| First Author | Hao L | Year | 2015 |
| Journal | FEBS Lett | Volume | 589 |
| Issue | 12 | Pages | 1331-1339 |
| PubMed ID | 25896020 | Mgi Jnum | J:221174 |
| Mgi Id | MGI:5638460 | Doi | 10.1016/j.febslet.2015.04.008 |
| Citation | Hao L, et al. (2015) Deficiency of cathepsin K prevents inflammation and bone erosion in rheumatoid arthritis and periodontitis and reveals its shared osteoimmune role. FEBS Lett 589(12):1331-9 |
| abstractText | Using rheumatoid arthritis (RA) and periodontitis mouse models, we demonstrate that RA and periodontitis share many pathological features, such as deregulated cytokine production, increased immune-cell infiltration, increased expression of Toll-like receptors (TLRs), and enhanced osteoclast activity and bone erosion. We reveal that genetic deletion of cathepsin K (Ctsk) caused a radical reduction in inflammation and bone erosion within RA joint capsules and periodontal lesions, a drastic decrease in immune-cell infiltration, and a significant reduction in osteoclasts, macrophages, dendritic and T-cells. Deficiency of Ctsk greatly decreased the expression of TLR-4, 5, and 9 and their downstream cytokines in periodontal gingival epithelial lesions and synovial RA lesions. Hence, Ctsk may be targeted to treat RA and periodontitis simultaneously due to its shared osteoimmune role. |
