Contrary to current views, most fractures in old-age occur after 65 years of age, are not vertebral, and are the result of greater loss of cortical rather than trabecular bone*. Thus, drugs that target the decay of cortical bone could reduce fracture risk and should be used to treat age-related bone loss, concludes an Article published in this week's edition of The Lancet.
For the past 70 years, osteoporosis research has focused on trabecular bone loss and fractures of the vertebrae, or back bones, which contain large amounts of trabecular bone. Yet, 80% of fractures in old age are non-vertebral and occur mainly at cortical sites.
To investigate the role of cortical bone loss and increased porosity on fracture risk, a team of Australian researchers led by Dr Roger Zebaze from the University of Melbourne used high-resolution x-ray computed tomography (CT) and electron microscopy to examine the effect of age on bone mineral density and cortical porosity, and compare cortical and trabecular bone loss from the distal radius (the most commonly broken bone in the arm) of 122 white adult women, and 24 postmortem specimens. This information was used to calculate age-related differences in cortical and trabecular bone mass and densities.
Findings showed that between ages 50 and 80 years bone mass at the distal radius was reduced—16% was lost between 50 and 64 years, and 84% after 65 years. Of the 106.5 mg hydroxyapatite (bone mineral) lost with age, 68% was cortical and 32% was trabecular.
Between ages 50 years and 80 years and older trabecular density at the distal radius decreased by 18.2mg hydroxyapatite per cm³before exclusion of cortical remnants, but 68.7 mg hydroxyapatite per cm³ after. Additionally, cortical density decreased by 127.8 mg hydroxyapatite per cm³ before porosity producing trabecularisation of the cortex was included and 374.3 mg hydroxyapatite per cm³after.
The researchers speculate that age-related increases in cortical porosity are underestimated by current methods used to measure bone mineral density and assess fracture risk. They suggest that because of trabecularisation of the cortex, cortical remnants that look similar to trabeculae are mistakenly viewed and calculated as trabecular bone loss by current methods.
"Accurate assessment of bone structure, especially porosity producing cortical remnants, could improve identification of individuals at high and low risk of fracture and therefore assist targeting of treatment", say the authors. "Present treatments reduce non-vertebral fractures by only 20%. Studies are needed to better define mechanisms causing fragility of cortical bone, and when research is complete, new targets might emerge."
In an accompanying Comment, David Burr from Indiana University School of Medicine in Indianapolis says that the study is important because it highlights how much bone loss in osteoporosis is cortical and emphasises that "drugs targeting cortical bone should be used to treat age-related bone loss late in life."
Dr Roger Zebaze, University of Melbourne, Melbourne, Australia.
T) + 61 3 9496 5489 E) zebaze@unimelb.edu.au
Dr David Burr, Indiana University School of Medicine, Indianapolis, USA.
T) +1 317 274 7496 E) dburr@iupui.edu
For full Article and Comment see: http://press.thelancet.com/porosity.pdf
Notes to Editors: *Trabecular bone is the porous spongy part of the inner bone and cortical bone forms the denser harder outer shell.
Journal
The Lancet