Martti Kvist

Achilles Tendon Injuries in Athletes

SummaryTwo-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 a 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.

The role of recreational sport activity in Achilles tendon rupture A clinical, pathoanatomical, and sociological study of 292 cases

During the last few decades, the incidence of tendon ruptures has increased in civilized countries. Our ma terial comprises 749 patients who had 832 tendon ruptures treated surgically between 1972 and 1985. There were no competitive athletes among the patients studied. There were 292 single ruptures of the Achilles tendon, 274 of the proximal biceps brachii, 113 of the extensor pollicis longus, and 70 of other tendons. Forty- eight patients had multiple ruptures and 35 patients had reruptures. Achilles tendon ruptures often occurred in recreational sports activities (59%), in contrast to other tendon ruptures (2%; P < 0.001). The mean age for patients who had Achilles tendon rupture was 35.2 years and for patients with other ruptures, 50.7 years (P < 0.001). There was a connection between the high incidence of blood group O and tendon ruptures (P< 0.001). In cases of multiple ruptures and reruptures, the frequency of blood group O was 71%. Sixty-two point three percent of the patients with Achilles tendon rupture were professionals or white collar workers, which is markedly more than in the Hungarian popula tion (12.7%; P < 0.001). Two hundred and six Achilles tendon ruptures were studied histologically, and all cases displayed pathological alterations. The results indicate that complete rupture of the Achilles tendon is usually a sequel to a sedentary life-style and participa tion in sports activities.

Histopathological findings in chronic tendon disorders

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.

Some biomechanical aspects of the foot and ankle in athletes with and without shin splints

Thirteen adult male athletes (long-distance runners and orienteerers without foot problems) and 35 male ath letes 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 tread mill. 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 < 0.05-0.01) angular displace ment 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 < 0.01) at the heel strike. Further, the shin splints group had a significantly greater (P < 0.01) angular displacement between the heel strike and the maximal everted position. The results suggest struc tural and functional differences in the feet and ankles between healthy athletes and those with shin splints.

Long-Term Prognosis for Jumper’s Knee in Male Athletes A Prospective Follow-up Study

Background: Little information is available on the long-term outcome of jumpers knee, a common problem among athletes. Purpose: Our aim was to determine the 15-year prognosis of jumpers knee. Study Design: Prospective case control. Methods: The prognosis for jumpers knee was studied using two groups: athletes with jumpers knee and nonsymptomatic control athletes. At baseline, all subjects participated in standardized clinical examinations and measurements, and 15 years later they were asked to respond to a questionnaire. Results: Twenty athletes with jumpers knee and 16 athlete control subjects responded (response rate 74% and 84%, respectively). The jumpers knee group reported significantly more knee symptoms according to their Kujala score and more knee pain after repeated squatting. Fifty-three percent of the subjects in the jumpers knee group (9 of 17) reported that they had quit their sports career because of their knee problem, compared with 7% of the control athletes (1 of 14). Patellar height was associated with knee symptoms at follow-up. Conclusion: Jumpers knee causes mild but long-lasting symptoms after an athletic career.

Mechanical loading regulates the expression of tenascin-C in the myotendinous junction and tendon but does not induce de novo synthesis in the skeletal muscle

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.

Chronic achilles paratenonitis in athletes: a histological and histochemical study

&NA; Pathological alterations of chronic Achilles paratenonitis were studied histologically and histochemically in tissue samples obtained operatively from 16 athletes with this complaint and from 3 control patients. The activities of 11 different enzymes lactate, succinate, malate, glucose‐6‐phosphate and glutamate dehydrogenases, lipoamide dehydrogenase and glutathione reductase (NADH2‐ and NADPH2‐diaphorases), acid and alkaline phosphatases, phosphorylase and leucylaminopeptidase ‐ were studied. Pathological findings were located diffusely around the tendon. A slight inflammatory cell reaction was found in all cases. The fatty areolar tissue was clearly thickened and edematous, and showed fibrinous exudations, widespread fat necrosis, considerable connective tissue proliferation and adhesion formation. The blood vessels showed profound degenerative and necrotizing changes. The thin membranes of the paratenon were clearly hypertrophied. Increased enzyme activities were mainly found in the fibroblasts, inflammatory cells and vascular walls. A moderate activity of lysosomal enzymes, an increased activity of enzymes of electron transport, anaerobic glycolysis, pentose phosphate shunt and decreased activity of those of aerobic energy metabolism were found. Simultaneously an increased amount of both neutral and acid mucopolysaccharides and a locally increased amount of elastic fibres were found in the inflamed paratenon. These results indicate that marked metabolic changes occur in paratenonitis, i.e. an increased catabolism and decreased oxygenation of the inflamed areas. The morphological alterations suggest that the gliding function of the paratenon may be impaired.

Chronic Achilles paratenonitis An immunohistologic study of fibronectin and fibrinogen

Pathological alterations in chronic Achilles paratenonitis were studied histologically and using immunofluores cence techniques for fibronectin and fibrinogen in tissue samples obtained operatively from 11 athletes with this complaint and from 4 male cadavers serving as con trols. The average duration of the paratenonitis was 20.4 months. The paratendineal fatty areolar tissue was clearly thickened and edematous, showing widespread fat necrosis and considerable connective tissue prolif eration. The blood vessels were often obliterated and degenerated. Fibronectin and fibrinogen were com monly found in the proliferating connective tissue areas and in the vascular walls. Exudates rich in fibrinogen and fibronectin were seen in the inflamed paratendineal tissues, but not in the controls. The results indicate that increased vascular permea bility and fibrin formation still persist in chronic Achilles paratenonitis and that marked obliterative and degen erative alterations of the blood vessels are frequent. The presence of fibronectin and fibrinogen points to an immature nature of scar tissue in chronic paratenonitis.

LOCATION AND DISTRIBUTION OF NON-COLLAGENOUS MATRIX PROTEINS IN MUSCULOSKELETAL TISSUES OF RAT

The study assessed immunohistochemically the location and distribution of various non-collagenous matrix proteins (fibronectin, laminin, tenascin-C, osteocalcin, thrombospondin-1, vitronectin and undulin) in musculoskeletal tissues of rat. Fibronectin and thrombospondin-1 were found to be ubiquitous in the studied tissues. High immunoreactivity of these proteins was found in the extracellular matrix of the anatomical sites where firm bindings are needed, i.e. between muscle fibres and fibre bundles, between the collagen fibres of a tendon and at myotendinous junctions, osteotendinous junctions and articular cartilage. Tenascin-C was found in the extracellular matrix of regions where especially high forces are transmitted from one tissue component to the other, such as myotendinous junctions and osteotendinous junctions. Laminin was demonstrated in the basement membranes of the muscle cells and capillaries of the muscle–tendon units. Osteocalc in immunoreactivity concentrated in the extracellular matrix of areas of newly formed bone tissue, i.e. in the subperiosteal and subchondral regions, osteoid tissue and mineralized fibrocartilage zone of the osteotendinous junction. Mild vitronectin activity could be seen in the extracellular matrix of the osteotendinous and myotendinous junctions, and high activity around the bone marrow cells. Undulin could be demonstrated in the extracellular matrix (i.e. on the collagen fibres) of the tendon and epimysium only. However, it was co-distributed with fibronectin and tenascin-C. Together, these findings on the normal location and distribution of these non-collagenous proteins in the musculoskeletal tissues help to form the basis of knowledge against which the location and distribution of the these proteins in various pathological processes could be compared.

Quantitative alterations in intramuscular connective tissue following immobilization: an experimental study in the rat calf muscles.

The purpose of the present investigation was to study the effect of immobilization in two different positions, shortened or lengthened, on the connective tissue and capillarization of the rat calf muscles. In 18 rats the left hind limb was immobilized so that the soleus and gastrocnemius muscles were in a lengthened position and tibialis anterior was in a shortened position, and in 18 rats vice versa. The right hind limbs were kept free to serve as controls. After 1, 2, and 3 weeks of immobilization, an equal number of rats were killed and the muscles were analyzed. The connective tissue muscle ratio was measured from histological sections by automatic image analyzer and the number of capillaries per 1000 muscle fibers was also recorded. In the intact muscles the proportions of intramuscular connective tissue in the soleus, gastrocnemius, and tibialis anterior were 2, 3, and 5%, respectively. During the immobilization period of 3 weeks the proportion of connective tissue increased significantly in all muscles, but the only significant difference between the positions was in the soleus muscle in which more connective tissue was found in the lengthened position, 54% vs 30% in the shortened position. The amount of capillaries decreased significantly during immobilization in all muscles to about 65% of normal capillar density, but the position of immobilization seemed to have no effect on this phenomenon. The increase in intramuscular connective tissue during immobilization seems to occur simultaneously with muscle atrophy and loss of muscle capillarity. The stretched position of immobilization seems to have an additional fibrotic effect if the immobilized muscle, such as soleus, consists mainly of type I fibers generally known to be more vulnerable to disuse atrophy than type II fibers.