BoneScore vs. DXA

BoneScore vs. DXA

Understanding the bone quality gap

Bone density testing was a breakthrough. It was never the whole answer.

DXA has been the standard of care for decades, and for good reason — it’s fast, widely available, and it changed how osteoporosis is diagnosed. But it measures one thing: bone mineral density. And density explains only part of why bone fractures.

What density leaves out

DXA estimates how much mineral is present by measuring how opaque bone is to X-rays. It doesn’t account for the bone matrix — the collagen, the microarchitecture, the tissue quality that determines whether bone resists a crack once it starts.

The result is a well-documented gap. Two-thirds of fractures are not attributable to osteoporosis and advancing age,1 and hip fractures occur in women who don’t meet the osteoporosis threshold.2 Most people who fracture were never classified as osteoporotic in the first place.

Simple assessments of bone mass or bone mineral content fail to take into account large contributions of bone geometry, microarchitecture, and material properties that effect the ultimate mechanical performance of bone.
— NIH/NIAMS Long-Range Plan

Density can be misleadingly normal — or even elevated

This is the failure mode that matters most clinically. In several conditions, bone quality deteriorates while density readings stay normal or rise, which can mask true fragility.

Type 2 diabetes is a clear example. These patients carry roughly a 70% increased fracture risk despite frequently presenting with normal or elevated bone density.3 Independent studies from Mayo Clinic, Columbia University, and the University of Gothenburg have each found compromised bone material quality in this population when measured by microindentation — quality a density scan doesn’t detect.4

The same pattern appears across other secondary causes of bone fragility, including chronic kidney disease, glucocorticoid therapy, and HIV.

In these patients, a normal T-score can be misleading.

Density changes too slowly to monitor treatment

DXA is typically repeated every two to five years, because that’s how long meaningful density change takes to register. That interval makes it a poor tool for answering the question clinicians actually face: is this treatment working? Bone material quality moves far faster — and it can be measured on a clinically useful timeline.
  • 7 weeks — measurable BMSi change in patients on osteoporosis therapy5
  • 3 months — a jumping exercise intervention produced a 7% BMSi increase, with no detectable change in volumetric BMD or bone microarchitecture6
That last finding is the important one. The bone was measurably adapting, and density-based tools registered nothing at all. These are questions density scanning can’t answer on a useful timeline. Is this drug working, or should we switch? When is it safe to pause therapy — and when does the patient need to restart? Did the change we made three months ago actually help? With DXA, the answer to all of these is: wait two years and scan again. A faster measure of bone quality makes it possible to ask them in months instead.

Access is a limitation

Even where DXA works well, most patients never receive it. Only about 9% of post-fracture Medicare patients are screened.

DXA requires a fixed, capital-intensive scanner and a dedicated appointment. OsteoProbe is handheld, portable, and radiation-free — deployable from major medical centers to small rural clinics and mobile units.

BoneScore® (BMSi) tracks measured bone strength across DXA-defined groups; density does not in the normal and osteopenic ranges. (Figure from 2026 CORR Publication7.)

Complements, not competitors

Density and material quality are two different properties of the same bone, and fracture risk depends on both. DXA remains the standard for diagnosing osteoporosis and should stay in the workup.

BoneScore® adds the dimension DXA was never designed to capture — particularly valuable in patients where density alone is least reliable: normal or near-normal BMD with clinical risk factors, secondary causes of bone fragility, and anyone whose treatment response you need to assess in months rather than years.

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References

  1. Mai HT, et al. J Clin Endocrinol Metab. 2019;104(8):3514–20. View source →
  2. Wainwright SA, et al. J Clin Endocrinol Metab. 2005;90(5):2787–93; Schuit SC, et al. Bone. 2004;34(1):195–202. View source →
  3. Company clinical development data; see also Murray CE & Coleman CM. Int J Mol Sci. 2019;20:4873. View source →
  4. Farr JM, et al. JBMR 2014;29(4):787–95; Nilsson AG, et al. JBMR 2017;32(5):1062–71; Furst JR, et al. J Clin Endocrinol Metab 2016;101(6):2502–10. View source →
  5. Mellibovsky L, et al. Bone tissue properties by reference-point indentation in glucocorticoid-treated patients. J Bone Miner Res. 2015;30:1651–6. View source →
  6. Sundh D, et al. A high-impact exercise intervention increases bone material strength index. J Bone Miner Res. 2018;33(7):1242–51. View source →
  7. Vaidya RS, et al. Impact Microindentation Evaluates Bone Strength, Bone Quality, and Fracture Susceptibility Across Skeletal Sites: A Cadaver Study. Clin Orthop Relat Res. 2026 Jul 2. View source →
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