TY - JOUR
T1 - Inflammatory osteolysis
T2 - A conspiracy against bone
AU - Mbalaviele, Gabriel
AU - Novack, Deborah V.
AU - Schett, Georg
AU - Teitelbaum, Steven L.
PY - 2017/6/1
Y1 - 2017/6/1
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=85020235195&partnerID=8YFLogxK
U2 - 10.1172/JCI93356
DO - 10.1172/JCI93356
M3 - Review article
C2 - 28569732
AN - SCOPUS:85020235195
SN - 0021-9738
VL - 127
SP - 2030
EP - 2039
JO - Journal of Clinical Investigation
JF - Journal of Clinical Investigation
IS - 6
ER -