Aim

This study aimed to evaluate the impact of intraoperative direct sonication on the yield of traditional culture and the time to positivity (TTP) of cultures obtained for periprosthetic joint infection (PJI), thereby assessing its potential to improve diagnostic efficiency and reduce contamination risk.

Osteoporosis accounts for a leading cause of degenerative skeletal disease in the elderly. Osteoblast dysfunction is a prominent feature of age-induced bone loss. While microRNAs regulate osteogenic cell behavior and bone mineral acquisition, however, their function to osteoblast senescence during age-mediated osteoporosis remains elusive. This study aims to utilize osteoblast-specific microRNA-29a (miR-29a) transgenic mice to characterize its role in bone cell aging and bone mass.

Young (3 months old) and aged (9 months old) transgenic mice overexpressing miR-29a (miR-29aTg) driven by osteocalcin promoter and wild-type (WT) mice were bred for study. Bone mineral density, trabecular morphometry, and biomechanical properties were quantified using μCT imaging, material testing system and histomorphometry. Aged osteoblasts and senescence markers were probed using immunofluorescence, flow cytometry for apoptotic maker annexin V, and RT-PCR.

Significantly decreased bone mineral density, sparse trabecular morphometry (trabecular volume, thickness, and number), and poor biomechanical properties (maximum force and breaking force) along with low miR-29a expression occurred in aged WT mice. Aging significantly upregulated the expression of senescence markers p16INK4a, p21Waf/Cip1, and p53 in osteoporotic bone in WT mice. Of note, the severity of bone mass and biomechanical strength loss, as well as bone cell senescence, was remarkably compromised in aged miR-29aTg mice. In vitro, knocking down miR-29a accelerated senescent (β-galactosidase activity and senescence markers) and apoptotic reactions (capsas3 activation and TUNEL staining), but reduced mineralized matrix accumulation in osteoblasts. Forced miR-29a expression attenuated inflammatory cytokine-induced aging process and retained osteogenic differentiation capacity. Mechanistically, miR-29a dragged osteoblast senescence through targeting 3′-untranslated region of anti-aging regulator FoxO3 to upregulate that of expression as evident from luciferase activity assessment.

Low miR-29a signaling speeds up aging-induced osteoblast dysfunction and osteoporosis development. Gain of miR-29a function interrupts osteoblast senescence and shields bone tissue from age-induced osteoporosis. The robust analysis sheds light to the protective actions of miR-29a to skeletal metabolism and conveys a perspective of miR-29a signaling enhancement beneficial for aged skeletons.

Aberrant infrapatellar fat metabolism is a notable feature provoking inflammation and fibrosis in the progression of osteoarthritis (OA). Irisin, a secretory subunit of fibronectin type III domain containing 5 (FNDC5) regulate adipose morphogenesis, energy expenditure, skeletal muscle, and bone metabolism. This study aims to characterize the biological roles of Irisin signaling in an infrapatellar fat formation and OA development.

Injured articular specimens were harvested from 19 patients with end-stage knee OA and 11 patients with the femoral neck fracture. Knee joints in mice that overexpressed Irisin were subjected to intra-articular injection of collagenase to provoke OA. Expressions of Irisin, adipokines, and MMPs probed with RT-quantitative PCR. Infrapatellar adiposity, articular cartilage damage, and synovial integrity verified with histomorphometry and immunohistochemistry.

Infrapatellar adipose and synovial tissues instead of articular cartilage exhibited Irisin immunostaining. Human OA specimens showed 40% decline in Irisin expression than the non-OA group. In vitro, the gain of Irisin function enabled synovial fibroblasts but not chondrocytes to display minor responses to the IL-1β provocation of MMP3 and MMP9 expression. Of note, Irisin signaling reduced adipogenic gene expression and adipocyte formation of mesenchymal progenitor cells. In collagenase-mediated OA knee pathogenesis, forced FNDC5 expression in articular compromised the collagenase-induced infrapatellar adipose hypertrophy, synovial hypercellularity, and membrane hyperplasia. These adipose-regulatory actions warded off the affected knees from cartilage destruction and gait aberrance. Likewise, intra-articular injection of Irisin recombinant protein mitigated the development of infrapatellar adiposity and synovitis slowing down the progression of cartilage erosion and walking profile irregularity. Affected joints and adipocytes responded to the Irisin recombinant protein treatment by reducing the expressions of cartilage-deleterious adipokines IL-6, leptin, and adiponectin through regulating PPAR&gamma, function.

Irisin dysfunction is relevant to the existence of end-stage knee OA. Irisin signaling protects from excessive adipogenesis of mesenchymal precursor cells and diminished inflammation and cartilage catabolism actions aggravated by adipocytes and synovial cells. This study sheds emerging new light on the Irisin signaling stabilization of infrapatellar adipose homeostasis and the perspective of the therapeutic potential of Irisin recombinant protein for deescalating knee OA development.

Introduction

Blood loss after TKA varied, but not uncommon with up to 1500 ml or a decrease in hemoglobin of 3–4 g/dL. In addition to improving prosthetic alignment, computer-assisted TKAs also contribute to reduced operative blood loss and systemic emboli. These observations imply that navigation TKAs may cause less microvascular endothelial damage than conventional TKAs. Cell adhesion molecules (CAMs) have been employed as markers for endothelial or vascular damage. We hypothesized serum levels of CAMs in patients receiving navigation TKAs may be different from those receiving conventional TKAs.

Over the past decades, computer-aided navigation system has experienced tremendous development for minimising the risks and improving the precision of the surgery. Nowadays, some commercially-available and self-developed surgical navigation systems have already been tested and proved successfully for clinical applications. However, all of these systems use computer screen to render the navigation information such as the real-time position and orientation of the surgical instrument, virtual path of preoperative surgical planning, so that the surgeons have to switch between the actual operation site and computer screen which is inconvenient and impact the continuity of surgery. In recent years, Augmented Reality (AR)- based surgical navigation is a promising technology for clinical applications. In the AR system, virtual and actual reality are mixed, offering real-time, high-quality visualisation of an extensive variety of information to the users.

Therefore, in this study, a pilot study of a surgical navigation system for orthopaedics based on optical see-through augmented reality (AR-SNS) is presented, which encompasses the preoperative surgical planning, calibration, registration, and intra-operative tracking. With the aid of AR-SNS, the surgeon wearing the optical see-through head-mounted display can obtain a fused image that the 3D virtual critical anatomical structures are aligned with the actual structures of patient in intra-operative real-world scenario, so that some disadvantages of the traditional surgical navigation are overcome (For example, surgeon is no longer obliged to switch between the real operation scenario and computer screen), and the safety, accuracy, and reliability of the surgery may be improved.

In this study, a biomimetic triphasic scaffold was constructed to mimic the native cartilage-subchondral bone tissue structure. This scaffold contained chondral layer, calcified zone of cartilage (CZC) and subchondral bone layer. The chondral layer was type II collagen sponge, the CZC and the subchondral bone layer were derived from normal pig knee by decellularization. In order to build separate microenvironment for chondral layer and subchondral bone layer, a dual-chamber bioreactor was designed by computer aided design, manufactured by 3D printer using Poly Lactic Acid, with CZC as the barrier of these two chambers. Culture medium in these two chambers was circulated separately by peristaltic pumps. Amniotic mesenchymal stem cells were seeded in this scaffold, fluorescence labeling was used for cell tracking, total DNA content analysis was used to indicate cell proliferation, and inducing medium was used to direct stem cells differentiation. After 7 days culture, the cells regularly distributed in the scaffold, cell adhesion and proliferation was not affected. No cell migration across CZC occurred. Total DNA content analysis showed that cells in scaffold increased in a time-dependent manner. Chondrogenic and osteogenic medium could induce stem cells in these two chambers to differentiate into chondrocytes and osteocytes, respectively. Our pilot study showed that the dual-chamber culture system with biomimetic triphasic scaffold was feasible, therefore this system will be further modified and tested in vivo.

Articular cartilage repair remains a challenge in orthopedic surgery, as none of the current clinical therapies can regenerate the functional hyaline cartilage tissue. In this study, we proposed a one-step surgery strategy that uses autologous bone marrow mesenchymal stem cells (MSCs) embedded in type II collagen (Col-II) gels to repair the full thickness chondral defects in minipig models. Briefly, 8 mm full thickness chondral defects were created in both knees separately, one knee received Col-II + MSCs transplantation, while the untreated knee served as control. At 1, 3 and 6 months postoperatively, the animals were sacrificed, regenerated tissue was evaluated by magnetic resonance imaging, macro- and microscopic observation, and histological analysis. Results showed that regenerated tissue in Col-II + MSCs transplantation group exhibited significantly better structure compared with that in control group, in terms of cell distribution, smoothness of surface, adjacent tissue integration, Col-II content, structure of calcified layer and subchondral bone. With the regeneration of hyaline-like cartilage tissue, this one step strategy has the potential to be translated into clinical application.

D-dimer is one of the useful laboratory tests to evaluate the incidence of venous thromboembolism (VTE) after the total knee arthroplasty (TKA). The most recent guideline for the prophylaxis of VTE points out the surgical procedure itself is a major risk factor for developing VTE.

Only a few literatures discuss the relationship of surgical procedures and the risk of venous thromboembolism. We therefore prospectively compare the difference of the perioperative plasma D-dimer levels between the patients undergoing navigation and convention TKA.

Two hundred consecutive total knee arthroplasties were performed between September 2011 and March 2013. The patients were randomised according to their registration to the orthopaedic clinic. Ninety-six patients (100 knees) underwent a navigation-assisted TKA and ninety-four patients (100 knees) had a conventional TKA. No intramedullary violation was done in the navigation-assisted TKA, while the intramedullary femoral guiding was adapted in the conventional group.

Pre-operative and post-operation day 1 plasma D-dimer levels were recorded and evaluated using Mann-Whitney U test. There was no difference in the demographic data and pre-operative D-dimer between the two groups (p=0.443). Significantly lower D-dimer levels on the post-operative day 1 were noted in the navigation group, when compared with the conventional group. (6.0 ± 4.4 mg/L vs 11.3 ± 9.6 mg/L, p = 0.000).

We demonstrated that lower D-dimer level is developed after the navigation-assisted TKA than the conventional one. Less incidence of VTE is expected and the finding may help to explain the fact that less systemic emboli in the navigation assisted TKA.