Assessment of Bone Quality, Quantity, and Turnover with Multiple Methodologies at Multiple Skeletal Sites

  • Charles Chesnut
  • Sharmila Majumdar
  • J. Gardner
  • A. Shields
  • David C. Newitt
  • E. Erickson
  • M. Glott
  • A. Kriegman
  • L. Mindeholm
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 496)

Abstract

The risk for osteoporotic fracture, and presumably the therapeutic prevention of such risk by osteoporosis therapies, is determined primarily by the parameters of bone quality (principally trabecular architecture and strength), bone quantity (bone mineral density), and bone turnover (markers of bone resorption such as pyridinolines and telopeptides). Other contributors are age, bone geometry (particularly of the femoral neck), and (extrinsic to the skeleton) falls. It is unclear as to the relative contributions of each of the intrinsic parameters to fracture risk, and particularly to the therapeutic prevention of such risk. Recent evidence1indicates that the therapeutic prevention of fracture is mediated to only a small extent by changes in quality; and there is a growing consensus that changes in turnover2 are equally important to changes in quantity to fracture reduction following osteoporosis therapies. The comparatively new hypothesis is that therapeutic prevention of osteoporotic fracture may be equally due to preservation or improvements in bone quality (trabecular architecture, strength, and material properties), based upon recent data with both raloxifene3 and salmon-calcitonin4 in which significant reduction in vertebral fracture is associated with only modest effects on bone quantity and turnover.

Keywords

Placebo Osteoporosis Perforation Crest Calcitonin 

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References

  1. 1.
    S. R. Cummings, D. M. Black, and T. M. Vogt. Changes in BMD substantially underestimate the anti-fracture effects of alendronate and other antiresorptive drugsJ. Bone Miner. Res.11:s102 (1996).Google Scholar
  2. 2.
    P. D. Delmas, How does antiresorptive therapy decrease the risk of fracture in women with osteoporosis?Bone27:1–3. (2000).PubMedCrossRefGoogle Scholar
  3. 3.
    B. Ettinger, D. M. Black, B. H. Mitlak, et al. Reduction of vertebral fracture risk in postmenopausal women with osteoporosis treated with raloxifeneJAMA282:637–645 1999.PubMedCrossRefGoogle Scholar
  4. 4.
    C. H. Chesnut, S. Silverman, K. Andriano, et al., A randomized trial of nasal spray salmon calcitonin in postmenopausal women with established osteoporosis: the Prevent Recurrence of Osteoporotic Fractures StudyAm. J. Med.109:267–276 (2000).PubMedCrossRefGoogle Scholar
  5. 5.
    C. H. Chesnut, Does ultrasound (US) estimate bone quality (BQUAL) or only bone quantity? Data from the QUEST study.J. Bone Miner. Res;15, S529. (2000).CrossRefGoogle Scholar
  6. 6.
    J. Gardner, E. Eriksen, S. Majumdar et al. In vivo assessment of trabecular microarchitecture (TMA) with bone biopsy histomorphometty (BX), microCT (mCT), and MRI.J Bone Miner. Res.15:S523 (2000).Google Scholar
  7. 7.
    Majumdar S, Newitt D, Eriksen EF, et al. Do MR derived measures of trabecular bone micro-architecture in the radius show any relationship to measures of tissue level and systemic bone remodeling in postmenopausal subjects? J Bone Miner Res 2000; 15:S403.Google Scholar
  8. 10.
    Laib, A., private communication.Google Scholar

Copyright information

© Springer Science+Business Media New York 2001

Authors and Affiliations

  • Charles Chesnut
    • 1
  • Sharmila Majumdar
    • 2
  • J. Gardner
    • 1
  • A. Shields
    • 1
  • David C. Newitt
    • 2
  • E. Erickson
    • 3
  • M. Glott
    • 4
  • A. Kriegman
    • 4
  • L. Mindeholm
    • 4
  1. 1.University of Washington Medical CenterUSA
  2. 2.Univeristy of CaliforniaSan FranciscoUSA
  3. 3.University of AarhusArahusUSA
  4. 4.NovartisEast Hanover/BaselSwitzerland

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