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British Journal of Sports Medicine 2002;36:392-393; doi:10.1136/bjsm.36.6.392
Copyright © 2002 BMJ Publishing Group Ltd & British Association of Sport and Exercise Medicine.
Br J Sports Med 2002;36:392-393
© 2002 British Journal of Sports Medicine

LEADER

Tendinopathies

Understanding tendinopathies

G A Murrell

Orthopaedic Research Institute, St George Hospital, University of New South Wales, Sydney, Australia

Correspondence to:
Correspondence to:
Professor Murrell, Research and Education Center, 4–10 South St, Kogarah, Sydney, NSW 2217, Australia;
admin@ori.org.au


Is apoptosis the heart of the problem?

Keywords: tendon; tendinopathy; apoptosis

The first 150 words of the full text of this article appear below.

One of the "banes" of most health professionals who look after athletes and workers is tendinopathies. What causes them? What gets them better? Recently there have been several advances that may contribute to our understanding of these disorders.

We all know that tendinopathies occur in the tendinous portion of musculotendinous units that cross joints, often two joints—for example, the extensor carpi radialis brevis in tennis elbow, the patellar tendon in jumpers knee—and that they occur in situations of repetitive, high, often eccentric loading. The classic pathology is a loss of the normal collagenous architecture and replacement with an amorphous mucinous material that lacks the parallel, longitudinal architecture of normal tendon.1 Soslowsky et al2 made a major advance when they developed an animal model that could reproduce many of the microscopic changes of supraspinatus tendinopathy. The model involved running rats on a treadmill for up to an hour a day . . . [Full text of this article]


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