Background/hypothesis: Shoulder pain in elite swimmers is common, and its pathogenesis is uncertain. Hypothesis/study design: The authors used a crosssectional study design to test Jobe's hypothesis that repetitive forceful swimming leads to shoulder laxity, which in turn leads to impingement pain. Methods: Eighty young elite swimmers (13-25 years of age) completed questionnaires on their swimming training, pain and shoulder function. They were given a standardised clinical shoulder examination, and tested for glenohumeral joint laxity using a non-invasive electronic laxometer. 52/80 swimmers also attended for shoulder MRI. Results: 73/80 (91%) swimmers reported shoulder pain. Most (84%) had a positive impingement sign, and 69% of those examined with MRI had supraspinatus tendinopathy. The impingement sign and MRIdetermined supraspinatus tendinopathy correlated strongly (r s =0.49, p<0.00001). Increased tendon thickness correlated with supraspinatus tendinopathy (r s =0.37, p<0.01). Laxity correlated weakly with impingement pain (r s =0.23, p<0.05) and was not associated with supraspinatus tendinopathy (r s =0.14, p=0.32). The number of hours swum/week (r s =0.39, p<0.005) and weekly mileage (r s =0.34, p=0.01) both correlated signifi cantly with supraspinatus tendinopathy. Swimming stroke preference did not. Conclusions: These data indicate: (1) supraspinatus tendinopathy is the major cause of shoulder pain in elite swimmers; (2) this tendinopathy is induced by large amounts of swimming training; and (3) shoulder laxity per se has only a minimal association with shoulder impingement in elite swimmers. These fi ndings are consistent with animal and tissue culture fi ndings which support an alternate hypothesis: the intensity and duration of load to tendon fi bres and cells cause tendinopathy, impingement and shoulder pain.

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This study has highlighted the variable response of AC in different topographical regions of meniscectomized joints to the altered mechanical stresses introduced by this surgical procedure. The AC at the joint margins, while thicker and richer in PG, was found to be biomechanically softer (lower shear modulus) than normal AC, and because of this, would be expected to undergo degenerative changes with time leading to the onset of OA.

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Application of topical nitric oxide improved early pain with activity, late functional measures, and outcomes of patients with extensor tendinosis.

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