Better prediction of outcome after total hip arthroplasty (THA) is warranted. Systemic inflammation and central neuroinflammation are possibly involved in progression of osteoarthritis and pain. We explored whether inflammatory biomarkers in blood and cerebrospinal fluid (CSF) were associated with clinical outcome, and baseline pain or disability, 12 months after THA. A total of 50 patients from the Danish Pain Research Biobank (DANPAIN-Biobank) between January and June 2018 were included. Postoperative outcome was assessed as change in Oxford Hip Score (OHS) from baseline to 12 months after THA, pain was assessed on a numerical rating scale, and disability using the Pain Disability Index. Multiple regression models for each clinical outcome were included for biomarkers in blood and CSF, respectively, including age, sex, BMI, and Kellgren-Lawrence score.Aims
Methods
This study examined the relationship between obesity (OB) and osteoporosis (OP), aiming to identify shared genetic markers and molecular mechanisms to facilitate the development of therapies that target both conditions simultaneously. Using weighted gene co-expression network analysis (WGCNA), we analyzed datasets from the Gene Expression Omnibus (GEO) database to identify co-expressed gene modules in OB and OP. These modules underwent Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment and protein-protein interaction analysis to discover Hub genes. Machine learning refined the gene selection, with further validation using additional datasets. Single-cell analysis emphasized specific cell subpopulations, and enzyme-linked immunosorbent assay (ELISA), protein blotting, and cellular staining were used to investigate key genes.Aims
Methods
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:
Given the function of adiponectin (ADIPOQ) on the inflammatory condition of obesity and osteoarthritis (OA), we hypothesized that the ADIPOQ gene might be a candidate gene for a marker of susceptibility to OA. We systematically screened three tagging polymorphisms (rs182052, rs2082940 and rs6773957) in the ADIPOQ gene, and evaluated the association between the genetic variants and OA risk in a case-controlled study that included 196 OA patients and 442 controls in a northern Chinese population. Genotyping was performed using the Sequenom MassARRAY iPLEX platform.Objectives
Methods
Activation of the leptin pathway is closely correlated with human knee cartilage degeneration. However, the role of the long form of the leptin receptor (Ob-Rb) in cartilage degeneration needs further study. The aim of this study was to determine the effect of increasing the expression of Ob-Rb on chondrocytes using a lentiviral vector containing Ob-Rb. The medial and lateral cartilage samples of the tibial plateau from 12 osteoarthritis (OA) patients were collected. Ob-Rb messenger RNA (mRNA) was detected in these samples. The Ob-Rb-overexpressing chondrocytes and controls were treated with different doses of leptin for two days. The activation of the p53/p21 pathway and the number of senescence-associated β-galactosidase (SA-β-gal)-positive cells were evaluated. The mammalian target of rapamycin (mTOR) signalling pathway and autophagy were detected after the chondrocytes were treated with a high dose of leptin.Objectives
Methods
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
Normal sagittal spine-pelvis-lower extremity alignment is crucial in humans for maintaining an ergonomic upright standing posture, and pathogenesis in any segment leads to poor balance. The present study aimed to investigate how this sagittal alignment can be affected by severe knee osteoarthritis (KOA), and whether associated changes corresponded with symptoms of lower back pain (LBP) in this patient population. Lateral radiograph films in an upright standing position were obtained from 59 patients with severe KOA and 58 asymptomatic controls free from KOA. Sagittal alignment of the spine, pelvis, hip and proximal femur was quantified by measuring several radiographic parameters. Global balance was accessed according to the relative position of the C7 plumb line to the sacrum and femoral heads. The presence of chronic LBP was documented. Comparisons between the two groups were carried by independent samples Objectives
Methods
To investigate psychosocial and biomedical outcomes following
total hip replacement (THR) and to identify predictors of recovery
from THR. Patients with osteoarthritis (OA) on the waiting list for primary
THR in North West England were assessed pre-operatively and at six
and 12 months post-operatively to investigate psychosocial and biomedical
outcomes. Psychosocial outcomes were anxiety and depression, social
support and health-related quality of life (HRQoL). Biomedical outcomes
were pain, physical function and stiffness. The primary outcome
was the Short-Form 36 (SF-36) Health Survey Total Physical Function.
Potential predictors of outcome were age, sex, body mass index,
previous joint replacement, involvement in the decision for THR,
any comorbidities, any complications, type of medication, and pre-operative
ENRICHD Social Support Instrument score, Hospital Anxiety and Depression
scores and Western Ontario and McMaster Universities osteoarthritis index
score.Objectives
Methods
Total hip replacement causes a short-term increase
in the risk of mortality. It is important to quantify this and to identify
modifiable risk factors so that the risk of post-operative mortality
can be minimised. We performed a systematic review and critical
evaluation of the current literature on the topic. We identified
32 studies published over the last 10 years which provide either
30-day or 90-day mortality data. We estimate the pooled incidence
of mortality during the first 30 and 90 days following hip replacement
to be 0.30% (95% CI 0.22 to 0.38) and 0.65% (95% CI 0.50 to 0.81),
respectively. We found strong evidence of a temporal trend towards
reducing mortality rates despite increasingly co-morbid patients.
The risk factors for early mortality most commonly identified are
increasing age, male gender and co-morbid conditions, particularly
cardiovascular disease. Cardiovascular complications appear to have
overtaken fatal pulmonary emboli as the leading cause of death after
hip replacement. Cite this article:
The development of tibiofemoral angle in children has shown ethnic
variations. However this data is unavailable for our population. We measured the tibiofemoral angle (TFA) and intercondylar and
intermalleolar distances in 360 children aged between two and 18
years, dividing them into six interrupted age group intervals: two
to three years; five to six years; eight to nine years; 11 to 12
years; 14 to 15Â years; and 17 to 18 years. Each age group comprised
30 boys and 30 girls. Other variables recorded included standing
height, sitting height, weight, thigh length, leg length and length
of the lower limb.Objectives
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