Background: Complex regional pain syndrome (CRPS)-related hand lesions are one of the complications following arthroscopic rotator cuff repair (ARCR). This study aimed to investigate the clinical outcomes of patients with CRPS-related hand lesions following ARCR. Methods: Altogether, 103 patients with ARCR were included in this study (mean age, 63.6±8.2 years; 66 males and 37 females; follow-up period, preoperative to 12 months postoperative). Clinical assessment included the Japanese Orthopaedic Association (JOA) score, University of California, Los Angeles (UCLA) score, Constant score, 36-item short form health survey (SF-36) score, and Quick Disabilities of the Arm, Shoulder, and Hand (QuickDASH) score from preoperative to 12 months postoperatively. The patients were either assigned to the CRPS group or non-CRPS group depending on CRPS diagnosis until the final follow-up, and clinical outcomes were then compared between the groups. Results: Of 103 patients, 20 (19.4%) had CRPS-related hand lesions that developed entirely within 2 months postoperatively. Both groups showed significant improvement in JOA, UCLA, and Constant scores preoperatively to 12 months postoperatively (P<0.0001). Comparisons between the two groups were not significantly different, except for SF-36 “general health perception” (P<0.05) at 12 months postoperatively. At final follow-up, three patients had residual CRPS-related hand lesions with limited range of motion and finger edema. Conclusions CRPS-related hand lesions developed in 19.4% of patients following ARCR. Shoulder or upper-limb function improved in most cases at 12 months, with satisfactory SF-36 patient-based evaluation results. Patients with residual CRPS-related hand lesions at the last follow-up require long-term follow-up.

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.

Background: Complex regional pain syndrome (CRPS)-related hand lesions are one of the complications following arthroscopic rotator cuff repair (ARCR). This study aimed to investigate the clinical outcomes of patients with CRPS-related hand lesions following ARCR. Methods: Altogether, 103 patients with ARCR were included in this study (mean age, 63.6±8.2 years; 66 males and 37 females; follow-up period, preoperative to 12 months postoperative). Clinical assessment included the Japanese Orthopaedic Association (JOA) score, University of California, Los Angeles (UCLA) score, Constant score, 36-item short form health survey (SF-36) score, and Quick Disabilities of the Arm, Shoulder, and Hand (QuickDASH) score from preoperative to 12 months postoperatively. The patients were either assigned to the CRPS group or non-CRPS group depending on CRPS diagnosis until the final follow-up, and clinical outcomes were then compared between the groups. Results: Of 103 patients, 20 (19.4%) had CRPS-related hand lesions that developed entirely within 2 months postoperatively. Both groups showed significant improvement in JOA, UCLA, and Constant scores preoperatively to 12 months postoperatively (P<0.0001). Comparisons between the two groups were not significantly different, except for SF-36 “general health perception” (P<0.05) at 12 months postoperatively. At final follow-up, three patients had residual CRPS-related hand lesions with limited range of motion and finger edema. Conclusions CRPS-related hand lesions developed in 19.4% of patients following ARCR. Shoulder or upper-limb function improved in most cases at 12 months, with satisfactory SF-36 patient-based evaluation results. Patients with residual CRPS-related hand lesions at the last follow-up require long-term follow-up.

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.

Massive rotator cuff tears (RCTs) are complicated by muscle atrophy, fibrosis, and intramuscular fatty degeneration, which are associated with postoperative tendon-to-bone healing failure and poor clinical outcomes. We evaluated muscle and enthesis changes in large tears with or without suprascapular nerve (SN) injury in a rat model. Methods: Sixty-two adult Sprague-Dawley rats were divided into SN injury (+) and SN injury (–) groups (n=31 each), comprising tendon (supraspinatus [SSP]/infraspinatus [ISP]) and nerve resection and tendon resection only cases, respectively. Muscle weight measurement, histological evaluation, and biomechanical testing were performed 4, 8, and 12 weeks postoperatively. Ultrastructural analysis with block face imaging was performed 8 weeks postoperatively. Results: SSP/ISP muscles in the SN injury (+) group appeared atrophic, with increased fatty tissue and decreased muscle weight, compared to those in the control and SN injury (–) groups. Immunoreactivity was only positive in the SN injury (+) group. Myofibril arrangement irregularity and mitochondrial swelling severity, along with number of fatty cells, were higher in the SN injury (+) group than in the SN injury (–) group. The bone-tendon junction enthesis was firm in the SN injury (–) group; this was atrophic and thinner in the SN injury (+) group, with decreased cell density and immature fibrocartilage. Mechanically, the tendon–bone insertion was significantly weaker in the SN injury (+) group than in the control and SN injury (+) groups. Conclusions: In clinical settings, SN injury may cause severe fatty changes and inhibition of postoperative tendon healing in large RCTs. Level of evidence: Basic research, controlled laboratory study