Research about Osteoporosis at the Clínic

Our main lines of osteoporosis research are the study of osteoporosis in liver diseases, where we analyse the effects of cholestasis on bone tissue at the cellular and clinical levels, and after organ transplantation, especially the liver. In addition, we also focus on early-onset and male osteoporosis, and the study of its genetic determinants; the loss of bone mass associated with spinal cord injury; and the diagnostic and therapeutic approach of symptomatic osteoporotic vertebral fracture. Another of the research interests is the study of bone replacement markers and their molecular mediators, with special interest in their clinical applicability.  

More recent areas of interest include the study of glucocorticoid-induced osteoporosis, and minority bone diseases such as brittle bone disease, hypophosphatasia and X-linked hypophosphatemic osteomalacia (XLH), among others. A coordinated and multidisciplinary approach to the care of patients with a recent fragility fracture (Fracture Liaison Service, FLS) for secondary fracture prevention has also been developed. 

Our contributions in the field of osteoporosis associated with chronic cholestasis are the identification of the main mechanism in this process being bone formation deficit, produced by the harmful effects of the products retained in cholestasis, such as bilirubin and bile acids, on osteoblasts. In addition, bilirubin itself increases viability and decreases the apoptosis of osteoclasts, which contributes to the appearance of osteoporosis in advanced liver diseases. From a clinical perspective, it has been shown that the main risk factors for developing osteoporosis are the duration and severity of liver damage, while bisphosphonate treatment reduces bone loss in this context. Regarding bone disease after liver transplantation, it has been determined that there is a high incidence of fractures afterwards, especially in patients who are elderly or who have osteoporosis. It has also been described that the prevalence of fractures in candidates for liver transplantation in the last decade is similar to that of two decades ago. In any case, the incidence of fractures after a transplant has been reduced due to improved immunosuppression and the application of specific prevention programmes. 

It has been shown that bone replacement markers are useful in Paget's bone disease therapy, since the aminoterminal propeptide of type 1 procollagen (P1NP), as a bone formation marker, and the aminoterminal telopeptide of type 1 collagen (NTx), as a marker of bone resorption, provide the best biochemical profiles to evaluate this disease. In addition, bone alkaline phosphatase and P1NP are the most sensitive markers to control the efficacy of treatment. The usefulness of tartrate-resistant acid phosphatase 5B (TRAP 5b) in the analysis of the disease has also demonstrated.

For glucocorticoid-induced osteoporosis, our group has shown that the Trabecular Bone Score (TBS) seems to have greater discriminative power than bone mineral density for evaluating risk fracture; and that hypogonadism is the main risk factor for the development of fractures in men and women treated with GC; while receiving boluses of GC is a significant factor for developing vertebral fractures.

Our group has also identified the most frequent factors associated with the development of osteoporosis in men; the clinical features of idiopathic osteoporosis in this population group; the special features of osteoporosis associated with chronic alcohol consumption (one of the most frequent causes of male osteoporosis); and the effect of alcoholic cessation on the evolution of bone mass and in bone replacement for these patients.

The most frequent causes of osteoporosis have been identified in young pre-menopausal woman while bone remodelling features have also been assessed, in addition to the study of genetic determinants in this population group, including the study of genetic determinants in osteoporosis associated with pregnancy. 

We also assessed the marked loss of bone mass that occurs after spinal cord injury at 20% per year, especially in the cortical bone; the molecular mechanisms related to this loss; and possible treatment. 

For the therapeutic approach of vertebral fractures due to symptomatic fragility, there have been several studies to analyse the usefulness of percutaneous vertebroplasty compared to conservative analgesic treatment in the evolution of pain and the quality of life of patients; with a similar analgesic effect being seen in both types of long-term treatment. However, worse pain evolution was seen in women, regardless of the treatment used or disease severity.  

Different contributions were made for minority bone diseases; including brittle bone disease, hypophosphatasia and X-linked hypophosphatemic osteomalacia (XLH). Thus, calcific periarthritis is described as a frequent manifestation in hypophosphatasia; cases of XLH have been characterised; and cardiac alterations described in patients with brittle bone disease.