Bone is capable of remodeling by bone resorbing osteoclasts, bone forming osteoblasts and osteocytes [ 15, 19, 22, 26].
Osteoprogenitor cells in turn give rise to and maintain the osteoblasts that synthesize new bone matrix on bone forming surfaces, the osteocytes within bone matrix that support bone structure, and the protective lining cells that cover the surface of quiescent bone.
Bone is composed of an organic phase that contains (i) bone forming cells (osteoblasts and osteocytes), (ii) bone resorbing cells (osteoclasts) and (iii) a matrix of collagen and non-collagenous proteins (osteoid), and a mineral phase of inorganic salts.
Gene expression was investigated in osteocytes and mature, bone forming osteoblasts.
We found that serum sclerostin levels were higher in Enpp1 −/− mice and that sclerostin mRNA expression was strongly increased in Enpp1 −/− osteocyte-like cells and mature, bone forming osteoblasts.
However, recent experimental evidences suggest that bisphosphonates may also inhibit apoptosis of both osteocytes and osteoblasts [5] and increase the bone forming potential of osteoblasts [6], implying that BMMSC/osteoblast lineage cells may actively participate in the recovery of osteoporosis.
Sclerostin mRNA expression was increased ~ 9-fold in osteocytes (Fig. 4D) and ~ 16-fold in mature, bone forming osteoblasts (Fig. 4E) derived from Enpp1 −/− mice.
This adaptive process is governed by mechanosensitive osteocytes that transduce the mechanical signals into chemical responses, i.e. the osteocytes release signaling molecules, which orchestrate the recruitment and activity of bone forming osteoblasts and/or bone resorbing osteoclasts.
In detail, osteocytes as well as fat cells, areas of solid mineralized bone, osteoblast lining cells throughout these areas, bone forming activity (Fig. 1B-C) and bone marrow (Fig. 1D) were observed in situ.
Following a period of secretory activity, osteoblasts undergo either apoptosis or terminal differentiation to form osteocytes surrounded by bone matrix.
