Thus, the activation of osteoclasts
is triggered by the balance between RANKL and OPG (12-13).
Osteoimmunology and the influence of proinflammatory cytokines on osteoclasts
. Biochem Med (Zagreb) 2013;23:43-63.
Comparison of osteoclastogenesis and resorption activity of human osteoclasts
on tissue culture polystyrene and on natural extracellular bone matrix in 2D and 3D.
Since circulating monocytes have two fates, either apoptosis or differentiation, they suggested that decreasing apoptosis is a mechanism for increasing monocyte survival and thus migration and differentiation into osteoclasts
However, some studies demonstrated that B cells and plasma cells in the bone microenvironment are significant sources of OPG [50-52], which is a neutralizing soluble decoy receptor that competes with RANKL, thus blocking the binding of RANKL and RANK, which eliminates the effect of RANKL on osteoclasts
Oh et al., "CHMP5 controls bone turnover rates by dampening NF-kB activity in osteoclasts
," The Journal of Experimental Medicine, vol.
It accomplished this by stimulating the proliferation of primitive bone marrow stem cells and their maturation into osteoblasts rather than other cells, such as bone-resorbing osteoclasts
In bone tissue, PTH increases osteoclast
formation and bone resorption by regulating the receptor activator of nuclear factor kappa B ligant (RANKL)/osteoprotegerin (OPG) expressed in osteoblasts.
The differentiated osteoclasts
cause bone resorption by dissolving inorganic calcium hydroxyapatite in acidic conditions and organic bone matrix by MMPs and cathepsin K [23-25].
For inducing RAW264.7 cell fusion and differentiation into mature multinucleated cells (MNC) or osteoclasts
, we cultured cells for 6 days in 35 ng/ml RANKL and stained them for detection of the marker protein tartrate-resistant acid phosphatase (TRAP) (Sigma-Aldrich, St.
Osteoblast increased in week 2 in all groups except in hydroxyapatite bovine, in which the number of osteoclasts
increased in week 2 and decreased in week 4.
AL is initiated by local inflammatory response to implant-derived wear particles that activate and recruit macrophages and osteoclasts
, thereby leading to fibrous tissue interface and periprosthetic bone resorption.