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Tendinopatia – eksentrisen harjoittelun merkitys kuntoutuksessa
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Suomalaisille lukijoille: Kirja on paperimuodossa loppuunmyyty, mutta siitä on saatavilla henkilökohtainen sähköinen versio ottamalla yhteyttä kirjoittajaan osoitteeseen jari.metsamuuronen@methelp.com. Kirjastolisenssejä välittää LM-info osoitteessa info@lminfo.com.
This is the original Finnish handbook which is the basis of the international "Essentials of Research Methods in Human Sciences" By SAGE. This book or its part are used in almost all universities in Finland. At some point, it was used in 26 different domains like education, psychology, nursing, sports, and management.
The etiology and pathogenesis to chronic tendon pain is unknown, and treatment is known to be difficult. Treatment is often based on opinions and not findings in scientific studies. Recent research, using the intra-tendinous microdialysis technique, has shown that in chronic painful Achilles-, patellar-, and extensor carpi radialis brevis (ECRB) tendons, there were no signs (normal Prostaglandin-2 levels) of a so-called chemical inflammation. Furthermore, in biopsies from chronic painful Achilles tendons, pro-inflammatory cytokines were not up-regulated, again showing the absence of an intra-tendinous inflammation. Consequently, if the purpose is to treat a chemical inflammation, there is no science backing up for treatment of theses conditions with anti-inflammatory agents (NSAIDs, corticosteroidal injections). Interestingly, Substance-P (SP) and Calcitonin Gene Regulated Peptide (CGRP) nerves have been demonstrated in close relation to vessels in biopsies from these chronic painful tendons, indicating the existence of a possible so-called neurogenic inflammation. Using ultrasonography (US) + color Doppler (CD), and immunhistochemical analyses of biopsies, a vasculo/neural(SP- and CGRP-nerves) ingrowth in the chronic painful tendinosis tendon, but not in the pain-free normal tendon, has recently been found. A specially designed treatment, using US- and CD-guided injections of the sclerosing agent Polidocanol, targeting the neovessels outside the tendon, has in pilot studies on chronic painful Achilles-, and patellar tendons been shown to cure the tendon pain in the majority of patients. A recent randomized double-blind study, verified the importance of injecting the sclerosing substance Polidocanol.
This study examined the concurrent age-related differences in muscle and tendon structure and properties. Achilles tendon morphology and mechanical properties and triceps surae muscle architecture were measured from 100 subjects [33 young (24 ± 2 yr.) and 67 old (75 ± 3 yr.)]. Motion analysis assisted ultrasonography was used to determine tendon stiffness, Young's modulus and hysteresis during isometric ramp contractions. Ultrasonography was used to measure muscle architectural features and size and tendon cross-sectional area. Older participants had 17 % lower (p < 0.01) Achilles tendon stiffness and 32 % lower (p < 0.001) Young's modulus than young participants. Tendon cross-sectional area was also 16 % larger (p < 0.001) in older participants. Triceps surae muscle size was smaller (p < 0.05) and gastrocnemius medialis muscle fascicle length shorter (p < 0.05) in old compared to young. Maximal plantarflexion force was associated with tendon stiffness and Young's modulus (r = 0.580, p < 0.001 and r = 0.561, p < 0.001, respectively). Comparison between old and young subjects with similar strengths did not reveal a difference in tendon stiffness. The results suggest that regardless of age, Achilles tendon mechanical properties adapt to match the level of muscle performance. Old people may compensate for lower tendon material properties by increasing tendon cross-sectional area. Lower tendon stiffness in older subjects might be beneficial for movement economy in low intensity locomotion and thus optimized for their daily activities.
Mechanical loading of human tendon stimulates collagen synthesis, but the relationship between acute loading responses and training status of the tendon is not clear. We tested the effect of prolonged load deprivation on the acute loading-induced collagen turnover in human tendons, by applying the same absolute load to a relative untrained Achilles tendon (2-week immobilization period prior to acute loading) and a habitually loaded contra-lateral Achilles tendon, respectively, within the same individuals. Eight untrained, healthy males had one lower limb totally immobilized for 2 weeks, whereas the contra-lateral leg was used habitually. Following the procedure both Achilles tendons and calf muscles were loaded with the same absolute load during a 1-h treadmill run. Tissue collagen turnover was measured by microdialysis performed post-immobilization but pre-exercise around both Achilles tendons and compared to values obtained by 72-h post-exercise. Power Doppler was used to monitor alterations in intratendinous blood flow velocity of the Achilles tendon and MRI used to quantitate changes in tendon cross-section area. Acute loading resulted in an increased collagen synthesis 72 h after the run in both Achilles tendons (p < 0.05) with no significant difference. No signs of acute tendon overloading were demonstrated by Power Doppler, and tendon cross-section area did not change as a result of immobilization and reloading. The present study indicates that 2 weeks of tendon load deprivation is not sufficient to affect the normal adaptive response to loading determined as increased collagen synthesis of peritendinous Achilles tendon tissue in humans.
Tendon disorders are a major problem for participants in competitive and recreational sports. To try to determine whether the histopathology underlying these conditions explains why they often prove recalcitrant to treatment, we reviewed studies of the histopathology of sports-related, symptomatic Achilles, patellar, extensor carpi radialis brevis and rotator cuff tendons.
The literature indicates that healthy tendons appear glistening white to the naked eye and microscopy reveals a hierarchical arrangement of tightly packed, parallel bundles of collagen fibres that have a characteristic reflectivity under polarised light. Stainable ground substance (extracellular matrix) is absent and vasculature is inconspicuous. Tenocytes are generally inconspicuous and fibroblasts and myofibroblasts absent.
In stark contrast, symptomatic tendons in athletes appear grey and amorphous to the naked eye and microscopy reveals discontinuous and disorganised collagen fibres that lack reflectivity under polarised light. This is associated with an increase in the amount of mucoid ground substance,which is confirmedwithAlcian blue stain. At sites of maximal mucoid change, tenocytes, when present, are plump and chondroid in appearance (exaggerated fibrocartilaginous metaplasia). These changes are accompanied by the increasingly conspicuous presence of cells within the tendon tissue, most of which have a fibroblastic or myofibroblastic appearance (smooth muscle actin is demonstrated using an avidin biotin technique). Maximal cellular proliferation is accompanied by prominent capillary proliferation and a tendency for discontinuity of collagen fibres in this area.Often, there is an abrupt discontinuity of both vascular and myofibroblastic proliferation immediately adjacent to the area of greatest abnormality. The most significant feature is the absence of inflammatory cells.
These observations confirmthat the histopathological findings in athletes with overuse tendinopathies are consistent with those in tendinosis — a degenerative condition of unknown aetiology. This may have implications for the prognosis and timing of a return to sport after experiencing tendon symptoms.
As the common overuse tendon conditions are rarely, if ever, caused by ‘tendinitis’, we suggest the term ‘tendinopathy’ be used to describe the common overuse tendon conditions.We conclude that effective treatment of athletes with tendinopathiesmust target the most common underlying histopathology, tendinosis, a noninflammatory condition.
Symptoms of jumper's knee (patellar tendinosis) are not easily quantified and this may explain why there are no evidence-based guidelines for managing the condition. A simple, practical questionnaire-based index of severity would facilitate jumper's knee research and subsequently, clinical management. Thus we devised and tested the Victorian Institute of Sport Assessment (VISA) questionnaire. The brief questionnaire assesses (i) symptoms, (ii) simple tests of function and (iii) ability to play sport. Six of the eight questions are scored on a visual analogue scale from 0–10 with 10 representing optimal health. The maximal VISA score for an asymptomatic, fully performing individual is 100 points and the theoretical minimum is 0 points. We found the VISA scale to have excellent short-term test-retest, and inter-tester reliability (both, r>0.95) as well as good short-term (one week) stability (r=0.87). Mean (SD) of the VISA scores ranged from 95 (8) points in asymptomatic control subjects to 55 (12) points in patients who presented to a sports medicine clinic with jumper's knee and 22 (17) points in patients before surgery for chronic jumper's knee. Six- and twelve-months after surgery VISA scores returned to 49 (15) and 75 (17) points respectively, mirroring clinical recovery. We conclude that the VISA score is a reliable index of the severity of jumper's knee that has potential to aid clinicians and researchers.
The maximum stresses to which a wide range of mammalian limb tendons could be subjected in life were estimated by considering the relative cross-sectional areas of each tendon and of the fibres of its muscle. These cross-sectional areas were derived from mass and length measurements on tendons and muscles assuming published values for the respective densities. The majority of the stresses are low. The distribution has a broad peak with maximum frequency at a stress of about 13 MPa, whereas the fracture stress for tendon in tension is about 100 MPa. Thus, the majority of tendons are far thicker than is necessary for adequate strength. Much higher stresses are found among those tendons which act as springs to store energy during locomotion. The acceptability of low safety factors in these tendons has been explained previously (Alexander, 1981). A new theory explains the thickness of the majority of tendons. The muscle with its tendon is considered as a combined system which delivers mechanical energy: the thickness of the tendon is optimized by minimizing the combined mass. A thinner tendon would stretch more. To take up this stretch, the muscle would require longer muscle fibres, which would increase the combined mass. The predicted maximum stress in a tendon of optimum thickness is about 10 MPa, which is within the main peak of the observed stress distribution. Individual variations from this value are to be expected and can be understood in terms of the functions of the various muscles.