An international group of scientists have found a chemical mediator that plays a key role in build up and breakdown of bones in the body.
The team have discovered a potential therapeutic target for bone-degenerating diseases, such as osteoporosis and rheumatoid arthritis.
The team have found a chemical mediator that plays a key role in build up and breakdown of bones in the body.
They hope that this mediator, which acts on cells that degrade bone, may provide a new target for developing new therapies for bone-degenerating diseases.
Bone degeneration, also known as bone resorption, is caused by specialized cells called osteoclasts.
Generally, bone degeneration is balanced by activity of bone-forming cells, called osteoblasts.
However, in people with bone-destructive disorders like osteoporosis, osteoclast activity surpasses the osteoblast activity and causes loss of bone density.
"Most current therapies for bone-degrading diseases target mature osteoclasts," Nature magazine quoted NIAID Director Dr Anthony S. Fauci as saying.
"Understanding how immature osteoclasts are recruited to the bone in the first place and targeting the signals that control that migration represents a potential new approach to treating and preventing debilitating joint and bone diseases," he added.
The research team led by Dr. Masaru Ishii, a visiting fellow from Osaka University in Japan, found that chemoattractant sphingosine-1-phosphate (S1P), which is associated with the trafficking of immune cells into and out of the lymph nodes, play a key role in bone metabolism.
During the study, they compared the bone density in mice having the S1P receptor on their cells' surfaces with that of mice lacking it.
And mice with functional S1P receptors had denser bones than mice lacking functional S1P receptors.
Ishii suggests that it may be possible to use combined therapies that target immature osteoclast migration and mature osteoclast function to treat and prevent bone-resorptive disorders.