Sentence examples for bone resorption through the from inspiring English sources

Bisphosphonates (BPs), synthetic analogs of pyrophosphate, are potent inhibitors of bone resorption through the inhibition of osteoclast activity and recruitment [ 14, 15].

In this particular system, RANKL, which is synthesized by the osteoblastic lineage cells, is essential for mediating bone resorption through the enhancement of osteoclast differentiation and proliferation.

After focal deposition, they inhibit bone resorption through the mechanism of internalization by osteoclasts that interfere with various vital biochemical processes [ 1– 6].

Conventional bisphosphonates were believed to inhibit bone resorption through the induction of osteoclast apoptosis after being taken up by these cells.

Furthermore, sclerostin contribution in the development of MM bone disease could be related to both a direct induction of OB suppression with reduced bone formation, and an indirect activation of osteoclast bone resorption through the unbalanced RANKL/OPG ratio.

Neutrophils can induce osteoclastic bone resorption through the expression of membrane-bound RANKL but could only mediate periodontal bone resorption if they are in close proximity to the bone [ 67].

This effect is upstream, or takes place ahead, of modification of bone resorption through this pathway, which is largely controlled by signaling through RANK/RANKL/OPG in OB 26 and OCY.

To summarize, T-614 – a novel immunomodulatory drug – appears to protect the joints from inflammation injury and osteoclastic bone resorption through skewing the response from primarily a Th17-driven one, and it does so to a greater degree in combination with MTX.

Indeed, a recent study by Nakamura and colleagues [ 86] reported that estrogen, acting via the ER-α, induced apoptosis in osteoclasts through activation of the Fas/FasL system and that this leads to suppression of bone resorption through truncating the short life span of differentiated osteoclasts.

Here phloretin appeared to allay estrogen deficiency-induced bone resorption through blocking the c-Src downstream signaling of Pyk2 and paxillin.

It has been reported that tanshinone IIA could inhibit osteoclast differentiation and suppresses bone resorption through disruption of the actin ring, and the precise inhibitory mechanism of Tanshinone VI on osteoclast differentiating might be through inhibiting RANKL expression and NF κB induction [ 20].