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Pigmented villonodular synovitis (PVNS) is a rare proliferative process of the synovium which most commonly affects the knee and occurs in either a localised (LPVNS) or a diffuse form (DPVNS). The effect of different methods of surgical synovectomy and adjuvant radiotherapy on the rate of recurrence is unclear. We conducted a systematic review and identified 35 observational studies in English which reported the use of surgical synovectomy to treat PVNS of the knee. A meta-analysis included 630 patients, 137 (21.8%) of whom had a recurrence after synovectomy. For patients with DPVNS, low-quality evidence found that the rate of recurrence was reduced by both open synovectomy (odds ration (OR) = 0.47; 95% CI 0.25 to 0.90; p = 0.024) and combined open and arthroscopic synovectomy (OR = 0.19, 95% CI = 0.06 to 0.58; p = 0.003) compared with arthroscopic surgery. Very low-quality evidence found that the rate of recurrence of DPVNS was reduced by peri-operative radiotherapy (OR = 0.31, 95% CI 0.14 to 0.70; p = 0.01). Very low-quality evidence suggested that the rate of recurrence of LPVNS was not related to the surgical approach. This meta-analysis suggests that open synovectomy or synovectomy combined with peri-operative radiotherapy for DPVNS is associated with a reduced rate of recurrence. Large long-term prospective multicentre observational studies, with a focus on both rate of recurrence and function, are required to confirm these findings.

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PURPOSE: To provide a comprehensive overview of the basic science and clinical evidence behind cartilage regeneration techniques as they relate to surgical management of chondral lesions in humans. METHODS: A descriptive review of current literature. RESULTS: Articular cartilage defects are common in orthopedic practice, with current treatments yielding acceptable short-term but inconsistent long-term results. Tissue engineering techniques are being employed with aims of repopulating a cartilage defect with hyaline cartilage containing living chondrocytes with hopes of improving clinical outcomes. Cartilage tissue engineering broadly involves the use of three components: cell source, biomaterial/membranes, and/or growth stimulators, either alone or in any combination. Tissue engineering principles are currently being applied to clinical medicine in the form of autologous chondrocyte implantation (ACI) or similar techniques. Despite refinements in technique, current literature fails to support a clinical benefit of ACI over older techniques such as microfracture except perhaps for larger (>4 cm) lesions. Modern ACI techniques may be associated with lower operative revision rates. The notion that ACI-like procedures produce hyaline-like cartilage in humans remains unsupported by high-quality clinical research. CONCLUSIONS: Many of the advancements in tissue engineering have yet to be applied in a clinical setting. While basic science has refined orthopedic management of chondral lesions, available evidence does not conclude the superiority of modern tissue engineering methods over other techniques in improving clinical symptoms or restoring native joint mechanics. It is hoped further research will optimize ease of cell harvest and growth, enhanced cartilage production, and improve cost-effectiveness of medical intervention.

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Purpose of this study is to conduct a meta-analysis comparing the results of open and arthroscopic Bankart repair using suture anchors in recurrent traumatic anterior shoulder instability. Using Medline Pubmed, Cochrane and Embase databases we performed a search of all published articles. We included only studies that compared open and arthroscopic repair using suture anchors. Statistical analysis was performed using chi-square test. Six studies met the inclusion criteria. The total number of patients was 501, 234 suture anchors and 267 open. The rate of recurrent instability in the arthroscopic group was 6% versus 6.7% in the open group; rate of reoperation was 4.7% in the arthroscopic group vs. 6.6% in open (difference not statistically significant). The difference was statistically significant only in the studies after 2002 (2.9% of recurrence in the arthroscopic group vs. 9.2% in open; 2.2% of reoperation in the arthroscopic group vs. 9.2% in open). Results regarding function couldn't be combined because of non-homogeneous scores reported in the original articles, but the arthroscopic treatment led to better functional results. Arthroscopic repair using suture anchors results in similar redislocation and reoperation rate compared to open Bankart repair; however, we need larger and more homogeneous prospective studies to confirm these findings.

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OBJECTIVE: The pathophysiology of non-traumatic osteonecrosis (ON) or avascular necrosis (AVN) of the femoral head remains poorly understood. Some studies have suggested the contribution of underlying thrombophilia as a mechanism; however, no specific thrombophilic factor has been consistently found in association with the disease. We are presenting data suggesting a role for endothelial cell activation rather than thrombophilia in ON. METHODS: A prospective consecutive cohort of 49 patients with a diagnosis of ON. The disease was considered idiopathic in five and secondary in 44 patients. The investigation included a coagulation and thrombophilia profile, endothelial cell activation and non-specific inflammatory markers as well as a biochemical profile. Statistical analysis using Fisher's exact test was obtained to assess correlation between endothelial cell markers and variables of inflammation. RESULTS: Patients with non-traumatic ON were not found to have a specific underlying thrombophilic factor compared with the general population. Out of 49 patients,19 had elevation of at least one endothelial cell markers. We found that activation of endothelial cell markers was independently correlated to ON but not correlated to the presence of inflammation (P = 1.0000). CONCLUSION: These results suggest that non-traumatic ON is not associated with a specific thrombophilic abnormality in those affected. This study demonstrates a potential association between regional endothelial dysfunction and ON. More studies are needed at a molecular level to further investigate the specific role of endothelium in the physiopathology of ON. A better understanding of the underlying mechanism could lead to potential preventive and therapeutic strategies of this devastating disease.

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