PAIN IN OSTEOARTHRITIS MICE: OVARIAN HORMONES REGULATE THE RESPONSE OF A2B ADENOSINE RECEPTORS

Other conference contribution, 2024

Pain in osteoarthritis (OA) is a complex phenomenon, attributable to alteration of the subchondral bone, local inflammation of the articular tissues, and increased responsiveness of the peripheral nerve to non-noxious stimuli. The decline of ovarian hormones after menopause might be responsible for the alteration of the joint tissues, predisposing women to an increased risk of developing more painful knee OA compared to men. This could be a direct consequence of the well-known effect of estrogens on bone metabolism, on the regulation of the inflammatory mechanisms, and/or the mutual regulation of endogenous molecules. Indeed, it has been previously shown that estrogen receptors regulate adenosine synthesis and the expression of adenosine receptors. Adenosine, by activating its receptors, has an important role in the regulation of pain, inflammation, bone, and cartilage metabolism.
The purpose of this study was to evaluate the effect of the pharmacological inhibition of the A2B adenosine receptors (A2BAR) in ovariectomized and control mice in the early and late stages of OA.