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SP0122 Osteoporosis and bone disease
  1. W.F. Lems
  1. Rheumatology, Vu medical centre, Amsterdam, Netherlands


Osteoporosis can be divided in primary osteoporosis and secondary osteoporosis. In the field of primary osteoporosis, the new focus is the diagnostic and therapeutic follow-up of individuals 50 years and over with a fracture. One of the big issues is how to implement that DXA-measurements will be adequately performed in all individuals 50 years and over with a fracture. Since it is nowadays possible to detect vertebral deformities with VFA (Vertebral Fracture Assessment), a software technique imaging the heights of the thoracal and lumbar vertebral bodies that can be used in one session with a BMD measurement, it is attractive to combine VFA with DXA of the lumbar spine and hip(s). Other critical points are how to integrate fall risk with bone related risk factors, and secondary osteoporosis: new data have shown that roughly 50% of fracture patients do have one or more secondary causes of osteoporosis.

For those patients who have already started with anti-osteoporotic therapy, one of the issues is how long to continue with anti-osteoporotic therapy (5 years? or more?), and what is the balance of the bisphosphonate related increased risk of subtrochanteric fractures versus the reduction in vertebral- and nonvertebral fractures.

What about secondary osteoporosis? Recent data in the field of osteo-immunology, the crosstalk between cytokines and bone, have elucidated that activated inflammatory cells at the sites of inflammation produce a wide spectrum of cytokines which stimulate local and generalised bone resorption, and which inhibit (in RA) or stimulate (in AS) bone formation. Osteoporosis related fragility fractures represent one of the most important complications that may occur in patients with rheumatic diseases; obviously these fractures may contribute to an important decrease in quality of life. Disease activity (inflammation), immobility and treatment with glucocorticoids are the main factors that increase the risk of osteoporotic fractures, on top of the background fracture risk based on, amongst others, age, body mass index and gender.

During the lecture, some topics will be discussed:

  • can both the local and generalised bone loss in RA be blocked with effective antirheumatic therapies?

  • the complex pathogenesis of bone loss and fractures in SLE;

  • the intriguing elevated loss of BMD and bone quality, with also local new bone formation in patients with ankylosing spondylitis.

Disclosure of Interest W. Lems Speakers Bureau: MSD, Lilly, Amgen, Servier, Novartis, Procter and Gamble, Will Pharma

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