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. 2013 Dec;22(12):1702-9.
doi: 10.1016/j.jse.2013.03.014. Epub 2013 May 8.

Evaluation of cartilage degeneration in a rat model of rotator cuff tear arthropathy

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Evaluation of cartilage degeneration in a rat model of rotator cuff tear arthropathy

Erik J Kramer et al. J Shoulder Elbow Surg. 2013 Dec.

Abstract

Background and hypothesis: Rotator cuff tears are the most common injury seen by shoulder surgeons. Glenohumeral osteoarthritis develops in many late-stage rotator cuff tear patients as a result of torn cuff tendons, termed "cuff tear arthropathy." However, the mechanisms of cuff tear arthropathy have not been fully established. It has been hypothesized that a combination of synovial and mechanical factors contribute equally to the development of cuff tear arthropathy. The goal of this study was to assess the utility of this model in investigating cuff tear arthropathy.

Materials and methods: We used a rat model that accurately reflects rotator cuff muscle degradation after massive rotator cuff tears through either infraspinatus and supraspinatus tenotomy or suprascapular nerve transection. Using a modified Mankin scoring system, we found significant glenohumeral cartilage damage after both rotator cuff tenotomy and suprascapular nerve transection after only 12 weeks.

Results: Cartilage degeneration was similar between groups and was present on both the humeral head and the glenoid. Denervation of the supraspinatus and infraspinatus muscles without opening the joint capsule caused cartilage degeneration similar to that found in the tendon transection group.

Conclusions: Our results suggest that altered mechanical loading after rotator cuff tears is the primary factor in cartilage degeneration after rotator cuff tears. Clinically, understanding the process of cartilage degeneration after rotator cuff injury will help guide treatment decisions in the setting of rotator cuff tears.

Level of evidence: Basic science study, animal model.

Keywords: Animal Model; Basic Science Study; Massive rotator cuff tear; arthropathy; articular cartilage; histology; osteoarthritis.

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Conflict of interest statement

Conflicts of Interest:

No authors have any conflicts of interest to disclose.

Figures

Figure 1
Figure 1
The humerus was divided into three discrete regions for analysis by dividing the arc of the humerus into thirds (a). An identical method was used for regional analysis of the glenoid (b). S = superior, M = middle, and I = inferior.
Figure 2
Figure 2
Coronal sections of the the glenohumeral joint at 5x. Note the structural irregularities, hypercellularity, loss of safranin-O staining, and loss of tidemark integrity in both surgical samples as compared to sham side (control).
Figure 3
Figure 3
Coronal sections of the inferior region of the humeral head at 10x. Note the structural irregularities, hypercellularity, loss of safranin-O staining, and loss of tidemark integrity in both surgical samples as compared to sham side (control). Arrows denote recessed tidemark.
Figure 4
Figure 4
Coronal sections of the inferior region of the glenoid at 10x. Note the structural irregularities, hypercellularity, loss of safranin-O staining, and loss of tidemark integrity in both surgical samples as compared to sham side (control). Arrows denote recessed tidemark.
Figure 5
Figure 5
Average total Mankin scores by cartilage type, region, and group. p-values: α1= 0.01,α2< 0.01, α3= 0.01, β1= 0.01, β2= 0.01, β3= 0.01, γ1= 0.01, γ2= 0.01, γ3= 0.01, δ1 = 0.01, δ2= 0.01, δ3 = 0.01.

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