Kusano and coworkers have shown that IL-1 β augments bone resorption in mouse calvaria culture in vitro, by inducing MMP-2, MMP-3, MMP-9, and MMP-13 production [ 53].
The coating with elevated anatase content and surface Ca/P ratio of ~2.0 disclosed a diminished osteoclast activity and adequate osteoblast differentiation, favoring an augmented bone matrix synthesis over resorption processes.
It is well established that both bone resorption and BFRs are increased during postmenopausal osteoporosis (Raisz, 2005; Feng and McDonald, 2011); however, the extent of increased bone resorption exceeds that of augmented bone formation, which causes an imbalance in favor of bone loss (Arlot et al., 1990; Ebeling et al., 1996; Tanizawa et al., 1999; Raisz, 2005; Eriksen, 2010).
To augment bone formation and inhibit excessive resorption simultaneously, we constructed a biodegradable magnesium-based implant integrated with the anti-catabolic drug zoledronic acid (ZA); this implant exhibits controllable, sustained release of magnesium degradation products and ZA in vitro.
The decrease in the number of osteoclast may lead to decreased bone resorption, and may augment the deposition of more densely mineralized bone, with reduced porosity and the temporary deficit of bone that occurs between bone resorption and formation.
TNF increases osteoclast formation and bone resorption both directly and by augmenting the sensitivity of maturing osteoclasts to the essential osteoclastogenic factor RANKL (the RANK ligand).
Several studies reported a high rate of bone resorption after insertion of implants in bone augmented ridges [4, 5].
Anti-resorptive agents all inhibit bone resorption.
In addition, accelerated bone turnover has in both traumatic and estrogen deficiency models (ovariectomy (OVX)) been shown to augment articular cartilage erosion [ 7, 11, 12, 44, 45], in which increased bone resorption alone results in increased articular cartilage damage [ 10, 37, 46].
Similar to their effects in sham rats, PGE2 and RC had synergistic effects in augmenting cancellous bone mass and architecture and maintaining the elevated bone formation but depressing bone resorption and activation frequency.
