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. Author manuscript; available in PMC: 2015 Jan 1.
Published in final edited form as: Calcif Tissue Int. 2013 Sep 4;94(1):25–34. doi: 10.1007/s00223-013-9774-y

Figure 3. Regulation of osteoblast and osteoclast production and function by osteocytes.

Figure 3

Osteocytes regulate bone formation through sost/sclerostin. Thus, bone formation induced by systemic elevation of PTH or local mechanical loading is associated with decreased expression of sclerostin. Osteocytes regulate bone resorption through pro- and anti-osteoclastogenic cytokines. Resorption under basal conditions, induced by PTH elevation or by PTHrP increased during lactation is regulated by RANKL through the PTH receptor (PTHR) expressed in osteocytes. Activation of Wnt signaling in osteocytes increases OPG expression leading to inhibition of resorption. Osteocyte apoptosis induced by immobilization, fatigue loading, sex steroid deficiency, or genetically induced by activating diphtheria toxin receptor signaling, is sufficient to recruit osteoclasts to specific bone areas and increase resorption; likely through a mechanism that increases RANKL expression in still-living osteocytes surrounding dead osteocytes. (Reprinted with kind permission of Elsevier, Basic and Applied Bone Biology, Chapter 2 Bone Cells, Bellido, Plotkin and Bruzzaniti).