimulus for the large

amount of hypervascularity is not known, however the biggest stim- ulus for neovascularisation in any tissue is hypoxia. It is possible that areas of a tendon become hypoxic with repeated loading during exercise. Another stimulus proposed is free radical release associated with perfusion/reperfusion seen in exercise (5). There may be other factors that act centrally rather than locally as it has been shown in rabbits that vascularity increased in both Achilles tendons if only one side underwent longitudinal tenotomy. There were no other changes seen in either collagen or structure (6).

The effect of hypervascularity in tendon is still debated, with pro- ponents suggesting a pos- itive benefit as vascularity improves repair. This can

Figure 1: An Achilles tendon demonstrating increased vas- cularity on colour Doppler

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