Targeting mRNA Stability Arrests Inflammatory Bone Loss

Silencing mitogen-activated protein kinase-activated protein kinase-2 arrests inflammatory bone loss.

p38 mitogen-activated protein kinases (MAPKs) are critical for innate immune signaling and subsequent cytokine expression in periodontal inflammation and bone destruction. In fact, previous studies show that systemic p38 MAPK inhibitors block periodontal disease progression. However, development of p38 MAPK inhibitors with favorable toxicological profiles is difficult. Here, we report our findi...

Inflammatory Periprosthetic Bone Loss

Total hip arthroplasty [THA] is one of the most successful and effective procedures developed for the treatment of pain and lack of mobility associated with end-stage arthritis such as osteoarthritis and rheumatoid arthritis. Approximately 1.5 million joint arthroplastic operations are performed annually worldwide. THA, although considered an excellent surgical procedure, can be complicated by ...

Bone loss in chronic inflammatory conditions.

Bone loss: Therapeutic approaches for preventing bone loss in inflammatory arthritis

Inflammatory arthritides are commonly characterized by localized and generalized bone loss. Localized bone loss in the form of joint erosions and periarticular osteopenia is a hallmark of rheumatoid arthritis, the prototype of inflammatory arthritis. Recent studies have highlighted the importance of receptor activator of nuclear factor-kappa B ligand (RANKL)-dependent osteoclast activation by i...

Stability of mRNA influences osteoporotic bone mass via CNOT3.

Osteoclastogenesis is under the control of posttranscriptional and transcriptional events. However, posttranscriptional regulation of osteoclastogenesis is incompletely understood. CNOT3 is a component of the CCR4 family that regulates mRNA stability, but its function in bone is not known. Here, we show that Cnot3 deficiency by deletion of a single allele induces osteoporosis. Cnot3 deficiency ...