Obesity, osteoporosis and bone metabolism.

Obesity and osteoporosis have become major global health problems over the last decades as their prevalence is increasing. The interaction between obesity and bone metabolism is complex and not fully understood. Historically, obesity was thought to be protective against osteoporosis;however, several studies have challenged this belief. Even though the majority of the studies suggest that obesity has a favourable effect on bone density, it is unclear what the effect of obesity is on skeletal microarchitecture. Additionally, the effects of obesity on skeletal strength might be site-dependent as obese individuals are at higher risk of certain fractures. Several mechanical, biochemical and hormonal mechanisms have been proposed to explain the association between the adipose tissue and bone. Mechanical loading has positive effects on bone health, but this may not suffice in obesity. Low-grade systemic inflammation is probably harmful to the bone and increased bone marrow adipogenesis may lead to decreased bone mass in obese individuals. Finally, visceral abdominal fat may exert different actions to the bone compared with the subcutaneous fat. Achieving a better understanding of the association between adipose and bone tissue may help to identify new molecular therapeutic targets that will promote osteoblastic activity and/or inhibit adipogenesis and osteoclastic activity.

Glucocorticoid-induced osteoporosis: an overview with focus on its prevention and management.

The widespread use of glucocorticoids (GCs) contributes to the effective management of several diseases and conditions. However, it comes at a price in the case of the bones causing glucocorticoid-induced osteoporosis (GIOP), the most common cause of secondary osteoporosis and fractures. Several scientific societies have issued comprehensive guidelines on the optimal management of patients receiving GCs with the aim of providing answers to three fundamental questions, namely, whom to treat, when to treat, and how to treat. Both common ground and different approaches exist among them. General preventive measures should start along with GC initiation, and the duration of GC therapy should be limited to the minimal effective range. A pre-existing fracture, age, gender, menopausal status, dose, and duration of GC treatment are key factors in the decision to initiate antiosteoporotic medication. Oral bisphosphonates are typically regarded as the first-line treatment choice for GIOP partly due to their cost-effectiveness. Denosumab is another valid option, but an "exit strategy" should be considered before its initiation due to the risk of rebound-associated vertebral fractures upon its discontinuation. Since impaired bone formation represents the main mechanism by which GCs negatively affect skeletal health, osteoanabolic therapies appear to be pathophysiologically the more appropriate and appealing option, although cost considerations currently limit their use to selected severe cases. Regardless of the agent selected to mitigate the impact of GCs on the skeleton, what is most crucial is that the treating physician correctly stratifies the risk and intervenes at the right time.