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There has been no consensus about how to determine the individual posterior tibial slope (PTS) intraoperatively. The purpose of this study was to investigate whether the tibial plateau could be used as a reference for reproducing individual PTS during medial unicompartmental knee arthroplasty (UKA). Preoperative computed tomography (CT) data from 48 lower limbs for medial UKA were imported into a three-dimensional planning software. Digitally reconstructed radiographs were created from the CT data as the lateral knee plain radiographs and the radiographic PTS angle was measured. Then, the PTS angles on the medial one-quarter and the center of the MTP (¼ and ½ MTP, respectively), and that on the medial tibial eminence (TE) were measured on the sagittal multiplanar reconstruction image. Finally, 20 lateral knee radiographs with an arthroscopic probe placed on the ¼ and the ½ MTP were obtained intraoperatively, and the angle between the axis of the probe and the tangent line of the plateau was measured. The mean radiographic PTS angle was 7.9 ± 3.0 degrees (range: 1.7–13.6 degrees). The mean PTS angles on the ¼ MTP, the ½ MTP, and the TE were 8.1 ± 3.0 degrees (1.2–13.4 degrees), 9.1 ± 3.0 degrees (1.4–14.7 degrees), and 9.9 ± 3.1 degrees (3.1–15.7 degrees), respectively. The PTS angles on the ¼ MTP and the ½ MTP were strongly correlated with the radiographic PTS angle (r =0.87 and 0.80, respectively, p

Introduction Nontuberculous mycobacterial (NTM) infections of the musculoskeletal system are uncommon. Such infections are typically acquired by direct inoculation after penetrating trauma, surgical procedures, or needle injections. There are no reported cases of NTM infection after arthrocentesis for idiopathic hemarthrosis of the knee. Here we report a case of NTM infection in the knee that developed after arthrocentesis for idiopathic hemarthrosis of the knee. Presentation of case The patient was an 85-year-old woman who experienced swelling of the left knee. An arthrocentesis was carried out, and hemarthrosis was found. The patient was referred to our hospital for repeated recurrence of hematoma of the knee. Significant swelling was observed in the suprapatellar sac. Magnetic resonance imaging examination revealed a mass at the suprapatellar sac. Laboratory data showed elevation of inflammatory markers. Debridement was performed under arthroscopy and samples were collected for culture. Although routine microbiological cultures were negative, the patient continued to experience knee swelling and laboratory data showed high C-reactive protein levels. Therefore, open debridement was carried out. At 4 weeks after the first surgical treatment, intraoperative cultures yielded Mycobacterium intracellulare. At this point, we diagnosed septic arthritis of the knee due to NTM infection. The patient showed an excellent prognosis with three-drug medical treatment for 1 year. Conclusion Clinically, diagnosis of septic arthritis due to NTM infection is not easy. Because selection of examination depends on clinical suspicion, NTM infections should be considered for patients with elevation of inflammatory markers after episodes of surgical procedures, and/or needle injections.

Sarcopenia is an aging-associated attenuation of muscular volume and strength and is the major cause of frailty and falls in elderly individuals. The number of individuals with sarcopenia is rapidly increasing worldwide; however, little is known about the underlying mechanisms of the disease. Sarcopenia often copresents with obesity, and some patients with sarcopenia exhibit accumulation of peri-organ or intra-organ adipose tissue as ectopic fat deposition, including atrophied skeletal muscle. In this study, we showed that transplantation of the perimuscular adipose tissue (PMAT) to the hindlimb thigh muscles of young mice decreased the number of integrin α7/CD29-double positive muscular stem/progenitor cells and that the reaction was mediated by PMAT-derived exosomes. We also found that the inhibition of cell proliferation was induced by Let-7d-3p miRNA that targets HMGA2, which is an important transcription factor for stem cell self-renewal, in muscular stem/progenitor cells and the composite molecular reaction in aged adipocytes. Reduction of Let-7 miRNA repressor Lin28 A/B and activation of nuclear factor-kappa B signaling can lead to the accumulation of Let-7d-3p in the exosomes of aged PMAT. These findings suggest a novel crosstalk between adipose tissue and skeletal muscle in the development of aging-associated muscular atrophy and indicate that adipose tissue-derived miRNAs may play a key role in sarcopenia.

Objectives: Interleukin (IL)-1β and matrix metalloproteinases (MMPs) play important roles in the pathogenesis of osteoarthritis. On the other hand, plasminogen activator inhibitor-1 (PAI-1), an inhibitor of fibrinolysis, exerts functions in the pathogenesis of various diseases. However, the functional roles of PAI-1 in the chondrocytes have been still remained unknown.Methods: In the present study, we investigated the roles of PAI-1 in the effects of IL-1β on the chondrocytes using wild-type and PAI-1-deficient mice.Results: IL-1β significantly elevated PAI-1 mRNA levels in the chondrocytes from wild-type mice. PAI-1 deficiency significantly blunted the mRNA levels of TGF-β and IL-6 enhanced by IL-1β in murine chondrocytes. Moreover, PAI-1 deficiency significantly decreased the mRNA levels of MMP-13, -3 and -9 as well as MMP-13 activity enhanced by IL-1β in the chondrocytes. In addition, PAI-1 deficiency significantly reversed type II collagen mRNA levels suppressed by IL-1β in the chondrocytes. On the other hand, active PAI-1 treatment significantly enhanced the mRNA levels of MMP-13, -3 and -9 as well as decreased type II collagen mRNA levels in the chondrocytes from wild-type mice.Conclusion: We first demonstrated that PAI-1 is involved in MMP expression enhanced by IL-1β in murine chondrocytes. PAI-1 might be crucial for the cartilage matrix degradation and the impaired chondrogenesis by IL-1β in mice.

Mechanical unloading induces disuse muscle atrophy and bone loss, but the details in mechanism involved in those pathophysiological conditions are not fully understood. Interaction between muscle and bone has been recently noted. Here, we investigated the roles of humoral factors linking muscle to bone during mechanical unloading using mice with hindlimb unloading (HU) and sciatic neurectomy (SNX). HU and SNX reduced muscle volume surrounding the tibia, tissue weights of soleus and gastrocnemius muscle, and trabecular bone mineral density (BMD) in the tibia of mice. Among humoral factors linking muscle to bone, HU and SNX reduced fibronectin type III domain-containing 5 (FNDC5) mRNA levels in the soleus muscle of mice. Simple regression analysis revealed that FNDC5 mRNA levels in the soleus muscle were positively related to trabecular BMD in the tibia of control and HU mice as well as sham and SNX mice. Moreover, FNDC5 mRNA levels were negatively correlated with receptor activator of nuclear factor-κB ligand (RANKL) mRNA levels in the tibia of control and HU mice. Irisin, a product of FNDC5, suppressed osteoclast formation from mouse bone marrow cells and RANKL mRNA levels in primary osteoblasts. FNDC5 mRNA levels elevated by fluid shear stress were antagonized by bone morphogenetic protein (BMP) and phosphatidylinositol 3-kinase (PI3K) signaling inhibitors in myoblastic C2C12 cells. In conclusion, the present study first showed that mechanical unloading reduces irisin expression in the skeletal muscle of mice presumably through BMP and PI3K pathways. Irisin might be involved in muscle/bone relationships regulated by mechanical stress in mice.

Background Subchondral osteopenia is important for the pathophysiology of osteoarthritis (OA). Although previous studies suggest that plasminogen activator inhibitor-1 (PAI-1), an inhibitor of fibrinolysis, is related to bone metabolism, its role in OA remains unknown. We therefore investigated the roles of PAI-1 in the subchondral bone in OA model mice. Methods Wild type (WT) and PAI-1-deficient (KO) mice were ovariectomized (OVX), and then destabilization of the medial meniscus (DMM) surgery was performed. Results DMM and OVX significantly decreased the trabecular bone mineral density of the subchondral bone evaluated by quantitative computed tomography in PAI-1 KO mice. The effects of OVX and/or PAI-1 deficiency on the OARSI score for the evaluation of the progression of knee degeneration were not significant. PAI-1 deficiency significantly augmented receptor activator nuclear factor κB ligand mRNA levels enhanced by IL-1β in mouse primary osteoblasts, although it did not affect osteoblast differentiation. Moreover, PAI-1 deficiency significantly increased osteoclast formation from mouse bone marrow cells. Conclusion We showed that PAI-1 deficiency accelerates the subchondral osteopenia after induction of OA in mice. PAI-1 might suppress an enhancement of bone resorption and subsequent subchondral osteopenia after induction of OA in mice.