Journal
ADVANCES IN ANATOMIC PATHOLOGY
Volume 14, Issue 1, Pages 42-45Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/PAP.0b013e31802ef4f2
Keywords
p38 mitogen-activated protein kinase; tumor necrosis factor-alpha; interleukin-1; osteoclast; inflammatory osteolysis
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Funding
- NCI NIH HHS [CA93796, CA098543] Funding Source: Medline
- NIAMS NIH HHS [AR046031] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [U10CA098543, R01CA093796] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [P30AR046031] Funding Source: NIH RePORTER
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Inflammatory osteolysis is a relatively frequent and incapacitating complication of rheumatoid arthritis and other inflammatory diseases, and is induced by accelerated osteoclast recruitment and activation in bone under the aegis of cytokines produced in the inflammatory environment. The success of antitumor necrosis factor-a and interleukin-1 therapy in correcting this condition highlights the central role of these cytokines in this process. Recent years have witnessed a revolution in understanding the molecular mechanism and pathogenesis of this family of diseases. It is now clear that p38 mitogen-activated protein kinase plays an essential role in the production of proinflammatory cytokines and cytokine-induced osteoclastogenesis, thus providing a potential therapeutic target for prevention of pathologic bone loss.
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