While interdisciplinary protocols and expedited surgical treatment improve management of geriatric hip fractures, the impact of such interventions on patients undergoing specifically arthroplasty for femoral neck fracture (FNF) has not been well studied. The aim of this study is to evaluate the efficacy of an interdisciplinary hip fracture protocol for patients undergoing arthroplasty for acute FNF. In 2017, our tertiary care institution implemented a standardized interdisciplinary hip fracture protocol. We conducted a retrospective review of adult patients who underwent hemiarthroplasty (HA) or total hip arthroplasty (THA) for FNF from July 2012 – March 2020, and compared patient characteristics, hospitalization characteristics, and outcomes between those treated before and after protocol implementation.Introduction
Methods
With the rising utilization of total joint arthroplasty, the role of simultaneous-bilateral surgery has expanding impact. The purpose of this study is to examine the risk of perioperative complications for this approach in total knee arthroplasty to inform shared decision making. We used nation-wide linked discharge data from the Hospital Cost and Utilization Project from 2005–2014 comparing outcomes of simultaneous-bilateral and staged-bilateral total knee arthroplasties (TKAs). Hierarchical logistic regression analysis was used to compare mortality within 30 days, 90 days and 1 year, perioperative risks within 30–60 days, and infection and mechanical complications within 1 year.Introduction
Methods
High tibial Osteotomy (HTO) realigns the forces in the knee to slow the progression of osteoarthritis. This study relates the changes in knee joint biomechanics during level gait to glutamate signalling in the subchondral bone of patients pre and post HTO. Glutamate transmits mechanical signals in bone and activates glutamate receptors to influence inflammation, degeneration and nociception in arthritic joints. Thus glutamate signalling is a mechanism whereby mechanical load can directly modulate joint pathology and pain. 3D motion analysis was used to assess level gait prior to HTO (n=5) and postoperatively (n=2). A biomechanical model of each subject was created in Visual3D (C-motion. Inc) and used for biomechanical analysis. Gene expression was analysed by RT-PCR from bone cores from anterior and posterior drill holes, subdivided according to medial or lateral proximal tibia from HTO patients (n=5).BACKGROUND
METHODS
To determine whether cycles of pivot shift testing prior to anterior cruciate ligament (ACL) reconstruction alters metabolite levels in synovial fluid. Testing for pivot shift is a standard aspect of the EUA prior to an ACL reconstruction. Teaching 2 trainees to perform the pivot test will result in the knee being pivoted 5 times. All cases were isolated ACL deficiency, without meniscal or chondral damage (n=3). Each knee had synovial fluid extracted under aseptic conditions following anaesthesia. The pivot shift test was then performed and demonstrated 5 times. After preparation of the knee for surgery, a second synovial fluid sample was extracted. The time between samples was 5 minutes. Synovial fluids were analysed using 500 MHz 1H NMR spectroscopy. Chemical shifts were referenced to known concentration NMR internal standard (TSP), peaks identified and peak integrals measured using the Bruker software Topspin 2.0.Purpose of study
Method
Glutamate is a neurotransmitter that transmits mechanical signals in bone (1) and activates glutamate receptors and transporters, in bone, cartilage, meniscus and synovium (2). Glutamate receptor activation influences inflammatory, degenerative and nociceptive pathways in arthritic joints (2). Thus glutamate signalling is a mechanism whereby mechanical load can directly influence joint pathology and pain. We have investigated components of glutamate signalling in the subchondral bone of patients with osteoarthritis to determine which are expressed and whether this varies in anatomical regions subject to different loads. Subchondral bone was sampled from tibial cuts derived from total knee arthroplasty (n=2, TKR, Kellgren Lawrence grade 3) and from tibial drill hole sites from high tibial osteotomy (n=5, HTO, KL grades 2 and 3) for osteoarthritis. RNA was extracted, reverse transcribed and RT-PCR performed for a housekeeping gene GAPDH, a glutamate transporters (EAAT-1, EAAT1ex9skip), glutamate receptors (NR2A and KA1), a bone matrix protein, osteocalcin, and signaling molecules (osteoprotegerin [OPG], RANKL). We found differential mRNA expression in different regions of subchondral bone. In one TKR patient, EAAT-1 expression was significantly reduced in the anterior zone versus the middle or posterior zones of the tibial plateau (ANOVA, p<0.001). HTO bone cores were subdivided medial/lateral and anterior/posterior. Good quality RNA was obtained from bone cores removed from drill holes during HTO surgery, with GAPDH, osteocalcin, EAAT-1, EAAT1ex9skip, NR2A, KA1, OPG and RANKL mRNA expression detected. In one patient, comparison of gene expression in bone cores obtained pre and post HTO revealed that EAAT1ex9skip was rarely detected in post-op bone whereas KA1 was rare in pre-op bone. This differential mRNA expression may be due to the altered loading through the joint caused by the osteotomy, although these on/off differences need to be quantified to confirm this. We have shown that glutamate transporters and receptors are expressed in human subchondral bone. Activation of these receptors and transporters by the increased synovial fluid concentrations of glutamate released in arthritis will influence pathological changes and nociception. In some patients, glutamate transporter mRNA expression appears to vary with anatomical location in bone, or after HTO surgery, consistent with our original discovery of this transporter as mechanically-regulated in bone (1). If glutamatergic signaling is mechanically regulated in the human knee, this will vary during arthritic disease progression and after joint realignment, providing a direct mechanism linking mechanical loading through the joint to pathology and pain in arthritis.
is the most common arthritic condition. OA causes joint pain, loss of mobility and significantly affects the quality of life for the affected individual. The major burden to patients with arthritis is pain. However, often radiological joint destruction and the extent of pain do not correlate. This causes a dilemma for clinicians in advising timing for joint replacement surgery. In arthritis, concentrations of the neurotransmitter, glutamate is increased within the synovial fluid activating both peripheral pain mechanisms and pathological processes (1). Other pathological/pain related metabolites are also released into synovial fluid, which provides a real time snap shot of the joint pathology. We have tested the hypothesis that ‘The increased levels of pain and disease-related metabolites within human synovial fluids from arthritic joints can be detected and quantified ex vivo using high resolution 1H-NMR.’ OA synovial fluid samples were obtained during arthroscopy or total knee replacements from patients with varying degrees of pain and pathology (cartilage graded 0-4; n=21). Pain perception was determined using the Oxford knee score and samples sub-classified as mild, moderate and severe pain. All samples were analysed using 500 MHz 1H NMR spectroscopy. Chemical shifts were referenced to a known concentration NMR internal standard (TSP), peaks identified by reference to published synovial fluid NMR spectra (2) and peak integrals measured using the Bruker software Topspin 2.0. Results: Using NMR we were able to detect around 26 metabolite-specific peaks in synovial fluid spectra (such as glutamate/glutamine, isoleucine, acetyl glucoproteins, beta-hydroxbutyrate, CH2 lipids, lactate, glucose). Some specific metabolites varied significantly with pain or pathological score. For example, we found significantly more glutamate/glutamine, isoleucine and beta-hydroxybutyrate (p<0.05, T test) in OA samples reporting mild to moderate levels of pain (n=14) compared to severe pain (n=7). Significantly more CH2 lipids (p<0.05, T-test) were also present in samples indicating severe pain compared to mild/moderate pain.Osteoarthritis (OA)
Method
Meniscal tears commonly occur after a traumatic twisting injury to the knee (acute) or can form over time (degenerate). Symptoms include pain, swelling, and ‘locking’ of the knee. These symptoms are also commonly associated with osteoarthritis (OA). In some cases of OA, degenerative meniscal tears can also be present making it difficult to determine the cause of symptoms. Furthermore, acute meniscal lesions may be associated with early stage OA but often no radiological signs are evident. Many metabolites associated with joint disorders are released into the synovial fluid providing a real-time snap shot of joint pathology. The ability to examine concentrations of specific metabolites within synovial fluid could provide invaluable clinical information about the cause and stage of joint pathology. We have tested the hypothesis that ‘high resolution 1H-NMR can discriminate between osteoarthritic and meniscal tear-related metabolites within human synovial fluids and aid in clinical diagnosis.’ Synovial fluid samples have been obtained during arthroscopy or knee replacement from patients with varying degrees of joint pathology (cartilage graded 0-4; meniscal tears classified as acute or degenerative). Samples were also taken from patients undergoing Anterior Cruciate Ligament (ACL) reconstruction with no additional pathology. Samples were analysed using 500 MHz 1H NMR spectroscopy. Chemical shifts were referenced to known concentration NMR internal standard (TSP), peaks identified by reference to published synovial fluid NMR spectra (1) and peak integrals measured using the Bruker software Topspin 2.0. Spectroscopy revealed a number of differences in metabolites between OA, meniscal tear and ACL pathologies. These included significantly increased concentrations of glutamate, n-acetyl glycoprotein and β-hydroxybutyrate in OA (n=10) and acute meniscal tears (n=6) compared to ACL samples (p<0.05, T-test, n=6). Specific metabolites were also able to discriminate between OA with no meniscal tear and OA with meniscal tear synovial fluids. For example, concentrations of n-acetyl glycoproteins, glutamate and CH3 lipids were significantly increased in OA without tears (n=10) compared to OA plus meniscal tears (n=12); conversely ceramide concentrations were significantly increased in OA plus tears compared to OA only samples (p<0.05, T-test).Method
Results
