Rotator cuff tears (RCTs) are the most common tendon injury seen in orthopedic patients. Massive RCT does not heal spontaneously and results in poor clinical outcomes. Muscle atrophy and fatty infiltration in rotator cuff muscles are major complications of chronic massive RCT and are thought to be the key factors responsible for the failure of attempted massive RCT repair. However, the pathophysiology of rotator cuff muscle atrophy and fat infiltration remains largely unknown, and no small animal model has been shown to reproduce the histologic and molecular changes seen in massive RCT. In this article, we report a novel rat massive RCT model, in which significant and consistent muscle atrophy and fat infiltration were observed in the rotator cuff muscles after rotator cuff tendon transection and denervation. The supraspinatus and infraspinatus muscle lost 25.4% and 28.9% of their wet weight 2 weeks after complete tendon transection, respectively. Six weeks after surgery, the average wet weight of supraspinatus and infraspinatus muscles decreased 13.2% and 28.3%, respectively. Significant fat infiltration was only observed in infraspinatus 6 weeks after tendon transection. Keywords: rotator cuff tear; muscular atrophy; fat infiltration Rotator cuff tears (RCTs) are one of the most common orthopedic conditions treated. Chronic RCTs lead to poor shoulder function, pain, and decreased quality of life.1 In the setting of chronic RCTs, studies have demonstrated that muscle atrophy and fatty infiltration are independent predictors of poor outcome following surgical repair.2,3 Understanding the factors that are responsible for muscle degeneration and atrophy as well as fatty infiltration may lead to pharmacologic treatments that will improve the outcomes of patients with massive RCTs.Massive RCTs, or tears that are greater than 4 cm, have been found to be associated with atrophy of the supraspinatus and infraspinatus muscle, as well as fatty infiltration of the muscle. 4 Cofield et al. 5 found that 94% of patients with a small RCT repair had a good or excellent outcome, compared to only 27% of patients with a massive RCT. Importantly, patients with large RCT with atrophy and fatty infiltration have poorer clinical outcomes than those that do not have atrophy and fatty infiltration. 4 Thus, it appears that the natural history of outcomes of large tears is due to the inelasticity and poor function of the muscle-tendon unit. Despite the importance of muscle quality and function in RCT, a majority of the studies on large and massive RCT have focused on improved repair techniques (i.e., single vs. double row repair 6,7 ) or biologic factors to improve tendon to bone healing. [8][9][10] There is no established small animal model for massive RCT. Although an acute animal model is not appropriate to test the degeneration of the tendon, it is likely appropriate to evaluate the atrophy and fatty infiltration that is seen in the setting of massive RCT. Gupta and Lee 11 have evaluated a rabbit model of RCT and demonstrat...

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Peri-tendinous injection of local anaesthetic, both alone and in combination with corticosteroids, is commonly performed in the treatment of tendinopathies. Previous studies have shown that local anaesthetics and corticosteroids are chondrotoxic, but their effect on tenocytes remains unknown. We compared the effects of lidocaine and ropivacaine, alone or combined with dexamethasone, on the viability of cultured bovine tenocytes. Tenocytes were exposed to ten different conditions: 1) normal saline; 2) 1% lidocaine; 3) 2% lidocaine; 4) 0.2% ropivacaine; 5) 0.5% ropivacaine; 6) dexamethasone (dex); 7) 1% lidocaine+dex; 8) 2% lidocaine+dex; 9) 0.2% ropivacaine+dex; and 10) 0.5% ropivacaine+dex, for 30 minutes. After a 24-hour recovery period, the viability of the tenocytes was quantified using the CellTiter-Glo viability assay and fluorescence-activated cell sorting (FACS) for live/dead cell counts. A 30-minute exposure to lidocaine alone was significantly toxic to the tenocytes in a dose-dependent manner, but a 30-minute exposure to ropivacaine or dexamethasone alone was not significantly toxic. Dexamethasone potentiated ropivacaine tenocyte toxicity at higher doses of ropivacaine, but did not potentiate lidocaine tenocyte toxicity. As seen in other cell types, lidocaine has a dose-dependent toxicity to tenocytes but ropivacaine is not significantly toxic. Although dexamethasone alone is not toxic, its combination with 0.5% ropivacaine significantly increased its toxicity to tenocytes. These findings might be relevant to clinical practice and warrant further investigation.