Bone matrix mineralization is preserved during early perimenopausal stage in healthy women

a paired biopsy study

B. M. Misof, P. Roschger, S. Blouin, Robert R. Recker, K. Klaushofer

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Summary: Bone matrix mineralization based on quantitative backscatter electron imaging remained unchanged during the first year of menopause in paired transiliac biopsy samples from healthy women. This suggests that the reported early perimenopausal reductions in bone mineral density are caused by factors other than decreases in the degree of mineralization. Introduction: It is unknown whether perimenopausal loss of bone mass is associated with a drop in bone matrix mineralization. Methods: For this purpose, we measured the bone mineralization density distribution (BMDD) by quantitative backscatter electron imaging (qBEI) in n = 17 paired transiliac bone biopsy samples at premenopausal baseline and 12 months after last menses (obtained at average ages of 49 ± 2 and 55 ± 2 years, respectively) in healthy women. For interpretation of BMDD outcomes, previously measured bone mineral density (BMD) and biochemical and histomorphometric markers of bone turnover were revisited for the present biopsy cohort. Results: Menopause significantly decreased BMD at the lumbar spine (−4.5 %) and femoral neck (−3.8 %), increased the fasting urinary hydroxyproline/creatinine ratio (+60 %, all p <0.01) and histomorphometric bone formation rate (+25 %, p <0.05), but affected neither cancellous nor cortical BMDD variables (paired comparison p > 0.05). Mean calcium concentrations of cancellous (Cn.CaMean) and cortical bone (Ct.CaMean) were within normal range (p > 0.05 compared to established reference data). Ct.CaMean was significantly correlated with Cn.CaMean before (R = 0.81, p <0.001) and after menopause (R = 0.80, p <0.001) and to cortical porosity of mineralized tissue (Ct.Po.) after menopause (R = −0.57, p = 0.02). Conclusions: Surprisingly, the BMDD was found not affected by the changes in bone turnover rates in this cohort. This suggests that the substantial increase in bone formation rates took place shortly before the second biopsy, and the bone mineralization changes lag behind. We conclude that during the first year after the last menses, the degree of bone matrix mineralization is preserved and does not contribute to the observed reductions in BMD.

Original languageEnglish
Pages (from-to)1795-1803
Number of pages9
JournalOsteoporosis International
Volume27
Issue number5
DOIs
StatePublished - May 1 2016

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Physiologic Calcification
Bone Matrix
Bone Density
Biopsy
Menopause
Menstruation
Bone Remodeling
Electrons
Postmenopausal Osteoporosis
Porosity
Femur Neck
Hydroxyproline
Osteogenesis
Fasting
Creatinine
Reference Values
Spine
Biomarkers
Calcium
Bone and Bones

All Science Journal Classification (ASJC) codes

  • Endocrinology, Diabetes and Metabolism

Cite this

Bone matrix mineralization is preserved during early perimenopausal stage in healthy women : a paired biopsy study. / Misof, B. M.; Roschger, P.; Blouin, S.; Recker, Robert R.; Klaushofer, K.

In: Osteoporosis International, Vol. 27, No. 5, 01.05.2016, p. 1795-1803.

Research output: Contribution to journalArticle

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title = "Bone matrix mineralization is preserved during early perimenopausal stage in healthy women: a paired biopsy study",
abstract = "Summary: Bone matrix mineralization based on quantitative backscatter electron imaging remained unchanged during the first year of menopause in paired transiliac biopsy samples from healthy women. This suggests that the reported early perimenopausal reductions in bone mineral density are caused by factors other than decreases in the degree of mineralization. Introduction: It is unknown whether perimenopausal loss of bone mass is associated with a drop in bone matrix mineralization. Methods: For this purpose, we measured the bone mineralization density distribution (BMDD) by quantitative backscatter electron imaging (qBEI) in n = 17 paired transiliac bone biopsy samples at premenopausal baseline and 12 months after last menses (obtained at average ages of 49 ± 2 and 55 ± 2 years, respectively) in healthy women. For interpretation of BMDD outcomes, previously measured bone mineral density (BMD) and biochemical and histomorphometric markers of bone turnover were revisited for the present biopsy cohort. Results: Menopause significantly decreased BMD at the lumbar spine (−4.5 {\%}) and femoral neck (−3.8 {\%}), increased the fasting urinary hydroxyproline/creatinine ratio (+60 {\%}, all p <0.01) and histomorphometric bone formation rate (+25 {\%}, p <0.05), but affected neither cancellous nor cortical BMDD variables (paired comparison p > 0.05). Mean calcium concentrations of cancellous (Cn.CaMean) and cortical bone (Ct.CaMean) were within normal range (p > 0.05 compared to established reference data). Ct.CaMean was significantly correlated with Cn.CaMean before (R = 0.81, p <0.001) and after menopause (R = 0.80, p <0.001) and to cortical porosity of mineralized tissue (Ct.Po.) after menopause (R = −0.57, p = 0.02). Conclusions: Surprisingly, the BMDD was found not affected by the changes in bone turnover rates in this cohort. This suggests that the substantial increase in bone formation rates took place shortly before the second biopsy, and the bone mineralization changes lag behind. We conclude that during the first year after the last menses, the degree of bone matrix mineralization is preserved and does not contribute to the observed reductions in BMD.",
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AU - Misof, B. M.

AU - Roschger, P.

AU - Blouin, S.

AU - Recker, Robert R.

AU - Klaushofer, K.

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N2 - Summary: Bone matrix mineralization based on quantitative backscatter electron imaging remained unchanged during the first year of menopause in paired transiliac biopsy samples from healthy women. This suggests that the reported early perimenopausal reductions in bone mineral density are caused by factors other than decreases in the degree of mineralization. Introduction: It is unknown whether perimenopausal loss of bone mass is associated with a drop in bone matrix mineralization. Methods: For this purpose, we measured the bone mineralization density distribution (BMDD) by quantitative backscatter electron imaging (qBEI) in n = 17 paired transiliac bone biopsy samples at premenopausal baseline and 12 months after last menses (obtained at average ages of 49 ± 2 and 55 ± 2 years, respectively) in healthy women. For interpretation of BMDD outcomes, previously measured bone mineral density (BMD) and biochemical and histomorphometric markers of bone turnover were revisited for the present biopsy cohort. Results: Menopause significantly decreased BMD at the lumbar spine (−4.5 %) and femoral neck (−3.8 %), increased the fasting urinary hydroxyproline/creatinine ratio (+60 %, all p <0.01) and histomorphometric bone formation rate (+25 %, p <0.05), but affected neither cancellous nor cortical BMDD variables (paired comparison p > 0.05). Mean calcium concentrations of cancellous (Cn.CaMean) and cortical bone (Ct.CaMean) were within normal range (p > 0.05 compared to established reference data). Ct.CaMean was significantly correlated with Cn.CaMean before (R = 0.81, p <0.001) and after menopause (R = 0.80, p <0.001) and to cortical porosity of mineralized tissue (Ct.Po.) after menopause (R = −0.57, p = 0.02). Conclusions: Surprisingly, the BMDD was found not affected by the changes in bone turnover rates in this cohort. This suggests that the substantial increase in bone formation rates took place shortly before the second biopsy, and the bone mineralization changes lag behind. We conclude that during the first year after the last menses, the degree of bone matrix mineralization is preserved and does not contribute to the observed reductions in BMD.

AB - Summary: Bone matrix mineralization based on quantitative backscatter electron imaging remained unchanged during the first year of menopause in paired transiliac biopsy samples from healthy women. This suggests that the reported early perimenopausal reductions in bone mineral density are caused by factors other than decreases in the degree of mineralization. Introduction: It is unknown whether perimenopausal loss of bone mass is associated with a drop in bone matrix mineralization. Methods: For this purpose, we measured the bone mineralization density distribution (BMDD) by quantitative backscatter electron imaging (qBEI) in n = 17 paired transiliac bone biopsy samples at premenopausal baseline and 12 months after last menses (obtained at average ages of 49 ± 2 and 55 ± 2 years, respectively) in healthy women. For interpretation of BMDD outcomes, previously measured bone mineral density (BMD) and biochemical and histomorphometric markers of bone turnover were revisited for the present biopsy cohort. Results: Menopause significantly decreased BMD at the lumbar spine (−4.5 %) and femoral neck (−3.8 %), increased the fasting urinary hydroxyproline/creatinine ratio (+60 %, all p <0.01) and histomorphometric bone formation rate (+25 %, p <0.05), but affected neither cancellous nor cortical BMDD variables (paired comparison p > 0.05). Mean calcium concentrations of cancellous (Cn.CaMean) and cortical bone (Ct.CaMean) were within normal range (p > 0.05 compared to established reference data). Ct.CaMean was significantly correlated with Cn.CaMean before (R = 0.81, p <0.001) and after menopause (R = 0.80, p <0.001) and to cortical porosity of mineralized tissue (Ct.Po.) after menopause (R = −0.57, p = 0.02). Conclusions: Surprisingly, the BMDD was found not affected by the changes in bone turnover rates in this cohort. This suggests that the substantial increase in bone formation rates took place shortly before the second biopsy, and the bone mineralization changes lag behind. We conclude that during the first year after the last menses, the degree of bone matrix mineralization is preserved and does not contribute to the observed reductions in BMD.

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