Clinical implications

Which Phase?

The therapist should always determine the phase of the inflammatory process before starting treatment. Acute traumatic injuries often present with a clear time of onset, but with overuse injuries, because of the insidious onset, it is more difficult to identify the current phase. Continuous reinjury as is common with overuse will repeatedly set back the progression of the inflammation phase, and therefore it is impossible to tell when the inflammatory process started. Because of this the therapist should always, unless proven otherwise assume that it is in the vascular inflammatory phase (Hujibregts and Smith 1999). Treatment of acute and chronic ligament/tendon injuries can be confusing because of the fine balance between adequate rest and preventing atrophy of surrounding muscles. This has led to the development of very detailed exercise programs of for example ACL, Achilles- and Patella tendon (Hyman and Rodeo 2000).

Healing of connective tissue

During the inflammation phase the tensile strength is dependant upon fibrin, which is very fragile, and tension could easily disrupt it. In order to control it is essential to limit the amount of post-injury oedema using ice, elevation compression. Other forms of management are NSAID´s and modified rest. Ultrasound and laser has shown to accelerate the inflammation process (Hunter 1994, Reid 1992).

In the regeneration phase it is important to maximize strength, the collagen fibres should relate to the undamaged tissue. Careful tensioning during this phase promotes correct alignment by remodelling the collagen fibres. The rate of increase in wound strength is proportional to the amount of collagen laid down (Hunter 1994).

Management in the remodelling phase is to minimize immobilization, balance functional stresses with increasing tissue strength, re-establish ROM and enhance proprioception (Reid 1992).
Prevention of scar tissue and contraction and promoting the correct orientation of collagen fibres is essential for the best functional outcome. The wound should be subjected to tension on a regular basis to promote extensibility of the scar tissue (Hunter 1994).

Modalities and pharmacology

There has been a great deal of research on the ability to influence the basic biology of tendon healing using pharmacological and physical modalities. Low intensity laser beam (photo stimulation) and electric stimulation has been shown to enhance tissue healing the research showed an increased total collagen production, but there were fewer cross-links per collagen molecules, the mechanism remains unclear. It is suggested that it promotes nucleic acid synthesis and cell division of human fibroblasts. Ultrasound has been reported to improve scar maturation and to decrease inflammatory cell infiltration into healing flexor tendon (Hyman and Rodeo 2000). A combination of ultrasound, electrical stimulation and laser stimulation was found to increase collagen synthesis and tensile strength in healing rabbit’s tendons (Gum and Reddy 1997).

Cold is useful in the immediate care of an acute tendon injury to decrease inflammation, oedema and pain. Heat has been shown to increase chemical activity, metabolic rate and tissue extensibility and decrease muscle spasm, pain and ischemia. Heat should not be used in the acute phase of the inflammation (Józsa and Kannus 1997) .
Various growth factors have been found to effect cell proliferation, matrix synthesis, and cell migration in intrasynnovial and extrasynnovial tendons, the most promising are (TGF, IGF-1 and PDGF). Ligaments treated with PDGF, IGF-1 and FGF had increases in strength, stiffness and breaking energy (Hyman and Rodeo 2000).

The current opinion on the use of NSAID´s in acute tendon strains and partial tendon ruptures should be administrated during the inflammation and proliferation phase (Józsa and Kannus 1997).

Tensile loading/stress

In the early stages of rehabilitation it is of great importance that the injured tissue is well protected. Maintaining the blood supply is critical to prevent necrosis of the collagen, and this may be a problem in areas with compromised vascularity because of friction, compression or torsion, for example achilles and supraspinatus tendon. It is also important to have a regime of progressive tensile stress, which will help the fibrillar alignment, appropriate cross-linking and normal mechanical properties, during subsequent phases. Research shows that exercise has a positive effect on mechanical and morphological characteristics of the injured tissue. There is a problem with applying a progressive regimen of tensile force to strengthen the tissue without reinjuring it (Hujibregts and Smith 1999).

Deep friction can in early phases enhance the mobilisation of tissue fluid, and in later stages stimulate fibre orientation, prevent cross linking and adhesions and increase blood flow.
Stretching should be used with increased tissue temperature and slow prolonged stretching to gain a permanent increase in ROM (Reid 1992).


The rehabilitation of ligaments depends on if the joint is stable or not, unstable joints may need bracing techniques or surgery. Injured ligaments have abnormal proprioception, which makes the proprioceptive training another factor to include in the rehabilitations program.
Joint position sense (JPS) in ACL deficient knees has been described as impaired, although knee stability can improve with exercise therapy, there may be no improvement in JPS. The role of JPS in the stability of ACL deficient knees remains unclear (Hyman and Rodeo 2000).

Heavy load eccentric calf muscle training for chronic achilles tendinosis

A study on eccentric training was conducted with 15 middle-aged recreational athletes, who had the diagnosis chronic achilles tendinosis (degenerative changes) and where selected for surgical treatment. They also had a control group with the same diagnostic criteria that underwent surgical treatment. The training group followed an eccentric training program 2 times a day for 12 weeks. The program included eccentric calf muscle training with both the knee extended and flexed (3×15 for each exercise). The patients were told to go ahead with the exercise even if they experienced pain. When they could perform the exercise without pain they were instructed to increase the load.

After 12 weeks the training group were all back to penury level. The control group were all back to pre-injury level after 6 months.

Possible explanations may be either the effect of stretching with a lengthening of the muscle-tendon unit, and consequently less strain during ankle joint motion. Or loading within muscle tendon unit with hypertrophy and increased tensile strength in the tendon, thus remodelling is induced from eccentric loading (Alfredson and Lorentzon 2000, Alfredson et al 1998).

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