Clinically important body weight gain following total hip arthroplasty: a cohort study with 5-year follow-up

SummaryObjectiveLiterature examining the effects of total hip arthroplasty (THA) on subsequent body weight gain is inconclusive. Determining the extent to which clinically relevant weight gain occurs following THA has important public health implications.DesignWe used multi-variable logistic regression to compare data from one of the largest US-based THA registries to a population-based control sample from the same geographic region. We also identified factors that increased risk of clinically important weight gain specifically among persons undergoing THA. The outcome measure of interest was weight gain of ≥5% of body weight up to 5 years following surgery.ResultsThe multi-variable adjusted [age, sex, body mass index (BMI), education, comorbidity and pre-surgical weight change] odds ratio for important weight gain was 1.7 [95% confidence interval (CI), 1.06, 2.6] for a person with THA as compared to the control sample. Additional arthroplasty procedures during the 5-year follow-up further increased odds for important weight gain (OR = 2.0, 95% CI, 1.4, 2.7) relative to the control sample. A patient with THA had increased risk of important post-surgical weight gain of 12% (OR = 1.12, 95% CI, 1.08, 1.16) for every kilogram of pre-operative weight loss.ConclusionsWhile findings should be interpreted with caution because of missing follow-up weight data, patients with THA appear to be at increased risk of clinically important weight gain following surgery as compared to peers. Patients less than 60 years and who have lost a substantial amount of weight prior to surgery appear to be at particularly high risk of important post-surgical weight gain

The synovial microenvironment of osteoarthritic joints alters RNA-seq expression profiles of human primary articular chondrocytes

Osteoarthritis (OA) is a disabling degenerative joint disease that prompts pain and has limited treatment options.To permit early diagnosis and treatment of OA, a high resolution mechanistic understanding of human chondrocytes in normal and diseased states is necessary. In this study, we assessed the biological effects of OArelated changes in the synovial microenvironment on chondrocytes embedded within anatomically intact cartilage from joints with different pathological grades by next generation RNA-sequencing (RNA-seq). We determined the transcriptome of primary articular chondrocytes derived from anatomically unaffected knees and ankles, aswell as fromjoints affected by OA. The GALAXY bioinformatics platformwas used to facilitate biological interpretations. Comparisons of patient samples by k-means, hierarchical clustering and principal component analyses together reveal that primary chondrocytes exhibit OA grade-related differences in gene expression, including genes involved in cell-adhesion, ECM production and immune response.We conclude that diseased synovial microenvironments in joints with different histopathological OA grades directly alter gene expression in chondrocytes. One ramification of this finding is that anatomically intact cartilage from OA joints is not an ideal source of healthy chondrocytes, nor should these specimens be used to generate a normal baseline for the molecular characterization of diseased joints