Cytokine-Mediated Bone Destruction in Rheumatoid Arthritis
Table 1
Roles of cytokines on osteoclastogenesis.
In Vitro
In Vivo
TNF-α
Osteoclastogenic (i) Upregulates the expression of RANKL and osteoclast activators (ii) Enhances osteoclast differentiation synergistically with RANKL or independently of RANKL (iii) Inhibits osteoclast apoptosis
Osteoclastogenic (i) Upregulates the expression of RANKL and osteoclast activators (ii) Induces osteoclastogenesis in the presence or absence of RANKL (iii) Plays a critical role in inflammatory arthritis (iv) Associated with estrogen-deficient osteoporosis and joint destruction in RA
Osteoclastogenic (i) Upregulates the expression of RANKL and osteoclast activators (ii) Enhances osteoclast differentiation synergistically with RANKL or independently of RANKL
Osteoclastogenic (i) Induces osteoclastogenesis in the presence or absence of RANKL (ii) Mediates TNF--induced osteoclastogenesis (iii) Participates in physiological bone metabolism (iv) Associated with estrogen-deficient osteoporosis
Osteoclastogenic (i) Upregulates the expression of RANKL and osteoclast activators (ii) Induces RANKL-dependent osteoclastogenesis
Osteoclastogenic (i) Enhances osteoclastogenesis in the prepubertal stage (ii) Supports osteoclastogenesis in callus formation during fracture healing (iii) Associated with bone loss from inflammatory arthritis and estrogen deficiency
Antiosteoclastogenic (i) Suppresses the RANK signaling pathway (ii) Diverts cells into the macrophage lineage
Antiosteoclastogenic (i) Suppresses the differentiation of early osteoclast precursor cells (ii) Decreases osteoclast formation, leading to reduced bone turnover
Osteoclastogenic (i) Induces the expression of RANKL and proinflammatory cytokines (ii) Increases sensitivity to RANKL (iii) Enhances osteoclastogenesis via prostaglandin E2 (PGE2) in osteoblasts
Osteoclastogenic (i) Induces the expression of RANKL and proinflammatory cytokines (ii) Mediates estrogen-deficient osteoporosis