1. Direct injury to skeletal muscle results in fragmentation and necrosis of muscle fibres, though this is patchy in distribution. 2. The sarcolemmal basement membranes form the interface along which fibre regeneration takes place. 3. Phagocytosis of disorganised sarcoplasm is an essential prelude to the reconstitution of severely damaged fibres. 4. Regeneration of injured muscle begins with proliferation of basophilic cells probably originating from muscle satellite cells. After a few days typical myoblast nuclear chains are present. By a week following injury the chains of myoblasts have formed myotubes, which possess myofibrils and sarcomeres. 5. By twelve days in the monkey and by eighteen days in man the muscle fibre regenerative process shows many new fibres which have not reached a mature diameter. 6. Much collagen may be formed in the tissue space at the site of injury. It appears that as the muscle fibres increase in diameter the collagen decreases in extent. 7. In the monkey by three weeks the muscle at the fracture site appears normal. This is also true in the specimens examined at four, six and twelve weeks. 8. In the monkeys the injured limb was immediately used to run and jump. A parallel intense and early activity of muscle and joints was a cardinal point in the management of this series of fracture patients. The clinical results were satisfactory. 9. It is concluded that in both the monkey and in man, given active limb movements, permanent and functionally useful muscle regeneration occurs following soft-tissue injury associated with a bone fracture

Aims

Improvements in the evaluation of outcomes following peripheral nerve injury are needed. Recent studies have identified muscle fatigue as an inevitable consequence of muscle reinnervation. This study aimed to quantify and characterize muscle fatigue within a standardized surgical model of muscle reinnervation.

The response of the muscle is critical in determining the functional outcome of limb lengthening. We hypothesised that muscle response would vary with age and therefore studied the response of the muscles during tibial lengthening in ten young and ten mature rabbits. A bromodeoxyuridine technique was used to identify the dividing cells.

The young rabbits demonstrated a significantly greater proliferative response to the distraction stimulus than the mature ones. This was particularly pronounced at the myotendinous junction, but was also evident within the muscle belly.

Younger muscle adapted better to lengthening, suggesting that in patients in whom a large degree of muscle lengthening is required it may be beneficial to carry out this procedure when they are young, in order to achieve the optimal functional result.

The nervous system is known to be involved in inflammation and repair. We aimed to determine the effect of physical activity on the healing of a muscle injury and to examine the pattern of innervation. Using a drop-ball technique, a contusion was produced in the gastrocnemius in 20 rats. In ten the limb was immobilised in a plaster cast and the remaining ten had mobilisation on a running wheel. The muscle and the corresponding dorsal-root ganglia were studied by histological and immunohistochemical methods.

In the mobilisation group, there was a significant reduction in lymphocytes (p = 0.016), macrophages (p = 0.008) and myotubules (p = 0.008) between three and 21 days. The formation of myotubules and the density of nerve fibres was significantly higher (both p = 0.016) compared with those in the immobilisation group at three days, while the density of CGRP-positive fibres was significantly lower (p = 0.016) after 21 days.

Mobilisation after contusional injury to the muscle resulted in early and increased formation of myotubules, early nerve regeneration and progressive reduction in inflammation, suggesting that it promoted a better healing response.

The anatomical studies, basic to our understanding of lumbar spine innervation through the sinu-vertebral nerves, are reviewed. Research in the 1980s suggested that pain sensation was conducted in part via the sympathetic system. These sensory pathways have now been clarified using sophisticated experimental and histochemical techniques confirming a dual pattern. One route enters the adjacent dorsal root segmentally, whereas the other supply is non-segmental ascending through the paravertebral sympathetic chain with re-entry through the thoracolumbar white rami communicantes.

Sensory nerve endings in the degenerative lumbar disc penetrate deep into the disrupted nucleus pulposus, insensitive in the normal lumbar spine. Complex as well as free nerve endings would appear to contribute to pain transmission.

The nature and mechanism of discogenic pain is still speculative but there is growing evidence to support a ‘visceral pain’ hypothesis, unique in the muscloskeletal system. This mechanism is open to ‘peripheral sensitisation’ and possibly ‘central sensitisation’ as a potential cause of chronic back pain.