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HomeIntroductionProgression of cuff failureTypical progressionConclusion

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Rotator Cuff Failure.

Last updated Tuesday, January 25, 2005

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Figure 4 - Major episodes of tendon tearing
Figure 4 - Major episodes of tendon tearing

Figure 5 - Creeping tears
Figure 5 - Creeping tears

Figure 6 - Degenerative lesions of the cuff generally start at the deep surface of the anterior insertion of the supraspinatus near the long head of the biceps
Figure 6 - Degenerative lesions of the cuff generally start at the deep surface of the anterior insertion of the supraspinatus near the long head of the biceps

Figure 7 - Limitation of tendon blood flow
Figure 7 - Limitation of tendon blood flow

Figure 8 - Articular and bursal sides
Figure 8 - Articular and bursal sides

Figure 9 - Full thickness defect
Figure 9 - Full thickness defect

Figure 10 - Additional fiber failure
Figure 10 - Additional fiber failure

Figure 11 - Infraspinatus and teres minor
Figure 11 - Infraspinatus and teres minor

Figure 12 - Destabilization of the long head tendon of the biceps
Figure 12 - Destabilization of the long head tendon of the biceps

Progression of cuff failure

Cuff failure may progress as major episodes of tendon tearing or as creeping tears involving relatively few fibers at a time with thinning of the cuff tendon.

Typical progression

Degenerative lesions of the cuff typically start at the deep surface of the anterior insertion of the supraspinatus near the long head of the biceps. Once these lesions begin, it is difficult for them to heal, because of the hostile environment, the compromised vascularity, the large loads, and the large deformations that the healing tissue must endure. Failure of one fiber or of groups of fibers places greater loads on the adjacent fibers, favoring their failure (the "zipper" phenomenon). When a tendon fiber fails, the muscle fiber to which it attaches produces retraction away from the site of disruption, increasing the gap needing to be closed. This retraction also places tension on the local vasculature leading to limitation of tendon blood flow in the area where healing is needed.

Rotator cuff tendon defects are subject to the effects of synovial fluid on both their articular and bursal sides; the fluid and its enzymes may remove the fibrin clot necessary for healing of the cuff lesion. In the absence of repair, the degenerative process tends to continue through the substance of the supraspinatus tendon to produce a full thickness defect in the anterior supraspinatus tendon. This full thickness defect tends to concentrate loads at its margin, facilitating additional fiber failure with smaller loads than those which produced the initial defect.

Once a supraspinatus defect is established, it typically propagates posteriorly through the remainder of the supraspinatus, then into the infraspinatus and teres minor. Further propagation of the cuff defect crosses the bicipital groove to involve the subscapularis, starting at the top of the lesser tuberosity and extending inferiorly. As the defect extends across the bicipital groove, it may be associated with rupture of the transverse humeral ligament and destabilization of the long head tendon of the biceps.


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