Unicompartmental knee arthroplasty (UKA) is the preferred treatment for anterior medial knee osteoarthritis (OA) owing to the rapid postoperative recovery. However, the risk factors for UKA failure remain controversial. The clinical data of Oxford mobile-bearing UKAs performed between 2011 and 2017 with a minimum follow-up of five years were retrospectively analyzed. Demographic, surgical, and follow-up data were collected. The Cox proportional hazards model was used to identify the risk factors that contribute to UKA failure. Kaplan-Meier survival was used to compare the effect of the prosthesis position on UKA survival.Aims
Methods
Approximately 15–20% of patients report chronic pain three months after total knee replacement (TKR). The STAR care pathway is a clinically important and cost-effective personalised intervention for patients with pain 3 months after TKR. The pathway comprises screening, assesment, onward referral for treatment and follow-up over one year. In a multicentre randomised controlled trial comparing the pathway with usual care, the pathway improved pain at 6 and 12 months. This study examined the longer-term clinical and cost-effectiveness of the STAR care pathway. STAR trial participants were followed-up at a median of 4 years post-randomisation. Co-primary outcomes were self-reported pain severity and interference in the replaced knee, assessed with the Brief Pain Inventory (BPI). Resource use from electronic hospital records was valued with UK reference costs.Abstract
Introduction
Methodology
Osteoarthritis (OA) is a degenerative disease resulting from progressive joint destruction caused by many factors. Its pathogenesis is complex and has not been elucidated to date. Advanced glycation end products (AGEs) are a series of irreversible and stable macromolecular complexes formed by reducing sugar with protein, lipid, and nucleic acid through a non-enzymatic glycosylation reaction (Maillard reaction). They are an important indicator of the degree of ageing. Currently, it is considered that AGEs accumulation in vivo is a molecular basis of age-induced OA, and AGEs production and accumulation in vivo is one of the important reasons for the induction and acceleration of the pathological changes of OA. In recent years, it has been found that AGEs are involved in a variety of pathological processes of OA, including extracellular matrix degradation, chondrocyte apoptosis, and autophagy. Clearly, AGEs play an important role in regulating the expression of OA-related genes and maintaining the chondrocyte phenotype and the stability of the intra-articular environment. This article reviews the latest research results of AGEs in a variety of pathological processes of OA, to provide a new direction for the study of OA pathogenesis and a new target for prevention and treatment. Cite this article:
Inflammatory response plays a pivotal role in the pathophysiological process of intervertebral disc degeneration (IDD). A20 (also known as tumour necrosis factor alpha-induced protein 3 (TNFAIP3)) is a ubiquitin-editing enzyme that restricts nuclear factor-kappa B (NF-κB) signalling. A20 prevents the occurrence of multiple inflammatory diseases. However, the role of A20 in the initiation of IDD has not been elucidated. The aim of the study was to investigate the effect of A20 in senescence of TNF alpha (TNF-α)-induced nucleus pulposus cells (NPCs). Immunohistochemical staining was performed to observe the expression of A20 in normal and degenerated human intervertebral discs. The NPCs were dissected from the tail vertebrae of healthy male Sprague-Dawley rats and were cultured in the incubator. In the experiment, TNF-α was used to mimic the inflammatory environment of IDD. The cell viability and senescence were examined to investigate the effect of A20 on TNF-α-treated NPCs. The expression of messenger RNA (mRNA)-encoding proteins related to matrix macromolecules (collagen II, aggrecan) and senescence markers (p53, p16). Additionally, NF-κB/p65 activity of NPCs was detected within different test compounds.Aims
Methods
X-linked hypophosphataemic rickets (XLHR) is a disease of impaired bone mineralization characterized by hypophosphataemia caused by renal phosphate wasting. The main clinical manifestations of the disorder are O-shaped legs, X-shaped legs, delayed growth, and bone pain. XLHR is the most common inheritable form of rickets, with an incidence of 1/20 000 in humans. It accounts for approximately 80% of familial cases of hypophosphataemia and serves as the prototype of defective tubular phosphate (PO43+) transport, due to extra renal defects resulting in unregulated The genome DNA samples of all members in the pedigree were extracted from whole blood. We sequenced all exons of the Objectives
Methods
Aging has been associated with decreases in muscle strength and bone quality. In elderly patients, paravertebral muscle atrophy is accompanied by vertebral osteoporosis. The purpose of this study was to use paravertebral injection of botulinum toxin-A (BTX) to investigate the effects of paravertebral muscle atrophy on lumbar vertebral bone quality. Forty 16-week-old female SD rats were randomly divided into four groups: (1) a control group (CNT); (2) a resection of erector spinae muscles group (RESM); (3) a botulinum toxin-A group (BTX) that was treated with local injection of 5U BTX into the paravertebral muscles bilaterally; and (4) a positive control group (OVX) that underwent bilateral ovariectomy. At 3 months post-surgery the lumbar vertebrae (L3 – L6) were collected. The BMDs of the RESM and BTX groups were significantly lower than that of the CNT group (P < 0.01). Micro-CT scans showed that rats in the three experimental groups had fewer trabeculae and trabecular connections than rats in the CNT group. The bone loss trend of the trabecular networks was most obvious in the OVX rats. Vertebral compression testing revealed that the three experimental groups had significantly lower maximum load, energy absorption, maximum stress, and elastic modulus values than the CNT group (P < 0.01), and these parameters were lowest in the OVX group (P < 0.05). Our results demonstrate that the new paravertebral muscle atrophy model using local BTX injection causes sufficient muscle atrophy and dysfunction to result in local lumbar vertebral bone loss and quality deterioration.
Previous genome-wide association studies (GWAS) have reported significant association of the single nucleotide polymorphism (SNP) rs8044769 in the fat mass and obesity-associated gene (FTO) with osteoarthritis (OA) risk in European populations. However, these findings have not been confirmed in Chinese populations. We systematically genotyped rs8044769 and evaluated the association between the genetic variants and OA risk in a case-controlled study including 196 OA cases and 442 controls in a northern Chinese population. Genotyping was performed using the Sequenom MassARRAY iPLEX platform.Objectives
Methods
The aim of this study was to evaluate the feasibility
of using the intact S1 nerve root as a donor nerve to repair an avulsion
of the contralateral lumbosacral plexus. Two cohorts of patients
were recruited. In cohort 1, the L4–S4 nerve roots of 15 patients
with a unilateral fracture of the sacrum and sacral nerve injury
were stimulated during surgery to establish the precise functional
distribution of the S1 nerve root and its proportional contribution
to individual muscles. In cohort 2, the contralateral uninjured
S1 nerve root of six patients with a unilateral lumbosacral plexus
avulsion was transected extradurally and used with a 25 cm segment
of the common peroneal nerve from the injured leg to reconstruct
the avulsed plexus. The results from cohort 1 showed that the innervation of S1 in
each muscle can be compensated for by L4, L5, S2 and S3. Numbness
in the toes and a reduction in strength were found after surgery
in cohort 2, but these symptoms gradually disappeared and strength
recovered. The results of electrophysiological studies of the donor
limb were generally normal. Severing the S1 nerve root does not appear to damage the healthy
limb as far as clinical assessment and electrophysiological testing
can determine. Consequently, the S1 nerve can be considered to be
a suitable donor nerve for reconstruction of an avulsed contralateral
lumbosacral plexus. Cite this article:
Corticosteroid use has been implicated in the
development of osteonecrosis of the femoral head (ONFH). The exact mechanism
and predisposing factors such as age, gender, dosage, type and combination
of steroid treatment remain controversial. Between March and July
2003, a total of 539 patients with severe acute respiratory syndrome (SARS)
were treated with five different types of steroid. There were 129
men (24%) and 410 women (76%) with a mean age of 33.7 years (21
to 59). Routine screening was undertaken with radiographs, MRI and/or
CT to determine the incidence of ONFH. Of the 129 male patients with SARS, 51 (39.5%) were diagnosed
as suffering from ONFH, compared with only 79 of 410 female patients
(19.3%). The incidence of ONFH in the patients aged between 20 and
49 years was much higher than that of the group aged between 50
and 59 years (25.9% (127 of 491) Cite this article:
