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Calcitonin, a hormone of thyroid gland, suppresses the osteoclastic activity. The osteoclasts do not have receptors for parathyroid hormone (PTH). However, PTH stimulates the osteoblasts to secrete the cytokine called osteoclast-stimulating factor, which is a potent stimulator of the osteoclastic activity. [1]
In addition to its effects on kidney and intestine, PTH increases the number and activity of osteoclasts. The increase in activity of already existing osteoclasts is the initial effect of PTH, and begins in minutes and increases over a few hours. [4] Continued elevation of PTH levels increases the abundance of osteoclasts.
The binding of RANKL to RANK (facilitated by the decreased amount of OPG available for binding the excess RANKL) stimulates osteoclast precursors, which are of a monocyte lineage, to fuse. The resulting multinucleated cells are osteoclasts, which ultimately mediate bone resorption. Estrogen also regulates this pathway through its effects on PTH.
Bone tissue is removed by osteoclasts, and then new bone tissue is formed by osteoblasts. Both processes utilize cytokine (TGF-β, IGF) signalling.In osteology, bone remodeling or bone metabolism is a lifelong process where mature bone tissue is removed from the skeleton (a process called bone resorption) and new bone tissue is formed (a process called ossification or new bone formation).
Feedback from physical activity maintains bone mass, while feedback from osteocytes limits the size of the bone-forming unit. [33] [34] [35] An important additional mechanism is secretion by osteocytes, buried in the matrix, of sclerostin, a protein that inhibits a pathway that maintains osteoblast activity. Thus, when the osteon reaches a ...
RANKL, through its ability to stimulate osteoclast formation and activity, is a critical mediator of bone resorption and overall bone density. Overproduction of RANKL is implicated in a variety of degenerative bone diseases, such as rheumatoid arthritis and psoriatic arthritis. In addition to degenerative bone diseases, bone metastases can also ...
Osteoclast maturation and activity is also regulated by activation of colony stimulating factor 1 receptor (CSF1R). [104] Menopause-associated increase production of TNF-α stimulates stromal cells to produce colony stimulating factor 1 (CSF-1) which activates CSF1R and stimulates osteoclasts to reabsorb bone. [105]
TRAF6 stimulates the activation of the c-jun N-terminal kinase (JNK) and nuclear factor kappa-b (NF-κB) pathways which trigger differentiation and activation of osteoclasts. This system is balanced by the relative expression of OPG to RANKL, which are highly regulated by many factors including hormones, immune signals, and growth factors.