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Background: Bone mineral density decreases after total knee arthroplasty and is believed to affect prosthetic fixation. Treatment with alendronate has been shown to improve short-term bone mineral density after total knee arthroplasty; however, the long-term effects of this therapy are unknown. The purpose of this study was to evaluate the long-term effects of a six-month course of alendronate on bone mineral density after total knee arthroplasty., Methods: Sixty patients were randomly assigned to receive either oral alendronate at a dosage of 10 mg/day for six months or no alendronate. The bone mineral density in the distal aspect of the femur and the proximal aspect of the tibia was measured preoperatively and at six, twelve, and thirty-six months after total knee arthroplasty., Results: Fifty-four patients (twenty-nine in the alendronate group and twenty-five in the control group) completed the study. The alendronate group showed significant increases in bone mineral density in the distal aspect of the femur compared with the controls at six months (+4.8% and -14.2%, respectively; p < 0.01) and twelve months (+1.6% and -11.5%, respectively; p < 0.01). No significant difference in bone mineral density was detected between the groups at thirty-six months (-3.9% and -12.2%, respectively; p = 0.08). Similar trends in bone mineral density changes were also observed in the proximal aspect of the tibia., Conclusions: A six-month course of alendronate initially increased bone mineral density at six and twelve months after total knee arthroplasty, but no difference was noted after thirty-six months. The effect of alendronate on bone mineral density after total knee arthroplasty may be limited after discontinuation of therapy.

Background: Bone mineral density around the knee is related to the mechanical properties of bone. Alendronate has been shown to be effective for the treatment of osteoporosis and for reducing the rate of osteoporotic fractures. The purpose of the present study was to investigate the effect of alendronate on bone mineral density in the distal part of the femur and proximal part of the tibia after total knee arthroplasty in women., Methods: Ninety-six women with an average age of seventy years who were undergoing total knee arthroplasty were randomly divided into two groups. Patients in the study group received oral alendronate at a dose of 10 mg/day for six months, whereas patients in the control group did not. The bone mineral density in the distal part of the femur and proximal part of the tibia was determined preoperatively and at six and twelve months postoperatively., Results: In the control group, the bone mineral density showed significant decreases of 13.8% (p < 0.001) and 7.8% (p = 0.003) in the distal part of the femur and of 6.5% (p = 0.002) and 3.6% (p = 0.141) in the proximal part of the tibia at six and twelve months, respectively. In the study group, however, the bone mineral density showed significant increases of 10.0% (p = 0.010) and 1.9% (p = 0.049) in the distal part of the femur and of 9.4% (p < 0.001) and 5.4% (p = 0.032) in the proximal part of the tibia at six and twelve months, respectively. The overall differences in bone mineral density between the study and control groups were significant (p = 0.011 for the proximal part of the tibia, and p = 0.033 for the distal part of the femur)., Conclusions: We found significant postoperative decreases in bone mineral density in the distal part of the femur and proximal part of the tibia in women who had undergone total knee arthroplasty. Oral administration of alendronate for six months postoperatively significantly improved the bone mineral density. While the clinical benefits of alendronate after total knee arthroplasty remain unproven and the duration of follow-up in the present study was quite short, the improvement in bone mineral density may have a clinically important effect on prosthetic fixation and the rate of periprosthetic fractures after total knee arthroplasty.

Background: This study investigated the effects of extracorporeal shockwave technology (ESWT) in osteoarthritis of the knee in rats. Materials and Methods: Thirty-six Sprague-Dawley rats were randomly divided into three groups with 12 rats in each group. Group I was the control group and received neither anterior cruciate ligament transection (ACLT) nor ESWT. In groups II and III, ACLT was performed in left knee and osteoarthritis (OA) was verified at 12 wk. Group II received no ESWT, and group III received ESWT at 12 wk after ACLT. Radiographs and bone mineral density (BMD) were obtained at 0, 12, and 24 wk. The animals were sacrificed at 24 wk. One half of the animals were subjected to bone strength test, and the other half for histomorphologic examination and immunohistochemical analysis. Results: Radiographs of the left knee showed progressive OA changes at 12 and 24 wk in group II, whereas, very subtle OA changes were noted in group I and group III. BMD and bone strength were significantly lower in group II compared with groups I and III, but no difference was noted between group I and group III. The cartilage degradations were significantly higher in group II compared with groups I and III, but no difference was noted between group I and group III. The subchondral bone remodeling was significantly less pronounced in group II compared with groups I and III, but no difference was noted between group I and group III. Conclusions: Application of ESWT to the subchondral bone of the medial tibia condyle showed regression of osteoarthritis of the knees in rats. [ABSTRACT FROM AUTHOR]

Abstract: Aims: Long-term glucocorticoid administration is known to induce bone deterioration. Glycogen synthase kinase-3β (GSK-3β) signaling reportedly participates in bone remodeling. This study investigated whether GSK-3β inhibitor could regulate glucocorticoid-induced inhibition of osteoblast differentiation in vitro or bone mass in vivo. Main methods: MC3T3-E1 osteoblasts were treated with kinase-inactive GSK-3β mutant and 6-bromoindirubin-3′-oxim (BIO) and then exposed to 1µM dexamethasone. Survival and osteoblast differentiation of cell cultures were assessed by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end-labeling, quantitative RT-PCR, and von Kossa staining. Mineral density, biomechanical properties and microenvironments of BIO- and glucocorticoid-treated rat bone tissues were analyzed using dual-energy X-ray absorptiometry, material testing, and histomorphometry, respectively. Key findings: Glucocorticoid decreased levels of phosphorylated Ser9-GSK-3β and β-catenin in osteoblast cultures. Kinase-inactive GSK-3β mutant and BIO treatments attenuated dexamethasone-induced inhibition of β-catenin, Runx2 abundance, and osteoblast differentiation but suppressed glucocorticoid-induced apoptosis of cell cultures. Exogenous BIO treatment alleviated methylprednisolone-induced impairment of mineral density, biomechanical strength, trabecular bone volume, osteoblast surface, and bone formation rate of rat bone tissue. BIO treatment also attenuated glucocorticoid-induced promotion of osteoclast surface and marrow adipocyte volume in bone tissue. Bone cells adjacent to glucocorticoid-stressed bone tissue displayed strong phosphorylated Ser9-GSK-3β and β-catenin immunostaining following BIO treatment. Significance: Inhibition of GSK-3β abrogated glucocorticoid-induced bone loss by increasing β-catenin- and Runx2-mediated osteoblast differentiation. Controlling GSK-3β signaling in bone cells may be a strategy for preventing glucocorticoid-induced osteopenia. [Copyright &y& Elsevier]