Osteoporosis is a major public health burden affecting 1 in 3 women and 1 in 5 men worldwide. It has a strong genetic component, but it can also be caused by environmental factors, like glucocorticoid intake, or associated to specific stages in life, like pregnancy. Moreover, osteoporosis can arise due to other comorbidities, like diabetes or chronic liver disease. In these cases, it is a risk factor that can negatively affect clinical management. There are different treatments available for osteoporosis, from antiresorptives targeting osteoclasts to anabolics targeting osteoblasts. However, they only reduce the fracture risk in about 20% and for some of them the individual response is highly variable. Therefore, better treatment alternatives are required. Understanding the role of genetic and metabolic markers in the development of the disease will help to improve the response to current treatments as well as to identify novel therapeutic targets.
Our group aims to investigate the molecular and metabolic mechanisms underlying primary and secondary osteoporosis and how they are genetically regulated. Moreover, we aim to functionally characterise genetic markers in bone involved in the response to treatment. To do so, we use in vitro and in vivo models for the disease and apply from routine cellular and molecular phenotyping and serum biomarker detection to state-of-the-art -omics approaches.
