Tendon

      Tendons attach muscle to bone and are composed of dense, regularly arranged fascicles, or groups of collagen bundles. The fascicles are surrounded by an epitenon and are closed within the paratendon (tendon sheath). The predominant cells are fibroblasts producing mostly type I collagen (85 per cent dry weight of tendon). Tendons transmit load from mus­cles to the bone and the collagen fibres tend to orientate themselves along stress lines. The collagen laid down in a healing tendon initially has a haphazard arrangement but when subjected to physiological strains the orientation returns to normal, with restoration of the mechanical properties of the tendon.

Tendon pathology may be divided into three types:

   paratendinitis;

 •  paratendinitis with tendinosis;

 •  pure tendinosis.

Paratendinitis is inflammation of the investing paratenon and may be diagnosed by eliciting tenderness around the full circumference of the tendon, the site of which does not move with the underlying tendon (Fig. 29.4). It is an extremely painful condition. Paratendinitis usually responds well to anti-inflammatory medication, local physical therapies such as friction massage and ultrasound, and occasionally an injection of local anaesthetic and corticosteroid into the paratenon (not into the tendon itself). If the paratendinitis becomes chronic it may be necessary to strip surgically the injured paratenon from the tendon.

    Tendinosis is a more sinister condition both to diagnose and to treat. It is usually asymptomatic and is present in an increasing proportion of all tendons with advancing age. The term covers a wide variety of pathological processes: hyaline degeneration, a decrease in the normal cell population and alterations in the matrix.

Treatment for tendinosus is difficult and patients should be warned against the likelihood of a ‘quick fix’. Physical therapies aimed at improving the blood supply to the degenerate areas are only moderately successful. Rehabilitation programmes should start with complete rest and only progress within the limits of pain. More recently the emphasis has been on eccentric loading and enhanced proprioceptive feedback to improve tendon healing. Surgical treatment for tendinosis is controversial but a distinction should be made between surgery to remove aggravating mechanical factors, for example subacromial decompression of the rotator cuff tendon, which has a good success rate, and surgery to the tendon itself which is less rewarding. However, encouraging results have been obtained after percutaneous, longitudinal tenorrhaphy of the Achilles tendon, although the risk of precipitating tendon rupture is always present.

Tendon rupture

Rupture is the end point of tendinosis in that there is histological evidence of degeneration present within every tendon that has ruptured. It seems that closed injury cannot rupture a normal tendon, failure always occurring at the musculotendinous junction in this instance.

The principles of treatment of a ruptured tendon are similar to those for treating fractures, namely to restore anatomy and maintain it whilst healing occurs. Tendon ends need to be apposed in order to minimise the gap that must be bridged by fibrous tissue. The larger the gap the greater the volume of scar tissue which has inferior biomechanical properties. A large tendon gap also decreases muscle strength by lengthening the musculotendinous unit and reducing the efficiency of its contractions.

All tendons will heal, and indeed this healing may to some extent be impaired by surgery. The surgeon must therefore be clear that benefit will ensue from his or her surgical inter­vention. The next point to remember is that the strength of any type of surgical repair will only ever be a small fraction of the strength of the intact tendon. Whilst the initial biomechanical properties of a repair may be improved by placing multiple sutures into the tendon ends, this apparent advantage is outweighed by the adverse effect on the vascular regeneration required to produce tendon healing.

Plantar flexing the ankle usually brings the tendon ends together after rupture of the Achilles tendon. Failure to produce tendon apposition may account for the relatively high rate of tendon re-rupture and weakness of calf muscle power in nonoperatively treated patients. In several instances the tendon ends can never be apposed by closed means; examples of this include rupture of the distal insertion of the biceps tendon on to the radial tuberosity and tears of the rotator cuff tendon. Surgery is then required to restore the anatomy whilst preserving the blood supply wherever possible. One advantage of surgical repair of a ruptured tendon is that a graduated rehabilitation programme to maintain muscle function and joint range of motion can be started within a week of surgery.