The study discovering a pharmaceutical target that, when activating; can reverse bone degradation caused by osteoporosis in mouse models of the disease. The most widely used drugs currently approving by the FDA to treat osteoporosis can prevent further bone loss, but they don’t help rebuild the bone.
Despite its apparent rigidity, bone is living tissue constantly being broken down and replaced by the body. Osteoporosis occurs when old tissue is lost faster than new tissue can be creating; causing the bone to become weak and brittle. The disease afflicts more than 40 million men and women in the United States alone and is most common in older women past menopause.
The role of popular biomedical devices made of calcium phosphate in promoting bone repair and regeneration. She discovered that the biochemical adenosine acting on the A2B receptor plays a particularly large role in promoting bone growth. It stood to reason that a lack of the chemical might play a role in the development of osteoporosis.
Target reverses osteoporosis
But the expression levels of two enzymes that help produce adenosine as well as the levels of adenosine traveling between cells. As predicted, they discovering that the mice’s lack of estrogen was causing all three to plummet. The researchers then testing to see if increasing the levels of adenosine in the mice would help reverse the damaging effects of the disease.
But rather than pumping in adenosine itself, they injected a non-hormonal small molecule produced by Bayer that activates the A2B receptor. Their bones were just as healthy as the control group without osteoporosis. Adenosine is creating naturally throughout the entire body; and has many roles such as modulating neurons and regulating blood flow to various organs.
Levels in the bone marrow
Despite the relevance of CD39/CD73 to bone health, the roles of these enzymes in bona fide skeletal disorders remain unknown. We demonstrate that CD39/CD73 expression and extracellular adenosine levels in the bone marrow; are substantially decreasing in animals with osteoporotic bone loss. Knockdown of estrogen receptors ESR1; and ESR2 in primary osteoprogenitors and osteoclasts undergoing differentiation showed decreased coexpression of membrane-bound CD39 and CD73 and lower extracellular adenosine.
Researchers can not simply dump a bunch of it into the bloodstream; to stop bone degradation without side effects. Targeting the adenosine A2B receptor using an agonist attenuated bone loss in ovariectomized mice. Together, these findings suggest a pathological association of purine metabolism; with estrogen deficiency and highlight the potential of A2B receptor as a target to treat osteoporosis.