[Arthroscopic treatment of eldly with massive rotator cuff tear].

Objective: To investigate the surgical technique and clinical efficacy of arthroscopic treatment of the elderly patients with massive rotator cuff tear. Methods: From June 2012 to June 2015, thirty-six patients with massive rotator cuff tear were treated with arthroscopic and followed up. The visual analog scale(VAS)pain score, University of California Los Angeles (UCLA) scores, Constant scores and American Shoulder and Elbow Surgeons scale(ASES)were used before and after the arthroscopic surgery. Results: All the patients were followed up for average of 18.5 (12 to 30) months.Before arthroscopic surgery, the VAS, UCLA, Constant, ASES were (6.1±2.2), (10.6±4.3), (40.3±10.5) and (28.8±18.5) points; the average flexion of the shoulder was (76.5±42.6)°, the average abduction of the shoulder was (72.4±35.2)°, the average external rotation of the shoulder was(26.6±22.2)° and the average internal rotation of the shoulder was (20.2±6.2)° respectively.These scores were improved to (1.4±1.2), (30.4±5.2), (82.6±12.6), and (78.8±22.6) points, the average flexion of the shoulder was improved to (152.8±25.6)°, the average abduction of the shoulder was improved to (120.6±32.8)°, the average external rotation of the shoulder was improved to (42.6±16.2)° and the average internal rotation of the shoulder was improved to (38.4±5.6)° after one-year follow-up period.Improvement in these scores and range of motion(ROM) were significant difference(P<0.05). Conclusion: Arthroscopic repair can effectively treat the eldly patient with massive rotator cuff tear and obviously improve the function of shoulder joint. The surgery has a clinical application value.

Protection against titanium particle-induced osteoclastogenesis by cyclooxygenase-2 selective inhibitor.

Wear particle-induced osteoclastogenesis is the most common cause of aseptic loosening in total joint arthroplasty. Although cyclooxygenase (COX)-2, an inducible regulator of prostaglandin E2 (PGE2) synthesis, is known to be involved in osteoclast differentiation, its effect on osteoclastogenesis in response to wear particles remains unclear. In this study, we investigated the role of COX-2 in the regulation of osteoclast differentiation in the osteoclast precursor cell line RAW264.7 stimulated with titanium (Ti) particles. The results showed COX-2 expression in the early stages of RAW264.7 differentiation when stimulated with receptor activator of nuclear factor kappa B ligand (RANKL) and Ti particles. Blockade of COX-2 by celecoxib, a COX-2 selective inhibitor, effectively reduced the expression of PGE2 and inhibited differentiation of RAW264.7 cells into tartrate-resistant acid phosphatase-positive (TRAP+) osteoclastic cells. Quantitative real-time polymerase chain reaction revealed that celecoxib inhibited mRNA expression of RANK, cathepsin K (CPK), TRAP, and the nuclear factor of activated T cells c1 (NFATc1) in RAW264.7 cells stimulated by Ti particles and RANKL. Moreover, exogenous PGE2 reversed the inhibitory effects of celecoxib. These results provide direct evidence that COX-2 dependent PGE2 induced by RANKL and Ti particles is required for osteoclastogenesis and suggests that reduced production of PGE2 by inactivation of COX-2 would provide a promising therapeutic target for the treatment of osteoclastogenesis induced by wear particles.

A novel sheep vertebral bone defect model for injectable bioactive vertebral augmentation materials.

New injectable bone substitutes have been developed that are, unlike polymethylmethacrylate, biologically active and have an osteogenic effect leading to osteogenesis and bone remodeling for vertebroplasty or kyphoplasty. In this study, we developed a sheep vertebral bone defect model to evaluate the new bioactive materials and assessed the feasibility of the model in vivo. Bone voids were experimentally created on lumbar vertebrae L2-L5 with L1 and L6 left intact as a normal control in mature sheep. The defect vertebrae L2-L5 in each sheep were randomized to receive augmentation with calcium phosphate cement (CPC) or sham. Vertebrae (L1-L6) were collected after 2 and 24 weeks of the cement augmentation and their strength and stiffness, as well as osseointegration activity and biodegradability, were evaluated. Finally, CPC significantly improved the strength and stiffness of vertebrae but did not yet restore it to the normal level at 24 weeks. Osteogenesis occurred at a substantially high level after 24 weeks of CPC augmentation or sham. Therefore, the sheep vertebral model with one void, 6.0 mm in diameter and 15.0 mm in depth, is replicable and can be used for evaluating the new injectable bioactive materials in vertebral augmentation or reconstruction.

A comparison of the proximal femoral nail antirotation device and dynamic hip screw in the treatment of unstable pertrochanteric fracture.

This prospective randomized study compared the outcome of elderly patients with an unstable pertrochanteric fracture, treated with a proximal femoral nail antirotation device (PFNA; n = 51) or a dynamic hip screw (DHS; n = 55). All patients in the DHS group and nine in the PFNA group had open reductions. Incisions were significantly shorter for the PFNA than the DHS group. Blood loss and the number of patients requiring post-operative blood transfusions were significantly greater, but operation and fluoroscopy times were significantly shorter, for the DHS versus the PFNA group. Time to mobilization with a frame was significantly shorter in the PFNA group, and post-operative complications were more common in the DHS group. Poor fracture reduction led to three revisions. All fractures in both groups united during follow-up. The PFNA allowed earlier mobilization and faster recovery than the DHS. The PFNA is a highly acceptable, minimally invasive implant for unstable fractures.

Inhibition of titanium particle-induced inflammatory osteolysis through inactivation of cannabinoid receptor 2 by AM630.

Wear particle could induce inflammatory osteolysis and is the primary pathological factor for aseptic loosening. Although it is known that cannabinoid receptor 2 (CB2) inhibits osteoclast differentiation, the effect on inflammatory osteolysis induced by wear particles remains unclear. This study examined the effect of CB2 in the regulation of osteoclast differentiation in a murine macrophage cell line (RAW264.7), which has been shown to be stimulated by titanium (Ti) particles and receptor activator of the NF-kappaB ligand (RANKL). Results showed that CB2 expression in RAW cells cultured with Ti particles and RANKL. CB2 inactivation by AM630, a CB2 selective antagonist, effectively inhibited osteoclastogenesis in the differentiation medium system. AM630 treatment (> or =100 nM) significantly reduced the number of tartrate-resistant acid phosphatase-positive cells when compared with the control. Real-time reverse transcription polymerase chain reaction analysis revealed that AM630 (100 nM) inhibited mRNA expression of RANK and cathepsin K in RAW cells stimulated by Ti particles and RANKL. Moreover, enzyme-linked immunosorbent assay showed that AM630 (100 nM) reduced protein expression of interleukin-1beta and tumor necrosis factor-alpha in RAW cells cultured with Ti particles. In addition, 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazoliumbromide revealed that AM630 had no toxic effect on RAW cells. These results suggested that CB2 inactivation by AM630 could provide a promising therapeutic target for treating or preventing aseptic loosening.