Objective. The aim of this study was to compare the functional outcome and complications in midshaft clavicle fractures receiving minimally invasive plate osteosynthesis and conventional open plating. Methods. Relevant studies were searched in the databases of Medline, EMBASE, Cochrane Library, Ovid, and Web of Science from inception to March 1, 2019. Pooled data were analyzed with Cochrane Collaboration’s Review Manager 5.3. Results. A total of 7 studies were included, of which 2 were randomized controlled trials, 3 were retrospective cohort studies, and 2 were prospective cohort studies including 316 patients. No statistical differences in functional outcome (weighted mean difference [WMD] = 0.99, P=0.12), operation time (WMD = −10.44, P=0.07) and time to bone union (WMD = −0.23, P=0.70) were observed between the two groups. However, minimally invasive plate osteosynthesis reduced rates of skin numbness (odds ratio (OR) = 0.25, 95% CI : 0.13 to 0.48; P<0.0001) and complications (OR = 0.33, 95% CI : 0.16 to 0.71; P=0.005) compared with conventional open plating. Conclusion. This systematic review and meta-analysis found no differences in terms of functional outcomes, operation time, and fracture healing time between minimally invasive plate osteosynthesis and conventional open plating. However, minimally invasive plate osteosynthesis had apparent advantages in rates of skin numbness and complications.

Simvastatin is effective in the treatment of osteoporosis, partly through the inhibition of the adipogenesis of bone-marrow derived mesenchymal stem cells (BMScs). The present study focused on the mechanisms responsible for the inhibitory effects of simvastatin on adipogenesis and examined the effects of simvastatin on the expression of peroxisome proliferator-activated receptor γ (PPARγ), chemerin, chemokine-like receptor 1 (cMKLR1), G protein-coupled receptor 1 (GPR1) and the adipocyte marker gene, adiponectin. BMScs were isolated from 4-week-old female Sprague-dawley (Sd) rats, and adipogenesis was measured by the absorbance values at 490 nm of Oil Red O dye. The expression of each gene was evaluated by western blot analysis or reverse transcription-quantitative PcR (RT-qPcR). The expression of chemerin increased during adipogenesis, while cMKLR1 exhibited a trend towards a decreased expression. On days 7 and 14, the simvastatin-treated cells exhibited a downregulated expression of chemerin, whereas the upregulated expression of its receptor, cMKLR1 was observed. The results also revealed that cMKLR1 is required for adipogenesis and the simvastatin-mediated inhibitory effect on adipogenesis. Simvastatin regulated adipogenesis by negatively modulating chemerin-cMKLR1 signaling. Importantly, simvastatin stimulation inhibited the upregulation of PPARγ and PPARγ-mediated chemerin expression to prevent adipogenesis. Treatment with the PPARγ agonist, rosiglitazone, partially reversed the negative regulatory effects of simvastatin. On the whole, the findings of the present study demonstrate that simvastatin inhibits the adipogenesis of BMScs through the downregulation of PPARγ and subsequently prevents the PPARγ-mediated induction of chemerin/cMKLR1 signaling.

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