Table 2.
The high degree of redundancy built in the osteocytic-driven bone resorption and stimuli impact on effector cells including osteoclasts, osteoblasts, and osteocytes themselves.
| Stimulus | Effect on osteocyte | Effect on cellular remodeling | Reference |
|---|---|---|---|
| Inflammatory cytokines (TNF-α, IL-1β, IL-6) | Expression of RANKL (TNFSF11) and Sclerostin (SOST) | Promotes osteoclastogenesis and halts osteoblast differentiation | (68–71) (72) |
| Apoptosis by Sex steroid deficiency Fatigue loading Weightlessness Glucocorticoids Aging |
Expression of RANKL and Sclerostin by neighboring osteocytes | Osteoclast recruitment and differentiation. Halts osteoblast differentiation. |
(73) (74, 75) (64) (30) (76) |
| (PTH/PTHr) signaling | Expression of RANKL Inhibition of Sclerostin |
Increases osteoclastogenesis and reduces osteoblast apoptosis | (77) |
| Phosphate homeostasis | Release of FGF 23 | Biphasic: Partially inhibits early differentiation Augments osteoclast activity at low concentrations |
(78) |
| Necrosis | Release of DAMPs (small nuclear ribonucleoprotein SAP -130) | Osteoclast recruitment and differentiation | (79) |
| Information trafficking loss by Cx 43 deletion | Expression of RANKL and HMGB 1 |
Osteoclast recruitment and differentiation | (80, 81) |
| Senescence | Acquiring SASP Expression of RANKL Reduced Wnt 16 and OPG (TNFRSF11B) |
(82, 83) | |
| Lactation and rapid release of calcium Parathyroid hormone-related peptide (PTHrP) |
Release of Cathepsin K (CTSK), tartrate acid phosphatase (Acp5), Matrix metalloproteinase 13 (MMP13), carbonic anhydrase 1, 2, and vacuole ATPase components | Induces osteocytic perilacunar remolding | (84, 85) |