ABSTRACT
In some patients with rotator cuff tear (RCT), the axial view of magnetic resonance imaging (MRI) shows subtle posterior decentering (PD) of the humeral head from the glenoid fossa. This is considered to result from a loss of centralization that is typically produced by rotator cuff function. There are few reports on PD in RCT despite the common occurrence of posterior subluxation in degenerative joint disease. In this study, we investigated the effect of PD in arthroscopic rotator cuff repair (ARCR). Methods: We conducted a retrospective study of consecutive patients who underwent ARCR at our institute and were followed-up for at least 1 year. PD was identified as a 2-mm posterior shift of the humeral head relative to the glenoid fossa in the axial MRI view preoperatively. The tear size and fatty degeneration (FD, Goutallier classification) were also evaluated using preoperative MRI. Retears were evaluated through MRI at 1 year postoperatively. Results: We included 135 shoulders in this study. Ten instances of PD (including seven retears) were observed preoperatively. Fifteen retears (three and 12 retears in the small/medium and large/massive tear groups, respectively) were observed postoperatively. PD was significantly correlated with tear size, FD, and retear occurrence (p<0.01 each). The odds ratio for PD in retears was 34.1, which was greater than that for tear size ≥3 cm and FD grade ≥3. Conclusions: We concluded that large tear size and FD contribute to the occurrence of PD. Furthermore, PD could be a predictor of retear after ARCR.
ABSTRACT
Local anesthetics often are used in rotator cuff tears as therapeutic tools, although some cases have reported that they have detrimental effects. Neurotropin (NTP) is used widely in Japan as a treatment for various chronic pain conditions and is shown to have protective effects on cartilage and nerve cells. In this study, we investigated the protective effect of NTP against lidocaine-induced cytotoxicity. Methods: Tenocytes from rotator cuff tendons were incubated with lidocaine, NTP, lidocaine with NTP, and a control medium. Cell viability was evaluated using the WST-8 assay. Cell apoptosis was detected via annexin V staining using flow cytometry. The expression of BCL-2 and cytochrome c, which are involved in the intrinsic mitochondrial pathway of apoptosis, was evaluated via Western blotting and immunohistochemical staining. Results: In the cell viability assay, lidocaine decreased cell viability in a dose-dependent manner, and NTP did not affect cell viability. Moreover, NTP significantly inhibited the cytotoxic effect of lidocaine. The flow cytometry analysis showed that lidocaine significantly induced apoptosis in tenocytes, and NTP considerably inhibited this lidocaine-induced apoptosis. Western blotting experiments showed that lidocaine decreased the protein expression of BCL-2, and that NTP conserved the expression of BCL-2, even when used with lidocaine. Immunohistochemical staining for cytochrome c showed that 0.1% lidocaine increased cytochrome c-positive cells, and NTP suppressed lidocaine-induced cytochrome c expression. Conclusions: NTP suppresses lidocaine-induced apoptosis of tenocytes by inhibiting the mitochondrial apoptotic pathway. Intra-articular/ bursal injection of NTP with lidocaine could protect tenocytes in rotator cuff tendons against lidocaine-induced apoptosis.