Metformin activates Wnt/ß-catenin for the treatment of diabetic osteoporosis.

BACKGROUND: With the deepening of social aging, the incidence rate of osteoporosis and diabetes continues to rise. More and more clinical studies show that diabetes is highly correlated with osteoporosis. Diabetes osteoporosis is considered as a metabolic bone disease of diabetes patients. This study aims to explore the role and mechanism of metformin (Met) in diabetic osteoporosis. METHODS: Mouse MC3T3-E1 cells were treated with Met (0.5 mM) and exposed to high glucose (HG, 35 mM). The cells were cultured in an osteogenic medium for osteogenic differentiation, and the cell proliferation ability was determined using Cell Counting Kit-8; Alkaline phosphatase (ALP) activity detection and alizarin red staining were utilized to evaluate the effect of Met on MC3T3-E1 osteogenic differentiation. Western blot was used to detect the expressions of osteogenesis-related proteins (Runx2 and OCN) as well as Wnt/ß-catenin signaling pathway-related proteins in MC3T3-E1 cells. RESULTS: HG inhibited proliferation and calcification of MC3T3-E1 cells, down-regulated ALP activity, and the expression of Runx2 and OCN in MC3T3-E1 cells. Meanwhile, the activity of the Wnt/ß-catenin signaling pathway was inhibited. Met treatment was found to significantly stimulate the proliferation and calcification of MC3T3-E1 cells under HG conditions, as well as increase the ALP activity and the protein expression level of Runx2 and OCN in the cells. As a result, osteogenic differentiation was promoted and osteoporosis was alleviated. Apart from this, Met also increased the protein expression level of Wnt1, ß-catenin, and C-myc to activate the Wnt/ß-catenin signaling pathway. CONCLUSION: Met can stimulate the proliferation and osteogenic differentiation of MC3T3-E1 cells under HG conditions. Met may also treat diabetic osteoporosis through Wnt/ß-catenin activation.

Comparison of D-dimer with CRP and ESR for diagnosis of periprosthetic joint infection.

BACKGROUND: Despite the availability of several biomarkers, the diagnosis of periprosthetic joint infection (PJI) continues to be challenging. Serum D-dimer assessment is a widely available test that detects fibrinolytic activities and has been reported as an inflammatory biomarker. However, quite a few articles have reported the diagnostic efficiency of D-dimer for PJI. METHODS: This prospective study enrolled patients who had undergone total joint arthroplasty, were suspected of PJI, and also prepared for revision arthroplasty. PJI was defined using the Musculoskeletal Infection Society criteria. In all patients, serum D-dimer level, erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP) level were measured preoperatively. We then compared the diagnostic efficiency of these three biomarkers. RESULTS: The median D-dimer level was significantly higher (p < 0.001) for the patients with PJI than for the patients with aseptic failure. With a sensitivity of 80.77% (95% CI, 65.62 to 95.92%) and a specificity of 79.63% (95% CI, 68.89 to 90.37%), the diagnostic efficiency of D-dimer did not outperform serum CRP (with a sensitivity of 84.61% and specificity of 64.81%) and ESR (with a sensitivity of 73.08% and specificity of 90.47%). CONCLUSIONS: Serum D-dimer as a marker for the diagnosis of PJI still requires more large-scale and detailed clinical trials.