Inflammatory osteolysis: a conspiracy against bone

There are many causes of inflammatory osteolysis, but regardless of etiology and cellular contexts, the osteoclast is the bone-degrading cell. Thus, the impact of inflammatory cytokines on osteoclast formation and function was among the most important discoveries advancing the treatment of focal ost...

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Bibliographic Details
Published in:The Journal of clinical investigation 2017-06, Vol.127 (6), p.2030-2039
Main Authors: Mbalaviele, Gabriel, Novack, Deborah V, Schett, Georg, Teitelbaum, Steven L
Format: Article
Language:English
Subjects:
Animals
Anti-inflammatory agents
Arthritis
Biomedical research
Bone and Bones - immunology
Bone and Bones - metabolism
Bone and Bones - pathology
Cytokines
Cytokines - physiology
Disease
Drug dosages
Etiology
Humans
Inflammasomes
Inflammasomes - metabolism
Inflammation
Inflammatory diseases
Ligands
Osteoclasts - physiology
Osteocytes - physiology
Osteolysis
Osteolysis - immunology
Osteolysis - metabolism
Osteolysis - pathology
Pathogenesis
Physiological aspects
Physiology
Review
Rheumatoid arthritis
Tumor necrosis factor-TNF
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Summary:There are many causes of inflammatory osteolysis, but regardless of etiology and cellular contexts, the osteoclast is the bone-degrading cell. Thus, the impact of inflammatory cytokines on osteoclast formation and function was among the most important discoveries advancing the treatment of focal osteolysis, leading to development of therapeutic agents that either directly block the bone-resorptive cell or do so indirectly via cytokine arrest. Despite these advances, a substantial number of patients with inflammatory arthritis remain resistant to current therapies, and even effective anti-inflammatory drugs frequently do not repair damaged bone. Thus, insights into events such as those impacted by inflammasomes, which signal through cytokine-dependent and -independent mechanisms, are needed to optimize treatment of inflammatory osteolysis.
ISSN:0021-9738
1558-8238
DOI:10.1172/jci93356