What causes the RANKL?
In inflammatory conditions, such as rheumatoid arthritis, the numbers of immune and accessory cells are increased in affected joints. Some of these cells produce RANKL in response to locally elevated levels of pro-inflammatory cytokines and other inflammatory mediators.
What is bone resorption caused by?
This can be caused by conditions such as hyperparathyroidism and hypovitaminosis D or even decreased hormonal production in the elderly. Some diseases with symptoms of decreased bone density are osteoporosis, and rickets. Some people who experience increased bone resorption and decreased bone formation are astronauts.
How does RANKL cause osteoporosis?
Perturbations in the ratio of OPG to RANKL have been demonstrated to occur with estrogen deficiency, hyperparathyroidism, and other disorders that stimulate bone resorption [32-34]. RANKL is also expressed by lymphocytes and synovial fibroblasts and may mediate bone loss associated with inflammatory conditions [35,36].
What stimulates RANKL?
RANKL expression is stimulated in osteoblast/stromal cells by most of the factors that are known to stimulate osteoclast formation and activity. It is highly expressed in lymph nodes, thymus and lung, and at low levels in a variety of other tissues including spleen and bone marrow .
What is RANKL in osteoporosis?
RANKL as a Promising Therapeutic Target for Osteoporosis RANKL is a homotrimeric transmembrane protein expressed by osteocytes, macrophages, osteoblasts, bone marrow stem cells and activated T lymphocytes (Lacey et al., 2012; Mori et al., 2013).
Which of the following factors promotes bone resorption?
Which of the following factors promotes bone resorption? presssure- osteoclasts are stimulated and bone resorption occurs.
What increases RANKL expression on osteoblasts?
While in vitro data suggest that PTH increases RANKL expression in osteoblasts, the depletion of mature osteoblasts in mice did not prevent the increase in RANKL or osteoclastogenesis induced by PTH.
What stimulates RANK Ligand?
Abstract. Receptor activator of NF-kappaB (RANK) ligand (RANKL), expressed by cells of the osteoblast lineage binds to RANK, induces signaling and a gene expression cascade that leads to osteoclast differentiation and activation.
What increases RANKL expression in osteoblasts?
Where does bone resorption occur?
We know resorption can happen at the root, but it can happen both internally and externally. External bone resorption – Develops on the exterior of the tooth in the site where your tooth connects to your jawbone. A sign that you may have external bone resorption are pink spots around the tooth on the gums.
Which cell is responsible for bone resorption?
Osteoclasts are multinucleated cells that play a crucial role in bone resorption.
What increases RANKL expression?
This is based on studies showing that, after PTH injection, RANKL expression is increased by osteoblast/stromal cells, leading to activation of existing osteoclasts and release by them of a factor(s) that stimulates new bone formation.
Why do osteoblasts release RANKL?
RANKL is expressed on osteoblasts and T cells. It binds the receptor RANK, which is produced on osteoclasts and their progenitors. The interaction of RANK with RANKL is required for osteoclast formation, differentiation, activation and survival.
Where is rankl found?
High protein expression of RANKL is commonly detected in the lungs, thymus and lymph nodes. Low protein expression is found in bone marrow, the stomach, peripheral blood, the spleen, the placenta, leukocytes, the heart, the thyroid, and skeletal muscle.
What is the role of RANKL?
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.
What does rank ligand do in bone?
Receptor activator of NF-κB (RANK) ligand (RANKL) induces the differentiation of monocyte/macrophage–lineage cells into the bone–resorbing cells called osteoclasts.
When RANKL binds to RANK what occurs?
RANKL is a transmembrane molecule expressed by mesenchymal cell and lymphocytes. The soluble form of RANKL is a consequence of proteolytic cleavage. RANKL binds to RANK on hematopoietic cells and activates cytoplasmic adaptor proteins (e.g., tumor necrosis factor receptor-associated factor 6, TRAF6).
What does RANK ligand do in bone?
What stimulates bone resorption?
Bone resorption is highly stimulated or inhibited by signals from other parts of the body, depending on the demand for calcium. Calcium-sensing membrane receptors in the parathyroid gland monitor calcium levels in the extracellular fluid.
What is bone resorption and why does it occur?
Bone resorption. Osteocyte activity plays a key role in this process. Conditions that result in a decrease in bone mass can either be caused by an increase in resorption or by a decrease in ossification. During childhood, bone formation exceeds resorption. As the aging process occurs, resorption exceeds formation.
How does calcium affect bone resorption?
High levels of calcium in the blood, on the other hand, leads to decreased PTH release from the parathyroid gland, decreasing the number and activity of osteoclasts, resulting in less bone resorption.
How does osteoporotic activity affect bone resorption?
At the same time, it has a direct effect on osteoclast activity. This results in an increased bone resorption rate and a decreased bone mineral density due to increased pit numbers and pit areas in the bone.