Factors Expressed in an Animal Model of Anteroinferior Glenohumeral Instability.

2015 
Shoulder dislocation is a common injury and most often occurs in the anteroinferior direction. During injury, the displaced humeral head stretches the capsuloligamentous structures, causing capsular tear4,28,35 and/or labral avulsion.5,6,11,17,18,25,35,36 Anteroinferior labral lesions often require surgical fixation due to persistent anterior glenohumeral instability.3,13,19,26 Despite the common nature of acute anterior glenohumeral dislocation, there is little information on the biologic and biochemical factors that are important in healing of the glenoid labrum. Bankart was the first to characterize the anatomic pathology of shoulder instability, calling the anteroinferior labral tear “the essential defect” in shoulder instability.16 The glenoid labrum is composed of fibrocartilaginous tissue at the junction of the capsule of the shoulder and the glenoid.27 Because of the absence of information available on glenoid labral healing, most information must be extrapolated from our knowledge of the knee meniscus. The glenoid labrum is similar to the meniscus in the knee in that only the peripheral margin has a significant vascular supply.1,10 The inner, avascular third of the meniscus has limited healing capacity while the outer two-thirds may heal by scar formation.2 Soluble mediators (eg, growth factors and cytokines) or physical factors (eg, mechanical compression or stretch) can have a significant influence on the metabolic activity of meniscal cells.15 Some of the important factors in meniscal healing include transforming growth factor–beta (TGF-β) and interleukin-1 (IL-1). Transforming growth factor–β1 (TGF-β1) stimulates mesenchymal cells to produce specific proteoglycans and type II collagen.34 The expression of proinflammatory cytokines such as IL-1 is known to be elevated in the presence of joint injury in the knee.14,21,37 This study was designed to develop an animal model of glenohumeral instability and to determine the immunohistochemical and mechanical changes that occur in the labrum in response to injury. Unlike the meniscus, there is currently no reliable animal model for glenoid labral injuries, and little is known about its capacity for healing. Soslowsky et al33 demonstrated that the bony, ligamentous, and muscular anatomy of the rat shoulder resembles that of the human, making it a good model to study shoulder pathology.8,30 These protocols are well established and applicable to the experimental design of this study as well.12,33 Based on studies of proinflammatory cytokines and growth factors in the meniscus, we hypothesized that, similarly, IL-1β, matrix metalloproteinases 3 and 13 (MMP3 and MMP13), TGF-β1, and collagen type III will be induced in the healing glenoid labrum and capsule in response to injury. This study also performed biomechanical testing to verify the ability of the model to create glenohumeral instability and to correlate the changes in growth factors and cytokines with biomechanical changes that occur.
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