Laszlo Jozsa

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.

Organization and distribution of intramuscular connective tissue in normal and immobilized skeletal muscles

Collagen fiber network is a major contributor to the coherence and tensile strength of normal skeletal muscle. Despite the well-recognized importance of the intramuscular connective tissue to the normal integrity and function of the skeletal muscle, the specific architecture including the location and three-dimensional orientation of the intramuscular connective tissue within the muscle tissue is poorly described. The structure of the intramuscular connective tissue was studied by immunohistochemistry, polarization microscopy (the crimp length and angle of the collagen fibers) and scanning electron microscope (SEM) in rat skeletal muscles (gastrocnemius, soleus and tibialis anterior) in normal situation and after 3 weeks of disuse (immobilization). Three separate networks of collagen fibers were distinguished by SEM in the normal endomysium; fibers running longitudinally on the surface of the muscle fibers (the main collagen orientation), fibers running perpendicularly to the long axis of the muscle fibers and having contacts with adjacent muscle fibers, and fibers attached to the intramuscular nerves and arteries. Similarly, the SEM analysis also disclosed three distinct collagen fiber networks running in different directions in the perimysium, but, contrary to the endomysium, the main fiber orientation could not be established. Immobilization resulted in a marked increase in the endo- and perimysial connective tissue, the majority of the increased endomysial collagen being deposited directly on the sarcolemma of the muscle cells. Immobilization also resulted in substantial increase in the number of perpendicularly oriented collagen fibers with contacts to two adjacent muscle fibers in the endomysium. Further, immobilization clearly disturbed the normal structure of the endomysium making it impossible to distinguish the various networks of fibers from each other. In the perimysium, immobilization-induced changes were similar, the number of longitudinally oriented collagen fibers was increased, the connective tissue was very dense, the number of irregularly oriented collagen fibers was markedly increased, and consequently, the different networks of collagen fibers could not be distinguished from each other. Of the three studied intact muscles, the crimp angle of the collagen fibers was lowest in the soleus and highest in the gastrocnemius muscle, and the crimp angle decreased over 10% in all muscles after the immobilization-period. Altogether, the above described quantitative and qualitative changes in the intramuscular connective tissue are likely to contribute to the deteriorated function and biomechanical properties of the immobilized skeletal muscle.

Achilles tendon injuries.

The Achilles tendon is the strongest tendon in the human body. Because most Achilles tendon injuries take place in sports and there has been an common upsurge in sporting activities, the number and incidence of the Achilles tendon overuse injuries and complete ruptures have increased in the industrialized countries during the last decades. The most common clinical diagnosis of Achilles overuse injuries is tendinopathy, which is characterized by a combination of pain and swelling in the Achilles tendon accompanied by impaired ability to perform strenuous activities. Most patients with Achilles tendon injury respond favorably to conservative treatment and only those who fail to respond to carefully followed nonoperative treatment should undergo surgery for repair. A complete rupture of the Achilles tendon usually occurs in sports that require jumping, running, and quick turns. Although histopathologic studies have shown that ruptured Achilles tendons include clear degenerative changes before the rupture, many of the Achilles tendon ruptures occur suddenly without any preceding signs or symptoms. Neither conservative nor operative treatment is a treatment of choice for the ruptured Achilles tendon. It is generally accepted that surgery should be performed on ruptured Achilles tendons in young, physically active patients and in those patients for whom the diagnosis or the treatment of the rupture has been delayed, whereas the results of conservative treatment are an acceptable outcome in older patients with sedentary lifestyles. Many important issues still remain unanswered concerning the cause, pathogenesis, diagnosis, and management of the Achilles tendon disorders. Only when these issues have been solved by well-controlled studies can tailored treatment protocols be created.

The effect of tenotomy and immobilisation on intramuscular connective tissue. A morphometric and microscopic study in rat calf muscles

The effect of tenotomy and of immobilisation in lengthened and shortened positions on the intramuscular connective tissue of the calf muscles of the rat was studied morphometrically and with a scanning electron microscope. Both tenotomy and immobilisation produced a marked increase in both the endomysial and the perimysial collagen networks, with a simultaneous decrease in intramuscular capillary density. The increase in connective tissue volume was more pronounced and occurred more rapidly in the soleus, which consists mainly of type I, slow-twitch fibres than in the gastrocnemius, which is mainly of type II, fast-twitch fibres. The relative volume of connective tissue increased in parallel with the duration of immobilisation or after tenotomy. There was slightly more increase after immobilisation in a shortened rather than in a lengthened position.

Treatment of tendon disorders

Tendon injuries and other tendon disorders are a source of major concern in competitive and recreational athletes and in many working conditions requiring repetitive movements. The exact etiology, pathophysiology, and healing mechanisms of the various tendon complaints are, however, only partly known and even origin of pain in the chronic tendon disorders is unknown. Thus, the treatment strategies recommended for tendon complaints vary considerably and the given treatment is frequently based on empirical evidence only. Corticosteroid injections are one of the most commonly used treatments for chronic tendon disorders. Despite their popularity, the biologic basis of their effect and the systematic evidence for their benefits are largely lacking. In addition to suppressing inflammation, the effects of local corticosteroid injections could be mediated through their effect on the connective tissue and adhesions between the tendon and the surrounding peritendinous tissues by inhibiting the production of collagen, other extracellular matrix molecules, and granulation tissue in these sites. Also, if the pain in tendinopathy is a result of stimulation of nociceptors by chemicals released by the damaged, degenerated tendon, corticosteroids might mediate their effect thorough alterations in the release of these noxious chemicals, the behavior of these receptors, or both. Achilles tendinopathy, rotator-cuff tendinopathy, tennis elbow, and trigger finger are among the most frequent tendon problems. There is good evidence, however, strongly supporting the use of local corticosteroid injections in the trigger finger only. This can be to the result of either a true lack of the effect or just a lack of good trials in the other complaints. Intimidation with adverse effects of peritendinous corticosteroid injections is based on case reports only rather than convincing data from controlled clinical studies. In light of the animal studies, corticosteroid injection into tendon substance should be avoided, although the true incidence of side effects after local corticosteroid injection(s) for tendon disorders is unknown. Also, the relevance of the steroid used, the tissue affected, the extent of the tendon problem, the duration of the symptoms, the phase of healing at the time of injections, and the postinjection events remain undetermined. Although a complete tendon rupture with loading after steroid injection has been reported, no reliable proof exists of the deleterious effects of peritendinous injections; conclusions in literature are based mainly on uncontrolled case reports that fail under scientific scrutiny, whereas scientifically rigorous studies have not been performed. An acute tendon disorder often responds favorably to early intervention with conservative treatment modalities. Local corticosteroid injections gives good short-term results in prolonged or subacute cases that do not respond to the conventional conservative treatments. Although corticosteroid injections are one of the most commonly used treatment modalities for chronic tendon disorders, there is an obvious lack of good trials defining the indications for and efficacy of such injections, and subsequently, many of the recommendations for the use of local corticosteroid injections do not rely on sound scientific basis. Thus, there is an obvious need for high-quality basic science studies and controlled clinical trials in examining the effects corticosteroids on various tendon disorders.

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.

Three-Dimensional infrastructure of Human Tendons

The three-dimensional ultrastructure of human tendons has been studied. Epitenon and peritenon consis of a dense network of longitudinal, oblique and transversal collagen fibrils crossing the tendon f

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.