CD14-deficiency protects against osteoarthritic subchondral bone sclerosis via enhanced osteoclastogenesis following joint injury
Osteoarthritis is one of the leading causes of disability worldwide. One of the hallmarks is subchondral sclerosis, or thickening of the bone in and around the joint. In this work, we used a mouse model of osteoarthritis to show that decreasing inflammatory signaling, through removal of CD14, protects against subchondral sclerosis, due to an increased presence of osteoclasts, cells that combat bone thickening. Osteoclasts without CD14 differentiate faster than osteoclasts with CD14, due to decreased Type I Interferon, an inflammatory cytokine.
Authors
- Christine B. Chung (ORCID: https://orcid.org/0000-0002-0821-5458)
- Jonathan J. Miner (ORCID: https://orcid.org/0000-0001-9551-2962)
- Kevin G. Burt
- Vu Nguyen (ORCID: https://orcid.org/0000-0002-4363-9803)
- Baofeng Hu (ORCID: https://orcid.org/0009-0003-2954-9056)
- Áurea Rodrigues Borges
- Carla R. Scanzello (ORCID: https://orcid.org/0000-0002-9290-188X)
- Kate Sharp
- Robert L Mauck
- Lance A Murphy
Institutions
- San Francisco VA Medical Center (US)
- Hospital of the University of Pennsylvania (US)
- University of California San Diego (US)
- Philadelphia VA Medical Center (US)
- University of Pennsylvania (US)
- Philadelphia University (US)
Publication Details
- Journal
- bioRxiv (Cold Spring Harbor Laboratory)
- Published
- 2026-02-11
- DOI
- https://doi.org/10.64898/2026.02.10.705094
- Primary Topic
- Osteoarthritis Treatment and Mechanisms
- Type
- article
- Field-Weighted Citation Impact
- 0.00