Giant cell arteritis (GCA) and polymyalgia rheumatica (PMR) are two common systemic inflammatory conditions with a combined lifetime risk of approximately 3.5% in women and 1.5% in men. They are intimately associated with the aging process, virtually never occurring prior to 50 years of age and becoming more common over time. The reasons for this are unclear, but likely relate in part to factors related to aging of the immune system. The treatment of both GCA and PMR is traditionally based on glucocorticoids, frequently requiring a prolonged treatment course over long periods of time. Other medications are belatedly entering our treatment armamentarium, but their exact place in treatment algorithms remains to be fully defined and it is likely glucocorticoids will remain a cornerstone of our treatment in GCA and PMR for the foreseeable future. As a result, people with GCA and PMR will continue to be exposed to a significant cumulative glucocorticoid burden with all of the attendant potential adverse events, including osteoporosis. The predominantly post-menopausal female population that most commonly develops PMR and GCA is also the population that is most affected by osteoporosis. Given the risk of glucocorticoid-induced osteoporosis and subsequent fragility fractures, a planned treatment approach from glucocorticoid initiation is needed in these conditions. For the majority of patients, this will entail ensuring sufficiency of calcium and vitamin D as well as antiresorptive treatments. In this article, we discuss considerations around optimisation of metabolic bone health in GCA and PMR.