[Effects of biologic antirheumatic treatments on bone metabolism in rheumatoid arthritis and ankylosing spondylitis].
Systemic inflammatory disorders like rheumatoid arthritis (RA) and ankylosing spondylitis (AS) are characterized by extensive dysregulation of bone metabolism recognized as focal articular bone erosions, juxta-articular and systemic bone loss. The complex interactions between bone cells, osteoprotegerin/RANKL pathway and a variety of inflammatory mediators are involved in the pathogenesis of focal and systemic osteopenia. Treatments with TNF-alpha blockers inhibit inflammation-induced bone resorption and might prevent structural bone damage in RA. In some studies with anti-TNF agents, an increase in BMD has been documented in spondyloarthropathies and in RA. The B-cell depleting antibody rituximab and the T-cell costimulation blocker abatacept are emerging as other effective treatment options in RA. Studies with anti- RANKL antibody Denosumab in RA demonstrate, that treatment targeting RANKL prevents development of erosions but not inflammation. This article reviews recent scientific literature regarding the effects of modern targeted therapies on bone turnover, bone mass and focal damage of joints.
Głuszko
Piotr
P
Zakład Reumatologii i Balneologii Uniwersytetu Jagiellońskiego, Collegium Medicum, Kraków. zruj@mp.pl
D018501:Antirheumatic Agents / Q000627:therapeutic use*; D001172:Arthritis, Rheumatoid / Q000150:complications / Q000188:drug therapy* / Q000378:metabolism; D001851:Bone Diseases, Metabolic / Q000209:etiology / Q000378:metabolism; D001842:Bone and Bones / Q000187:drug effects / Q000378:metabolism*; D006801:Humans; D053244:Osteoprotegerin / Q000378:metabolism; D053245:RANK Ligand / Q000378:metabolism; D013167:Spondylitis, Ankylosing / Q000150:complications / Q000188:drug therapy* / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*
D018501:Antirheumatic Agents; D053244:Osteoprotegerin; D053245:RANK Ligand; D014409:Tumor Necrosis Factor-alpha