DIAGNOSIS

ACHILLES TENDINOPATHY UNDERSTANDING

By Professor Nicola Maffulli MD, MS, PhD, FRCS (Orth) and Mr Pankaj Sharma MRCS

INTRODUCTION Achilles tendinopathy is common among athletes participating in racquet sports, track and field, volleyball and soccer. Following greater participation in recreational and competitive sporting activities, the incidence of Achilles tendinopathy has increased in recent years. However, Achilles tendinopathy does not exclusively affect athletes. In this paper we review the aetiology and man- agement of Achilles tendinopathy.

ANATOMY The Achilles tendon is a confluence of the gastrocnemius and soleus muscles. The soleus muscle lies deep to the gastrocnemius muscle, arising from the posterior surface of the upper tibia. The tendon inserts on the posterior surface of the calcaneus distal to the posterior-superior calcaneal tuberosity. The Achilles tendon is not encased in a true synovial sheath, but is surrounded by paratenon composed of a single layer of cells. This tissue is richly vascularised and is responsible for a significant portion of the blood supply to the tendon (1). This supply comes through a series of transverse vincula, which function as passageways for blood vessels to reach the tendon. The Achilles tendon also receives blood from vessels originating at the musculotendinous and osteo- tendinous junctions.

At about 12 to 15 cm proximal to its insertion rotation of the ten- don begins, becoming more marked in the distal most 5 to 6 cm of the tendon. The tendon spirals approximately 90°, with the medial fibres rotating posteriorly and the posterior fibres rotating laterally. Angiographic injection techniques have demonstrated a zone of hypovascularity 2 to 7 cm proximal to the tendon inser- tion (1).

Healthy tendons are brilliant white with a fibroelastic texture. Within the extracellular matrix network, tenoblasts and tenocytes constitute about 90-95% of the cellular elements of tendons and lie between the collagen fibres along the long axis of the tendon (2).

BIOMECHANICS Tendons transmit force generated by muscle to bone and act as a

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buffer by absorbing external forces to limit muscle damage. Tendons exhibit high mechanical strength, good flexibility and an optimal level of elasticity to perform their unique role (2). The ten- sile strength of tendons is related to thickness and collagen con- tent and a tendon with an area of 1cm2 500-1000 kg (3).

is capable of supporting

AETIOLOGY AND PATHOPHYSIOLOGY Tendon injuries can be acute or chronic and are caused by intrin- sic or extrinsic factors, either alone or in combination. In acute trauma, extrinsic factors predominate. Overuse injuries generally have a multifactorial origin. Tendon vascularity, gastrocnemius- soleus dysfunction, age, gender, body weight and height, pes cavus and lateral ankle instability are common intrinsic factors. Excessive motion of the hindfoot in the frontal plane, especially a lateral heel strike with excessive compensatory pronation, is thought to cause a ‘whipping action’ on the Achilles tendon, and predispose it to tendinopathy (4).

Changes in training pattern, poor technique, previous injuries, footwear and environmental factors such as training on hard, slip- pery or slanting surfaces are extrinsic factors which may predispose athletes to Achilles tendinopathy (4).

Excessive loading of tendons during vigorous physical training is regarded as the main pathological stimulus for degeneration (5). Tendons respond to repetitive overload beyond physiological threshold by either inflammation of their sheath, degeneration of their body, or a combination of both (6). It remains unclear whether different stresses induce different responses. Active repair of fatigue damage must occur, or tendons would weaken and even- tually rupture (7).

The repair mechanism is probably mediated by resident tenocytes, which continually monitor the extracellular matrix (8). Failure to adapt to recurrent excessive loads results in the release of cytokines leading to further modulation of cell activity (9). Tendon damage may even occur from stresses within physiological limits, as frequent cumulative microtrauma may not allow enough time for repair (5).

The aetiology of tendinopathy remains unclear and many factors www.sportex.net