Premenopausal Trabecular Bone Loss is Associated with a Family History of Fragility Fracture

J. C. Prior; C. L. Hitchcock; Y. M. Vigna; V. Seifert-Klauss

doi:10.1055/s-0042-103751

GebFra - DGGG-Gesellschaftsausgaben, Inhaltsverzeichnis

Geburtshilfe Frauenheilkd 2016; 76(08): 895-901
DOI: 10.1055/s-0042-103751

Original Article

GebFra Science

Georg Thieme Verlag KG Stuttgart · New York

Premenopausal Trabecular Bone Loss is Associated with a Family History of Fragility Fracture

Prämenopausaler trabekulärer Knochendichteverlust ist mit einer Familienanamnese für niedrig-traumatische Frakturen assoziiert

J. C. Prior

¹Centre for Menstrual Cycle and Ovulation Research, Division of Endocrinology, University of British Columbia, Vancouver, BC, Canada

²Dept. of Medicine, University of British Columbia, Vancouver, BC, Canada

³Vancouver Coastal Health Research Institute, Vancouver, BC, Canada

,

C. L. Hitchcock

¹Centre for Menstrual Cycle and Ovulation Research, Division of Endocrinology, University of British Columbia, Vancouver, BC, Canada

,

Y. M. Vigna

¹Centre for Menstrual Cycle and Ovulation Research, Division of Endocrinology, University of British Columbia, Vancouver, BC, Canada

,

V. Seifert-Klauss

⁴Frauenklinik und Poliklinik, Gynecologic Endocrinology and Interdisciplinary Osteoporosis Center (IOZ), Klinikum rechts der Isar, TUM Munich, Germany

› Institutsangaben

Abstract

Introduction: Although a fragility fracture family history (FFFH+) has repeatedly been shown to be associated with lower bone mineral density (BMD), its relationship to human BMD change is unclear. Animal research, however, documented that different purebred strains within rodent species have wide ranges in rates of bone acquisition during growth as well as in change post-ovariectomy. Our objective was to compare the rate of premenopausal spinal trabecular BMD change between women with and without a general family history of fragility fracture. Participants and Methods: Healthy premenopausal community women participated in prospective observational studies at two academic medical research centres: Vancouver, Canada (n = 66) and Munich, Germany (n = 20). The primary outcome was annual spinal BMD change, measured by quantitative computed tomography (QCT). The two studies employed similar methodologies for assessing QCT and FFFH. Results: Volunteer community participants had a mean age of 36.0 (SD, 6.9) years, body mass index 22.5 (2.4) and baseline QCT of 150.2 (22.5) mg/cm³ trabecular bone. The rates of BMD change were similar in both cities: − 3.5 (5.1)/year Vancouver, − 2.0 (3.4)/year Munich (95 % CI of difference: − 3.9, 0.9). Over a third of the women (31 of the 86, 36 %) reported FFFH+. Those with and without a FFFH were similar in demographics, nutrition, exercise, menstrual cycle and luteal phase lengths and physiological measures (serum calcium, osteocalcin and estradiol). However, women with FFFH+ lost trabecular BMD more rapidly: FFFH+, − 4.9 (5.0), FFFH−, − 2.2 (4.4) mg/cm³/year (95 % CI diff − 0.7 to − 4.8, F_1.83 = 7.88, p = 0.006). FFFH+ explained 7.7 % of the variance in QCT volumetric trabecular spinal bone change/year in these healthy premenopausal women. Conclusion: This study shows for the first time that having a history of a fragility fracture in a family member is associated with a greater rate of premenopausal spinal trabecular bone loss.

Key words

osteoporosis - QCT - bone turnover - menstrual cycle - estrogen - genetics

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References
1 Kanis JA, Johansson H, Oden A et al. A family history of fracture and fracture risk: a meta-analysis. Bone 2004; 35: 1029-1037
2 Peacock M, Turner CH, Econs MJ et al. Genetics of osteoporosis. Endocr Rev 2002; 23: 303-326
3 Eisman JA. Genetics of osteoporosis. Endocr Rev 1999; 20: 788-804
4 Kanis JA, Johnell O, Oden A et al. Risk of hip fracture according to the World Health Organization criteria for osteopenia and osteoporosis. Bone 2000; 27: 585-590
5 Lentle B, Cheung AM, Hanley DA et al. Scientific Advisory Council of Osteoporosis Canada. Osteoporosis Canada 2010 guidelines for the assessment of fracture risk. Can Assoc Radiol J 2011; 62: 243-250
6 Kanis JA, Oden A, Johnell O et al. The use of clinical risk factors enhances the performance of BMD in the prediction of hip and osteoporotic fractures in men and women. Osteoporos Int 2007; 18: 1033-1046
7 Seeman E, Hopper JL, Bach LA et al. Reduced bone mass in daughters of women with osteoporosis. N Engl J Med 1989; 320: 554-558
8 MacInnis RJ, Cassar C, Nowson CA et al. Determinants of bone density in 30- to 65-year-old women: a co-twin study. J Bone Miner Res 2003; 18: 1650-1656
9 Abrahamsen B, Hjelmborg JV, Kostenuik P et al. Circulating amounts of osteoprotegerin and RANK ligand: genetic influence and relationship with BMD assessed in female twins. Bone 2005; 36: 727-735
10 Karasik D, Myers RH, Cupples LA et al. Genome screen for quantitative trait loci contributing to normal variation in bone mineral density: the Framingham Study. J Bone Miner Res 2002; 17: 1718-1727
11 Richards JB, Rivadeneira F, Inouye M et al. Bone mineral density, osteoporosis, and osteoporotic fractures: a genome-wide association study. Lancet 2008; 371: 1505-1512
12 Ichikawa S, Koller DL, Padgett LR et al. Replication of previous genome-wide association studies of bone mineral density in premenopausal American women. J Bone Miner Res 2010; 25: 1821-1829
13 Buie HR, Moore CP, Boyd SK. Postpubertal architectural developmental patterns differ between the L3 vertebra and proximal tibia in three inbred strains of mice. J Bone Miner Res 2008; 23: 2048-2059
14 Bouxsein ML, Myers KS, Shultz KL et al. Ovariectomy-induced bone loss varies among inbred strains of mice. J Bone Miner Res 2005; 20: 1085-1092
15 Garnero P, Arden NK, Griffiths G et al. Genetic influence on bone turnover in postmenopausal twins. J Clin Endocrinol Metab 1996; 81: 140-146
16 Melton 3rd LJ, Khosla S, Atkinson EJ et al. Relationship of bone turnover to bone density and fractures. J Bone Miner Res 1997; 12: 1083-1091
17 Berger C, Langsetmo L, Joseph L et al. CaMos Research Group. Association between change in BMD and fragility fracture in women and men. J Bone Miner Res 2009; 24: 361-370
18 Christian JC, Yu PL, Slemenda CW et al. Heritability of bone mass: a longitudinal study in aging male twins. Am J Hum Genet 1989; 44: 429-433
19 Kelly PJ, Nguyen T, Hopper J et al. Changes in axial bone density with age: a twin study. J Bone Mineral Res 1993; 8: 11-17
20 Bainbridge KE, Sowers M, Lin X et al. Risk factors for low bone mineral density and the 6-year rate of bone loss among premenopausal and perimenopausal women. Osteoporos Int 2004; 15: 439-446
21 Brot C, Jensen LB, Sørensen OH. Bone mass and risk factors for bone loss in perimenopausal Danish women. J Intern Med 1997; 242: 505-511
22 Prior JC, Vigna YM, Schechter MT et al. Spinal bone loss and ovulatory disturbances. N Engl J Med 1990; 323: 1221-1227
23 Prior JC, Vigna YM, Schulzer M et al. Determination of luteal phase length by quantitative basal temperature methods: validation against the midcycle LH peak. Clin Invest Med 1990; 13: 123-131
24 Bedford JL, Prior JC, Hitchcock CL et al. Detecting evidence of luteal activity by least-squares quantitative basal temperature analysis against urinary progesterone metabolites and the effect of wake-time variability. Eur J Obstet Gynecol Reprod Biol 2009; 146: 76-80
25 Prior JC, Vigna YM, Barr SI et al. Ovulatory premenopausal women lose cancellous spinal bone: a five year prospective study. Bone 1996; 18: 261-267
26 Seifert-Klauss V, Mueller JE, Luppa P et al. Bone metabolism during the perimenopausal transition: a prospective study. Maturitas 2002; 41: 23-33
27 Seifert-Klauss V, Link T, Heumann C et al. Influence of pattern of menopausal transition on the amount of trabecular bone loss. Results from a 6-year prospective longitudinal study. Maturitas 2006; 55: 317-324
28 Cann CE, Genant HK, Ettinger B et al. Spinal mineral loss in oophorectomized women. Determination by quantitative computed tomography. JAMA 1980; 244: 2056-2059
29 Kalender WA, Felsenberg D, Genant HK et al. The European Spine Phantom—a tool for standardization and quality control in spinal bone mineral measurements by DXA and QCT. Eur J Radiol 1995; 20: 83-92
30 Kalender WA, Felsenberg D, Louis O et al. Reference values for trabecular and cortical vertebral bone density in single and dual-energy quantitative computed tomography. Eur J Radiol 1989; 9: 75-80
31 Rosenbrock H, Seifert-Klauss V, Kaspar S et al. Changes of biochemical bone markers during the menopausal transition. Clin Chem Lab Med 2002; 40: 143-151
32 Moayyeri A, Hammond CJ, Hart DJ et al. The UK Adult Twin Registry (TwinsUK Resource). Twin Res Hum Genet 2013; 16: 144-149
33 Waugh EJ, Polivy J, Ridout R et al. A prospective investigation of the relations among cognitive dietary restraint, subclinical ovulatory disturbances, physical activity, and bone mass in healthy young women. Am J Clin Nutr 2007; 86: 1791-1801
34 Bedford JL, Prior JC, Barr SI. A prospective exploration of cognitive dietary restraint, subclinical ovulatory disturbances, cortisol and change in bone density over two years in healthy young women. J Clin Endocrinol Metab 2010; 95: 3291-3299
35 Li D, Hitchcock CL, Barr SI et al. Negative spinal bone mineral density changes and subclinical ovulatory disturbances—prospective data in healthy premenopausal women with regular menstrual cycles. Epidemiol Rev 2014; 36: 137-147
36 Barr SI, Prior JC. The menstrual Cycle: Effects on Bone in premenopausal Women. In: Draper HH, ed. Advances in Nutritional Research, Nutrition and Osteoporosis. New York: Plenum Press; 1993
37 Popat VB, Calis KA, Vanderhoof VH et al. Bone mineral density in estrogen-deficient young women. J Clin Endocrinol Metab 2009; 94: 2277-2283
38 Biver E, Durosier C, Chevalley T et al. Prior ankle fractures in postmenopausal women are associated with low areal bone mineral density and bone microstructure alterations. Osteoporos Int 2015; 26: 2147-2155