Inhibition of cyclooxygenase-2 activity in subchondral bone modifies a subtype of osteoarthritis

Manli Tu, Mi Yang, Nanxi Yu, Gehua Zhen, Mei Wan, Wenlong Liu, Baochao Ji, Hairong Ma, Qiaoyue Guo, Peijian Tong, Li Cao, Xianghang Luo, Xu Cao

Research output: Contribution to journalArticlepeer-review

11 Scopus citations

Abstract

Osteoarthritis (OA) causes the destruction of joints. Its pathogenesis is still under investigation, and there is no effective disease-modifying therapy. Here, we report that elevated cyclooxygenase-2 (COX-2) expression in the osteocytes of subchondral bone causes both spontaneous OA and rheumatoid arthritis (RA). The knockout of COX-2 in osteocytes or treatment with a COX-2 inhibitor effectively rescues the structure of subchondral bone and attenuates cartilage degeneration in spontaneous OA (STR/Ort) mice and tumor necrosis factor-α transgenic RA mice. Thus, elevated COX-2 expression in subchondral bone induces both OA-associated and RA-associated joint cartilage degeneration. The inhibition of COX-2 expression can potentially modify joint destruction in patients with arthritis.

Original languageEnglish (US)
Article number29
JournalBone Research
Volume7
Issue number1
DOIs
StatePublished - Dec 1 2019

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Histology
  • Physiology

Fingerprint

Dive into the research topics of 'Inhibition of cyclooxygenase-2 activity in subchondral bone modifies a subtype of osteoarthritis'. Together they form a unique fingerprint.

Cite this