Aortic stenosis is common and potentially fatal. Recent key insights into the pathophysiology of this disease suggest it is likely to represent a self-perpetuating cycle of injury where tissue calcification is the major driver. Also, the mechanisms governing this appear closely related to calcium homeostasis and bone metabolism. Manipulation of these processes may offer a means by which aortic stenosis progression can be inhibited using drugs currently licensed to treat osteoporosis. Indeed, a prospective randomized controlled trial is currently underway for determining whether denosumab or bisphosphonates can slow aortic stenosis disease. If successful, this would meet a major unmet clinical need.