In active RA, bone resorption is increased and bone formation is normal or
reduced in comparison to healthy controls. This uncoupling of bone formatio
n and resorption with a negative remodelling balance lends to generalized b
one loss.
The pathogenesis of this altered bone metabolism is multifactorial, involvi
ng non-disease-specific factors (such as age, female sex and postmenopausal
status) and disease-specific factors. Disease-specific factors are associa
ted with disease activity (inflammatory cells and cytokines; hypogonadism),
disease outcome (especially reduced mobility), and disease medication (e.g
. corticosteroids).