COPD, Bone Metabolism, and Osteoporosis

doi:10.1378/chest.10-1427

COPD, Bone Metabolism, and Osteoporosis

An Lehouck, MSc,
Steven Boonen, MD, PhD,
Marc Decramer, MD, PhD and
Wim Janssens, MD, PhD

From the Respiratory Division (Ms Lehouck and Drs Decramer and Janssens) and the Center of Metabolic Bone Diseases (Dr Boonen), University Hospital Gasthuisberg, Katholieke Universiteit Leuven, Leuven, Belgium.

Correspondence to:
Wim Janssens, MD, PhD, Respiratory Division, University Hospital Gasthuisberg, KUL, Herestraat 49, 3000 Leuven, Belgium; e-mail: wim.janssens{at}uz.kuleuven.be

Abstract

COPD and osteoporosis are strongly associated because of common risk factors such as age, smoking, and inactivity. In addition, COPD-related systemic inflammation, vitamin D deficiency, and the use of systemic corticosteroids enhance ongoing bone destruction. Osteoporosis, in turn, may cause fragility fractures, which further impair mobility and increase morbidity and mortality. Vertebral compression fractures and rib cage fractures in patients with COPD may also reduce pulmonary function or enhance exacerbations. Early prevention and treatment of osteoporosis in COPD is, therefore, important and should be based on integrated risk assessment tools such as FRAX, which take bone mineral density, history of fragility fractures, and population-specific clinical factors into account. As long as intervention studies focusing on the bone in COPD are lacking, a more rigorous application of existing treatment guidelines of osteoporosis in general is mandatory.

Footnotes

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).
Funding/Support: This study was supported by the Funds for Scientific Research-Flanders [Grant 059809N] and the Institute for Promotion of Innovation Through Science and Technology-Flanders [Grant 335102].