Bone remodeling is a complex process that is regulated by an interplay between circulating hormones and locally produced factors that act in a concerted manner to regulate osteoblast and osteoclast activity. There has been recently increasing interest in the role that the nervous system and neurotransmitters play in the regulation of bone remodeling. Reflecting this fact, the endocannabinoid pathway has recently been implicated as are important regulator of bone turnover and bone mass. The type 2 cannabinoid receptor (CB2) has been reported to regulate bone mass, but conflicting results have been reported with regard to its effects on bone resorption and osteoclast function. In this study [1], the authors investigated the role that CB2 plays in regulating bone mass and osteoclast function using a combination of pharmacological and genetic approaches.

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Calcineurin is a protein phosphatase that regulates several physiological processes and is the target for cyclosporine A. Pharmacological inhibition of calcineurin by low concentrations of cyclosporin A increases osteoblast differentiation in vitro and bone mass in vivo. To determine whether calcineurin exerts direct actions on osteoblasts, the authors of a recent study [1] generated mice lacking a calcineurin regulatory subunit selectively in osteoblasts.
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Cardiovascular disease and osteoporotic fractures are two major public health problems. Cardiovascular disease and osteoporosis coexist in women: progression of aortic calcifications has been associated with faster bone loss. Low BMD has been shown to predict cardiovascular events and cardiovascular mortality, whereas the association between the extension of aortic calcifications and hip fracture risk is controversial. In contrast to these findings in women, few studies concern the relationship between osteoporosis and cardiovascular disease in men.
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