Bone metabolism in rheumatoid arthritis

J.W.G. Jacobs¹, R.N.J. de Nijs¹, W.F. Lems², J.W.J. Bijlsma¹

¹Department of Rheumatology & Clinical Immunology, University Medical Center Utrecht, Utrecht; ²Department of Rheumatology, Free University Hospital Amsterdam, The Netherlands.

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

Key words
Bone metabolism, bone, bone formation, osteoblasts, bone resorption, bone loss, osteoclasts, bone markers, hypogonadism, androgens, cytokines, bone histomorphometry, osteoporosis, osteopenia, rheumatoid arthritis.

Please address correspondence and reprint requests to: Dr. J.W.G. Jacobs, Department of Rheumatology and Clinical Immunology, University Medical Center Utrecht, PO Box 85500, 3508 GA Utrecht, The Netherlands.
E-mail: g.dekruyf@digd.AZU.nl.

Clin Exp Rheumatol 2000; 18 (Suppl. 21): S5-S11.
© Copyright Clinical and Experimental Rheumatology 2000.