Cancellous and cortical bone architecture and turnover at the iliac crest of postmenopausal osteoporotic women treated with parathyroid hormone 1-84

Robert R. Recker, S. P. Bare, S. Y. Smith, A. Varela, M. A. Miller, S. A. Morris, J. Fox

Research output: Contribution to journalArticle

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Abstract

Treatment with parathyroid hormone [PTH(1-84)] increases lumbar spine bone mineral density and decreases vertebral fractures, but its effects on bone microarchitecture are unknown. We obtained iliac crest biopsies from postmenopausal osteoporotic women given placebo (n = 8) or 100 μg PTH(1-84) for 18 (n = 8) or 24 (n = 7) months to assess cancellous and cortical bone formation and structure. At 18 months, cancellous bone volume (BV/TV) measured by microcomputed tomography and histomorphometry was 45-48% higher in subjects treated with PTH(1-84) versus placebo, a result of higher trabecular number (Tb.N) and thickness. The higher Tb.N appeared to result from intratrabecular tunneling. Connectivity density was higher and structure model index was lower, indicating a better connected and more plate-like trabecular architecture. Cancellous bone formation rate (BFR) was 2-fold higher in PTH(1-84)-treated subjects, primarily because of greater mineralizing surface. Osteoblast and osteoid surfaces were a nonsignificant 58% and 35%, respectively, higher with PTH(1-84) treatment. Osteoclast and eroded surface were unaffected by PTH(1-84). There were no effects of PTH(1-84) treatment on cortical thickness, or endocortical or periosteal BFR, but cortical porosity tended to be higher. Although cancellous BFR was lower at 24 than at 18 months, measures of cancellous and cortical bone structure were similar at both timepoints. The bone produced by PTH(1-84) had normal lamellar structure and mineralization with no abnormal histology. In conclusion, when compared with placebo, treatment of osteoporotic women with PTH(1-84) was associated with higher BV/TV and trabecular connectivity, with a more plate-like architecture, all consistent with the lower vertebral fracture incidence.

Original languageEnglish
Pages (from-to)113-119
Number of pages7
JournalBone
Volume44
Issue number1
DOIs
StatePublished - Jan 2009

Fingerprint

Bone Remodeling
Parathyroid Hormone
Osteogenesis
Placebos
Cancellous Bone
Cortical Bone
Bone and Bones
X-Ray Microtomography
Porosity
Osteoclasts
Therapeutics
Osteoblasts
Bone Density
Histology
Spine
Biopsy
Incidence

All Science Journal Classification (ASJC) codes

  • Physiology
  • Endocrinology, Diabetes and Metabolism
  • Histology

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Cancellous and cortical bone architecture and turnover at the iliac crest of postmenopausal osteoporotic women treated with parathyroid hormone 1-84. / Recker, Robert R.; Bare, S. P.; Smith, S. Y.; Varela, A.; Miller, M. A.; Morris, S. A.; Fox, J.

In: Bone, Vol. 44, No. 1, 01.2009, p. 113-119.

Research output: Contribution to journalArticle

Recker, Robert R. ; Bare, S. P. ; Smith, S. Y. ; Varela, A. ; Miller, M. A. ; Morris, S. A. ; Fox, J. / Cancellous and cortical bone architecture and turnover at the iliac crest of postmenopausal osteoporotic women treated with parathyroid hormone 1-84. In: Bone. 2009 ; Vol. 44, No. 1. pp. 113-119.
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abstract = "Treatment with parathyroid hormone [PTH(1-84)] increases lumbar spine bone mineral density and decreases vertebral fractures, but its effects on bone microarchitecture are unknown. We obtained iliac crest biopsies from postmenopausal osteoporotic women given placebo (n = 8) or 100 μg PTH(1-84) for 18 (n = 8) or 24 (n = 7) months to assess cancellous and cortical bone formation and structure. At 18 months, cancellous bone volume (BV/TV) measured by microcomputed tomography and histomorphometry was 45-48{\%} higher in subjects treated with PTH(1-84) versus placebo, a result of higher trabecular number (Tb.N) and thickness. The higher Tb.N appeared to result from intratrabecular tunneling. Connectivity density was higher and structure model index was lower, indicating a better connected and more plate-like trabecular architecture. Cancellous bone formation rate (BFR) was 2-fold higher in PTH(1-84)-treated subjects, primarily because of greater mineralizing surface. Osteoblast and osteoid surfaces were a nonsignificant 58{\%} and 35{\%}, respectively, higher with PTH(1-84) treatment. Osteoclast and eroded surface were unaffected by PTH(1-84). There were no effects of PTH(1-84) treatment on cortical thickness, or endocortical or periosteal BFR, but cortical porosity tended to be higher. Although cancellous BFR was lower at 24 than at 18 months, measures of cancellous and cortical bone structure were similar at both timepoints. The bone produced by PTH(1-84) had normal lamellar structure and mineralization with no abnormal histology. In conclusion, when compared with placebo, treatment of osteoporotic women with PTH(1-84) was associated with higher BV/TV and trabecular connectivity, with a more plate-like architecture, all consistent with the lower vertebral fracture incidence.",
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