In the field of osteo-immunology, the crosstalk between cytokines and bone, new data have elucidated that activated inflammatory cells at the site of inflammation produce a wide spectrum of cytokines which not only upregulate RANKl and stimulate local and generalized bone resorption, but also interfere with the Wnt-signaling pathway, with an inhibiting effect on bone formation. Obviously, this may lead to rapid bone loss and decreased bone quality in patients with systemic inflammatory rheumatic diseases, such as RA, PMR and SLE. As a consequence, both generalised and local bone loss (erosions) in RA may be limited in patients with adequate suppression of disease activity. This has been demonstrated in RA-patients treated with low dose glucocorticoids, but also in a longterm observational study in SLE. In contrast, bone loss at the spine and hips is much larger in glucocorticoid-treated patients after heart or liver transplantation.
For primary osteoporosis, implementation is still the major challenge for the coming years. Unfortunately, no diagnostic procedures and/or therapeutic interventions are done in the majority of fracture patients 50 years and over! The first step is to perform a DXA-measurement, preferably followed by a VFA (Vertebral Fracture Assesment), a fall-risk evaluation, and a screening for (underlying) secondary osteoporosis. While earlier data have shown that adherence to treatment was around 50% in osteoporotic patients 1 year after starting treatment, recent data have elucidated that adherence to therapy in fracture patients could be above 85%!
How should osteoporotic patients be treated?
– lifestyle measures are still very important: adequate supply of calcium and vitamin D, stop smoking, limit alcohol intake, fall-prevention, regular weigh-bearing exercises;
– oral bisphosphonates are first choice of treatment, zoledronic acid and denosumab are attractive alternatives for those who do not intolerate these drugs;
– teriparatide is a unique osteo-anabolic drug, since it not only more or less preserves the BMD, by blocking osteoclast activity (such as bisphosphonates), but by building up new bone;
– new exciting drugs are under development: odanacatib, a cathepsin K inhibitor, which seems to uncouple bone metabolism, since bone resorption is depressed, while bone formation is unchanged, and monoclonal antibodies against sclerostin, which seem to have a stronger bone formation stimulating effect than the currently available drugs.
Disclosure of Interest W. Lems Conflict with: Merck, Takeda, Eli Lily, Novartis, Will Pharma, Servier, Amgen