Y magnetic resonance imaging (MRI) of the knee. Methods: This was a retrospective study of 125 patients undergoing primary ACL reconstruction between July 2013 and May 2017. Another 125 patients without any organic knee joint injury were served as controls. The shape of intercondylar notch, the intercondylar notch width index, the intercondylar notch height index, the α angle, the β angle, and the medial and lateral tibial plateau slope were measured with MRI and compared. The data were compared by binary logistic regression to find the risk factors. Results: The two groups differed in the proportion of male patients (70.4% vs. 52.0%, χ2 = 8.911, P = 0.003), but gender was excluded as a risk factor for ACL injury with regression analysis (odds ratio = 1.476, 95% confidence interval [CI]: 0.689–3.160, P = 0.317). The injured group was found to have a smaller notch width index (95% CI = 7.960E-23–2.154E-9, P < 0.001), a larger β angle (95% CI = 1.311–1.785, P < 0.001), and a larger lateral tibial plateau slope (95% CI = 1.201–1.683, P < 0.001). The cutoff values of notch width index, β angle, and the lateral tibial plateau slope were 0.252, 38.5°, and 7.5°, respectively. Conclusions: In this study, a narrow intercondylar notch (intercondylar notch width index 7.5°), and larger β angle (>38.5°) might be the factors associated with ACL injury. Trial Registration: ChiCTR-RRC-17014116; http://www.chictr.org.cn/showproj.aspx?proj=24119 ....

Osteoarthritis (OA), the most common form of human joint disease, is characterized by progressive degeneration of the articular cartilage, synovitis and subchondral osteoporosis. Chondrocyte apoptosis is the primary pathogenic mechanism of OA and is considered to be a potential therapeutic target. Sulforaphane (SFN), a dietary isothiocyanate obtained from cruciferous vegetables, has been reported to exert an anti‑apoptotic effect by activating sirtuin 1 (SIRT1). To the best of our knowledge, however, the effects of SFN on apoptotic responses in OA have not been reported. In the present study, SFN was shown to significantly inhibit chondrocyte apoptosis while enhancing expression levels of SIRT1 in a H₂O₂‑induced OA mouse model. The anti‑apoptotic effect of SFN was reversed by SIRT1 small interfering RNA, implying that SIRT1 exerted a protective role against the effect of SFN on chondrocytes. The expression levels of C/EBP homologous protein, 78‑kDa glucose regulated protein, Bax, Bcl‑2 and cleaved caspase 3 were found to be downregulated in SFN‑treated mice. Furthermore, SFN ameliorated cartilage degradation in the OA mouse model. These findings indicate that SFN exerted an anti‑apoptotic effect on chondrocytes and ameliorated OA in vivo by activating the SIRT1 signaling pathway.

Purpose: To restore rotation center exactly in total hip arthroplasty (THA) is technically challenging for patients with end-stage osteoarthritis due to developmental dysplasia of the hip (DDH). The technical difficulty is attributable to the complex acetabular changes. In this study, we investigated the pathomorphology of acetabulum and Harris fossa of Crowe types I to IV and discussed the method of restoring rotation center of the hip. Methods: This study retrospectively reviewed 56 patients (59 hips) who underwent cementless THA due to end-stage osteoarthritis of DDH. The pathomorphology of acetabulum and Harris fossa was observed during operations. Using the preoperative and postoperative pelvic radiographs, the vertical and the horizontal distances of hip rotation center were measured in order to evaluate the effects of restoring rotation center of the hip. Results: Adult DDH acetabulum could be classified into four basic pathological types which include the shallow cup shape, the dish shape, the shell shape, and the triangular shape. Adult DDH Harris fossa could be classified into four pathological types, including the crack shape, the closed shape, the triangle shape, and the shallow shape, in accordance with the osteophyte coverage. The vertical and horizontal distances of hip rotation center on the pelvic radiographs before and after operations were as follows: the preoperative vertical distance of hip rotation center was (39.96 ± 5.65) mm, and the postoperative one was (13.83 ± 2.66) mm; the preoperative horizontal distance of hip rotation center was (42.15 ± 6.42) mm, and the postoperative one was (28.12 ± 4.56) mm. Conclusions: The acetabulum and Harris fossa can display different pathological types on account of different degrees of dislocation and osteophyte hyperplasia in the end-stage osteoarthritis of adult DDH. The hip rotation center can be accurately restored by locating the acetabular center with Harris fossa and acetabular notch as the marks.

Background: The objectives of this study was to explore the activation of the extracellular-signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) signaling pathway and osteogenesis-related factors in the subchondral bone of patients with knee osteoarthritis (OA). Methods: Ten patients with primary OA who underwent total knee arthroplasty in the Department of Arthritis Surgery of our hospital were enrolled, and subchondral bone tissue samples were obtained during the operation. He staining and saffron staining were used to observe the arrangement of chondrocytes in the patient tissues. The protein expression levels of JNK, p-JNK, ERK, p-ERK, Runx2 and OMD in subchondral bone were detected by Western Blot. Knee osteoarthritis mice were established. He staining was used to observe the arrangement of subchondral bone cells in the knee joint of mice. Cellular mineralized nodules were determined by alizarin red staining. Results: Firstly, in general and staining, it was observed that the subchondral bone lesions of knee OA participants were obvious. Compared with normal knee joints, the levels of phosphorylation-c-Jun N-terminal kinase (P-JNK) and phosphorylation-extracellular-signal-regulated kinase (P-ERK) in the subchondral bone of knee arthritis participants were significantly increased (P<0.05). The level of osteomodulin (OMD) was significantly reduced (P<0.05). Secondly, compared with normal mice, the levels of JNK, P-JNK, OMD, ERK, and P-ERK in the model group were significantly different (P<0.05). At 2–8 weeks, the JNK and P-JNK levels in the mice model group increased significantly over time (P<0.05), and the OMD level decreased significantly over time (P<0.05). The levels of ERK and P-ERK fluctuated over time. Thirdly, osteoblasts were treated with different concentrations of anisomycin, and stained with alizarin red after continuous culture for 24 and 48 h, respectively. It was found that all the cells were stained with orange-red mineralized nodules. As the concentration of anisomycin was increased, the number of cell mineralization nodules was significantly larger, and the positive rate of chemical nodules increased. Different concentrations of anisomycin were given to interfere with the osteoblasts of mice. When anisomycin was administered at a dose of 25 ng, the OMD level reached the highest level. When the concentration of anisomycin was increased, the osteocalcin (OCN) level also showed an upward trend. Conclusions: The process by which the JNK signaling pathway regulates OMD may be closely related to the pathological changes of subchondral bone in patients with knee OA, and is involved in the occurrence and development of knee arthritis.

The fracture healing outcome is largely dependent on the quantities as well as osteogenic differentiation capacities of mesenchymal stem cells (MSCs) at the lesion site. Herein, macrophage membrane (MM)-reversibly cloaked nanocomplexes (NCs) are engineered for the lesion-targeted and hierarchical co-delivery of short stromal derived factor-1α peptide (sSDF-1α) and Ckip-1 small interfering RNA (Ckip-1 siRNA, siCkip-1) to promote bone repair by concurrently fostering recruitment and osteogenic differentiation of endogenous MSCs. To construct the NCs, a membrane-penetrating α-helical polypeptide first assembles with siCkip-1, and the cationic NCs are sequentially coated with catalase and an outer shell of sSDF-1α-anchored MM. Due to MM-assisted inflammation homing, intravenously injected NCs could efficiently accumulate at the fractured femur, where catalase decomposes the local hydrogen peroxide to generate oxygen bubbles that drives the shedding of sSDF-1α-anchored MM in the extracellular compartment. The exposed, cationic inner core thus enables robust trans-membrane delivery into MSCs to induce Ckip-1 silencing. Consequently, sSDF-1α-guided MSCs recruitment cooperates with siCkip-1-mediated osteogenic differentiation to facilitate bone formation and accelerate bone fracture healing. This study provides an enlightened strategy for the hierarchical co-delivery of macromolecular drugs into different cellular compartments, and it also renders a promising modality for the management of fracture healing.