In summary, radiation-induced death of marrow cells is associated with 1) a transient increase in bone formation due, at least in part, to activation of bone lining cells, and 2) an increase in bone resorption due to increased osteoclast perimeter.
In healthy joints, RANKL expression has been described in bone lining cells of osteoblast lineage, synovial T cells, and chondrocytes [ 9, 15- 19], whereas in inflamed arthritic joints, it is detected in synovial fibroblasts, T and B cells, osteoclasts, and chondrocytes [ 6, 20- 23].
Bone remodeling is a multicellular and multispatial event that takes place with the close cooperation among the cells that constitute the so-called basic multicellular unit (BMU), which includes osteoclasts, osteoblasts, osteocytes embedded in the bone matrix, the bone lining cells, and the capillary blood supply (reviewed in [ 21]).
Bone lining cells have the capability to form bone, following no former bone resorption, in reaction to bone anabolic agents and may govern mineral homeostasis with the composite of osteoblasts and osteocytes (Kerschnitzki et al. 2013).
The function of bone lining cells is not well clear, but these cells seem to play an important role in coupling bone resorption to bone formation [ 9].
Bone lining cells lineup the resting surface.
Bone lining cells appear microscopically as relatively undifferentiated cells that line the bone.
The BRC seems to be connected to bone lining cells on bone surface, which in turn are in communication with osteocytes enclosed within the bone matrix [ 13, 14].
Cells of osteoblastic origin, including osteoblasts, osteocytes and bone lining cells are believed to act as mechanosensors in bone tissue.
- In vivo, osteoblasts differentiate either to bone lining cells or to osteocytes; about two-thirds undergo apoptosis.
