Resistin promotes the abnormal Type I collagen phenotype of subchondral bone in obese patients with end stage hip osteoarthritis

Research output: Contribution to journalArticle

Authors

Colleges, School and Institutes

External organisations

  • MRC-ARUK Centre for Musculoskeletal Ageing Research; School of Immunity and Infection; Birmingham University Medical School; Birmingham B15 2TT UK
  • Royal Orthopaed Hosp

Abstract

The purpose of this study was to determine the effect of adiposity on the architecture and composition of hip OA subchon-dral bone, and to examine the pathological role of adipokines. Femoral heads were collected from normal-weight or over-weight/obese patients with hip OA. Structural parameters of subchondral bone were determined by MicroCT and type I collagen a1/a2 ratio was determined by SDS PAGE and by qRT-PCR in ex-vivo bone explants. The serum concentration of adipokines was determined by Luminex. The effect of resistin on primary OA osteoblasts was determined by analysis of Wnt pathway signal transduction, bone nodule formation, and osteoblast metabolic activity. Subchondral bone from over-weight/obese hip OA patients exhibited reduced trabecular thickness, increased bone surface/bone volume ratio, and an
increase in the Type I collagen a1/a2, compared to normal-weight hip OA patients. The serum concentration of resistin was higher in overweight/obese OA patients, compared to normal-weight OA patients. Stimulation of normal-weight bone explant with recombinant resistin increased the Type I collagen a 1/a2 ratio. Stimulation of primary OA osteoblasts with recombinant resistin increased Wnt signalling activation, osteoblast metabolic activity, and bone nodule formation. Increased adiposity in hip OA patients is associated with altered subchondral bone architecture and type I collagen composition.

Details

Original languageEnglish
Article number4042
JournalScientific Reports
Volume7
Early online date22 Jun 2017
Publication statusPublished - 2017

Keywords

  • ageing, bone