Two-thirds of Achilles tendon injuries in competitive athletes are paratenonitis and one-fifth are insertional complaints (bursitis and insertion tendinitis). The remaining afflictions consist of pain syndromes of the myotendineal junction and tendinopathies. The majority of Achilles tendon injuries from sport occur in males, mainly because of their higher rates of participation in sport, but also with tendinopathies a gender difference is probably indicated. Athletes in running sports have a high incidence of Achilles tendon overuse injuries. About 75% of total and the majority of partial tendon ruptures are related to sports activities usually involving abrupt repetitive jumping and sprinting movements. Mechanical factors and a sedentary lifestyle play a role in the pathology of these injuries. Achilles tendon overuse injuries occur at a higher rate in older athletes than most other typical overuse injuries. Recreational athletes with a complete Achilles tendon rupture are about 15 years younger than those with other spontaneous tendon ruptures. Following surgery, about 70 to 90% of athletes have a successful comeback after Achilles tendon injury. Surgery is required in about 25% of athletes with Achilles tendon overuse injuries and the frequency of surgery increases with patient age and duration of symptoms as well as occurrence of tendinopathic changes. However, about 20% of injured athletes require a re-operation for Achilles tendon overuse injuries, and about 3 to 5% are compelled to abandon their sports career because of these injuries. Myotendineal junction pain should be treated conservatively. Partial Achilles tendon ruptures are primarily treated conservatively, although the best treatment method of chronic partial rupture seems to be surgery. Complete Achilles tendon ruptures of athletes are treated surgically, because this increases the likelihood of athletes reaching preinjury activity levels and minimises the risk of re-ruptures. Marked forefoot varus is found in athletes with Achilles tendon overuse injuries, reflecting the predisposing role of ankle joint overpronation. Athletes with the major stress in lower extremities have often a limited range of motion in the passive dorsiflexion of the ankle joint and total subtalar joint mobility, which seems to be predisposing factor for these injuries. Various predisposing transient factors are found in about one-third of athletes with Achilles tendon overuse injuries; of these, traumatic factors (mostly minor injuries) predominate. The typical histological features of chronically inflamed paratendineal tissue of the Achilles tendon are profound proliferation of loose, immature connective tissue and marked obliterative and degenerative alterations in the blood vessels. These changes cause continuing leakage of plasma proteins, which may have an important role in the pathophysiology of these injuries. The chronically inflamed paratendineal tissues of the Achilles tendon do not seem to have enough capacity to form mature connective tissue.

Tendon injuries and other tendon disorders represent a common diagnostic and therapeutic challenge in sports medicine, resulting in chronic and long‐lasting problems. Tissue degeneration is a common finding in many sports‐related tendon complaints. In the great majority of spontaneous tendon ruptures, chronic degenerative changes are seen at the rupture site of the tendon (1). Systemic diseases and diseases specifically deteriorating the normal structure of the tendon (i.e. foreign bodies, and metabolic, inherited and infectious tendon diseases) are only rarely the cause of tendon pathology. Inherited diseases, such as various hereditary diseases with disturbed collagen metabolism and characteristic pathological structural alterations (Ehlers‐Danlos syndrome, Marfani syndrome, homocystinuria (ochronosis)), represent approximately 1% of the causes of chronic tendon complaints (2), whereas foreign bodies are somewhat more common and are found in less than 10% of all chronic tendon problems (1). Rheumatoid arthritis and sarcoidosis are typical systemic diseases that cause chronic inflammation in tendon and peritendinous tissues. Altogether, these ‘specific’disorders represented less than 2% of the pathological alterations found in the histological analysis of more than 1000 spontaneously ruptured tendons (1, 3, 4). In this material, degenerative changes were seen in a great majority of the tendons, indicating that aspontaneous tendon rupture is a typical clinical end‐state manifestationof a degenerative process in the tendon tissue. The role of overuse in the pathogenesis of chronic tendon injuries and disorders is not completely understood. It has been speculated that when tendon is overused, it becomes fatigued and loses its basal reparative ability, the repetitive microtraumatic processes thus overwhelming the ability of the tendon cells to repair the fiber damage. The intensive repetitive activity, which often is eccentric by nature, may lead to cumulative microtrauma which further weakens the collagen cross‐linking, non‐collagenous matrix, and vascular elements of the tendon. Overuse has also been speculated to cause chronic tendon problems, by disturbing the micro‐ and macrovasculature of the tendon and resulting in insufficiency in the local blood circulation. Decreased blood flow simultaneous with an increased activity may result in local tissue hypoxia, impaired nutrition and energy metabolism, and together these factors are likely to play an important role in the sequence of events leading to tendon degeneration (4). A sedentary lifestyle has been proposed as a main reason for poor basal circulation of the tendon, and presumably is at least partly responsible for the high number of tendon problems in people with a sedentary lifestyle who occasionally take part in high physical activity sports events.

Jumper's knee causes mild but long-lasting symptoms after an athletic career.

Tenascin-C is a hexabrachion-shaped matricellular protein with a very restricted expression in normal musculoskeletal tissues, but it is expressed abundantly during regenerative processes of these tissues and embryogenesis. To examine the importance of mechanical stress for the regulation of tenascin-C expression in the muscle-tendon unit, the effects of various states of mechanical loading (inactivity by cast-immobilization and three-varying intensities of subsequent re-activity by treadmill running) on the expression of tenascin-C were studied using immunohistochemistry and mRNA in situ hybridization at the different locations of the muscle-tendon unit of the rat gastrocnemius muscle, the Achilles tendon complex. This muscle-tendon unit was selected as the study site, because the contracting activity of the gastrocnemius-soleus muscle complex, and thus the mechanical loading-induced stimulation, is easy to block by cast immobilization. Tenascin-C was expressed abundantly in the normal myotendinous and myofascial junctions, as well as around the cells and the collagen fibers of the Achilles tendon. Tenascin-C expression was not found in the normal skeletal muscle, although it was found in blood vessels within the muscle tissue. Following the removal of the mechanical loading-induced stimulation on the muscle-tendon unit by cast immobilization for 3 weeks, the immonoreactivity of tenascin-C substantially decreased or was completely absent in the regions expressing tenascin-C normally. Restitution of the mechanical loading by removing the cast and allowing free cage activity for 8 weeks resulted in an increase in tenascin-C expression, but it could not restore the expression of tenascin-C to the normal level (in healthy contralateral leg). In response to the application of a more strenuous mechanical loading stimulus after the removal of the cast (after 8 weeks of low- and high-intensity treadmill running), the expression of tenascin-C was markedly increased and reached the level seen in the healthy contralateral limb. Tenascin-C was abundantly expressed in myotendinous and myofascial junctions and in the Achilles tendon, but even the most strenuous mechanical loading (high-intensity treadmill running) could not induce the expression of tenascin-C in the skeletal muscle. This was in spite of the marked immobilization-induced atrophy of the previously immobilized skeletal muscle,which had been subjected to intensive stress during remobilization. mRNA in situ hybridization analysis confirmed the immunohistochemical results for the expression of tenascin-C in the study groups. In summary, this study shows that mechanical loading regulates the expression of tenascin-C in an apparently dose-dependent fashion at sites of the muscle-tendon unit normally expressing tenascin-C but can not induce de novo synthesis of tenascin-C in the skeletal muscle without accompanying injury to the tissue. Our results suggest that tenascin-C provides elasticity in mesenchymal tissues subjected to heavy tensile loading.

Thirteen adult male athletes (long-distance runners and orienteerers without foot problems) and 35 male athletes with shin splints were compared with respect to: 1) the position of the lower leg and the heel while standing, 2) the passive range of mobility in the subtalar joint, and 3) the angular displacement between the calcaneus and the midline of the lower leg (Achilles tendon angle) while running with bare feet on a treadmill. In standing, the two groups differed statistically significantly in the Achilles tendon angle, which values were greater in the shin splint group. With respect to passive mobility, the athletes with shin splints had significantly greater (P less than 0.05-0.01) angular displacement values in inversion, eversion, and in their sum than the control group. While running, the Achilles tendon angle of the shin splint group was significantly greater (P less than 0.01) at the heel strike. Further, the shin splints group had a significantly greater (P less than 0.01) angular displacement between the heel strike and the maximal everted position. The results suggest structural and functional differences in the feet and ankles between healthy athletes and those with shin splints.

The conservative management of chronic calcaneal paratenonitis is time-consuming and often unsatisfactory. A new, safe and simple technique is described. The crural fascia on both sides ofthe tendon is incised and left open, adhesions around the tendon are trimmed away, the strongly hypertrophied portions of the paratenon are removed and mobilisation is begun Immediately after operation. Between 1961 and 1978 201 such operations were performed on 182 patIents 62 of whom were top-ranking Finnish athletes. Only five patients were not athletes. The results, including early return to full activity, were excellent in 169, good in 25 and poor in seven cases. After operation one ofthe patients gained an Olympic gold medal; others also have attained international prominence.

After 3 wk of immobilization, the effects of free cage activity and low- and high-intensity treadmill running (8 wk) on the morphology and histochemistry of the soleus and gastrocnemius muscles in male Sprague-Dawley rats were investigated. In both muscles, immobilization produced a significant (P < 0.001) increase in the mean percent area of intramuscular connective tissue (soleus: 18.9% in immobilized left hindlimb vs. 3.6% in nonimmobilized right hindlimb) and in the relative number of muscle fibers with pathological alterations (soleus: 66% in immobilized hindlimb vs. 6% in control), with a simultaneous significant (P < 0.001) decrease in the intramuscular capillary density (soleus: mean capillary density in the immobilized hindlimb only 63% of that in the nonimmobilized hindlimb) and muscle fiber size (soleus type I fibers: mean fiber size in the immobilized hindlimb only 69% of that in the nonimmobilized hindlimb). Many of these changes could not be corrected by free remobilization, whereas low- and high-intensity treadmill running clearly restored the changes toward control levels, the effect being most complete in the high-intensity running group. Collectively, these findings indicate that immobilization-induced pathological structural and histochemical alterations in rat calf muscles are, to a great extent, reversible phenomena if remobilization is intensified by physical training. In this respect, high-intensity exercise seems more beneficial than low-intensity exercise.

Factors predisposing to patellar chondropathy (the PC group) and inferior patellar apicitis (jumper's knee - the PA group) were sought by means of a questionnaire, detailed quantitative physical measurements and radiological examination in male athletes. There were 20 athletes in the two groups who had typical symptoms and signs of each disorder. A group of 20 high-level athletes without knee symptoms served as a control group. The factors found in the PC group which differed significantly from those in the control group included increased anterior drawer sign (p less than 0.05), increased passive mediolateral patellar range of movement (p less than 0.001) and increased hyperextension (p less than 0.05). More leg length inequality (p less than 0.001) and patella alta (p less than 0.05) was observed in the PA group than in the controls. There was statistically significant positive correlation between the different measurements of knee laxity (anterior drawer sign, passive mediolateral patellar movement and hyperextension) in the 60 cases. The correlation coefficient between the length of the patellar tendon and passive mediolateral patellar movement was 0.82 (p less than 0.001).