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ABCC5 functions to promote osteolytic bone destruction through the recruitment and enhanced formation of osteoclasts.
These cancers cells secrete factors such as parathyroid hormone-related protein (PTHrP) which stimulate osteoclast-mediated bone destruction through the RANK/RANKL/OPG signaling pathway [ 22, 27].
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Similarly, there are several ways in which T cells might be regulatory in an effector state like this: for example, they might control bone destruction through interaction with the osteoprotegrin system [ 23] or through the regulation of cytokines such as IFN-β, tumour necrosis factor-α or IL-4 [ 24- 26].
Therapy with both TNF antagonists and local corticosteroids modulates the RANKL/OPG system, inhibiting bone destruction through distinct mechanisms.
It typically acts as a decoy receptor that binds to RANKL and prevents its association with RANK with the net result of preventing excessive bone destruction through activation of osteoclasts[39].
These findings therefore suggest that in vivo blockade of endogenous IL-23 has an effect on preventing bone destruction through a decrease in inflammatory cytokines associated with bone destruction.
In collagen-induced and adjuvant arthritis models, intraperitoneal or intraarticular injection of IFNβ resulted in reduction of disease activity and inhibition of cartilage and bone destruction through a significant decrease of TNF and IL-6 expression and an enhancement of IL-10 responses at the site of inflammation [ 20, 38, 39].
By blocking TNFα, adalimumab can attenuate cartilage and bone destruction partially through the downregulation of matrix metalloproteinases [ 13].
Lymphoma usually causes permeative bone destruction and invades the skull base through the foramina[ 71, 72 ].
The bone destruction observed in the joints of patients with RA presents a challenging clinical problem.
X-ray showed a 7 cm bone destruction in the medial cortex of the proximal femur.
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