Rotator cuff defect healing: a biomechanical and histologic analysis in an animal model.

Rotator cuff tears are one of the most common causes of pain and disability in the upper extremity. With the use of an animal model, we studied the healing response of a controlled defect in the normal supraspinatus tendon and in a tendon with a reduced intrinsic healing capacity. In 36 Sprague-Dawley rats, defects (2 mm x 2 mm) were created in the supraspinatus tendons bilaterally. To model a tendon with an intrinsically reduced capacity to heal, the tissue adjacent to the defect area in the left shoulder was treated with in situ freezing. The contralateral tendon was not frozen. After 3 (n = 12), 6 (n = 12), and 12 (n = 12) weeks, animals were killed and underwent histologic (n = 4 from each group) and biomechanical (n = 8 from each group) evaluation. An additional group of untreated animals served as a normal control group. On histologic evaluation 78% of tendons had persistent defects (defined as incomplete closure of the defect site). Over time, the tissue from both groups demonstrated an improved histologic grade but did not reach normal levels, even at 12 weeks. No histologic differences were found between defect healing in normal tendons and in those treated with in situ freezing. On biomechanical evaluation there were also no significant differences between treatment groups. Over time, an improvement occurred in tissue properties, indicating that some healing of the defects had occurred. However, these tissue properties remained an order of magnitude lower than those of normal control tendons. These findings indicate that there is an active but inadequate repair response to the defect in the rat supraspinatus tendon, which is not significantly worsened by in situ freezing of the tissue around the defect. This model has applications toward the study of techniques to improve or accelerate cuff defect healing.

Coracoacromial ligament: in situ load and viscoelastic properties in rotator cuff disease.

The coracoacromial ligament plays a role in rotator cuff disease. The changes in the in situ load and viscoelastic properties of the coracoacromial ligament in shoulders with rotator cuff tears were evaluated. Coracoacromial ligaments from 16 cadaveric shoulders (8 with rotator cuff tears, 8 without tears) were evaluated via biomechanical testing of bone ligament bone specimens. An in situ load existed in the coracoacromial ligaments of 19.6 +/- 15.4 N (rotator cuff tear) and 18.3 +/- 9.8 N (no rotator cuff tear). This difference was not statistically significant. Cyclic loading of the ligaments demonstrated a greater drop in peak stress in rotator cuff tear shoulders than in normal shoulders, whereas the stress relaxation response was not different. These changes in the coracoacromial ligament in shoulders with cuff tears may be attributable to ultrastructural changes within the ligament as a result of an altered loading environment. It remains unknown whether they occur as a result of a rotator cuff tear or if they contribute to the pathogenesis of cuff disease.

Development and use of an animal model for investigations on rotator cuff disease.

Although both intrinsic and extrinsic factors have been implicated in the cause of rotator cuff disease, previous studies have not been designed to test hypotheses of this disease, partly because of the lack of an appropriate animal model. Thirty-three animals were evaluated according to a 34 item checklist of criteria to determine their appropriateness as an animal model for investigations on the rotator cuff. Only the rat shoulder satisfactorily fulfilled all criteria, with a prominent supraspinatus tendon passing under an enclosed arch. Once the rat was identified, 36 rats were randomized to three experimental groups. One group (n = 12) was treated with an intratendinous injection of bacterial collagenase simulating an acute intrinsic injury, another group (n = 12) was treated with an acromial alteration to reduce the subacromial space simulating an external compression, and the third group (n = 12) was treated with a combination of both modifications. Significant increases in cellularity, number of fibroblasts, and collagen disorganization were seen in all experimental tendons compared with a contralateral control group. Semiquantitative grading of histologic sections revealed marked changes in all groups at 4 and 8 weeks. Injuries appeared to be healing at 12 weeks except in the combination group, which seemed to demonstrate persistent alterations. This study supports the rat as an appropriate model for investigating rotator cuff disease. In addition, this study demonstrates that both intrinsic and extrinsic alterations can induce changes in the supraspinatus tendon, which may have similarities to human tendon disease.