Skip to main page content
Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2010 Oct 31;2010:845180.
doi: 10.4061/2010/845180.

Progesterone and Bone: Actions Promoting Bone Health in Women

Affiliations
Free PMC article

Progesterone and Bone: Actions Promoting Bone Health in Women

Vanadin Seifert-Klauss et al. J Osteoporos. .
Free PMC article

Abstract

Estradiol (E(2)) and progesterone (P(4)) collaborate within bone remodelling on resorption (E(2)) and formation (P(4)). We integrate evidence that P(4) may prevent and, with antiresorptives, treat women's osteoporosis. P(4) stimulates osteoblast differentiation in vitro. Menarche (E(2)) and onset of ovulation (P(4)) both contribute to peak BMD. Meta-analysis of 5 studies confirms that regularly cycling premenopausal women lose bone mineral density (BMD) related to subclinical ovulatory disturbances (SODs). Cyclic progestin prevents bone loss in healthy premenopausal women with amenorrhea or SOD. BMD loss is more rapid in perimenopause than postmenopause-decreased bone formation due to P(4) deficiency contributes. In 4 placebo-controlled RCTs, BMD loss is not prevented by P(4) in postmenopausal women with increased bone turnover. However, 5 studies of E(2)-MPA co-therapy show greater BMD increases versus E(2) alone. P(4) fracture data are lacking. P(4) prevents bone loss in pre- and possibly perimenopausal women; progesterone co-therapy with antiresorptives may increase bone formation and BMD.

Figures

Figure 1
Figure 1
This photomicrograph (at 400 power magnification) shows human osteoblasts in culture after 28 days stained to show Alkaline Phosphatase production as dark blue. (a) Estradiol at a physiological concentration. (b) Estradiol alone for 7 days combined with Progesterone for 21 days. Note the lack of alkaline phosphatase staining in (a) exposed to estrogen alone, and the marked ALP staining indicating osteoblast differentiation/maturation induced by the addition of progesterone, (b) This figure is reprinted from [20] with permission from authors (Schmidmayr M and Seifert-Klauss V). Publisher permission provided.
Figure 2
Figure 2
This diagram illustrates changes in Total Body (black circle) and Spine (black square) Bone Mineral Content (BMC) adjusted for body size in a population-based cohort of adolescents (mean 11.8 years old) by Tanner Stages on the X-axis. It is drawn from data in Table 3 [28]. Endocrine Society permission provided.
Figure 3
Figure 3
This graph shows the multivariable regression for the mean and the 95% confidence interval of the change in total body bone mineral density (BMD) over 3 years in relationship to time since menarche in 38 peripubertal girls studied prospectively [30]. The vertical line shows the earliest, in a subset of 13 girls who provided menstrual calendar data and salivary progesterone levels, that ovulation could be diagnosed [34]. Reprinted with permission of the authors. Society for Bone and Mineral Research permission provided.
Figure 4
Figure 4
Intra-cycle follicular-luteal phase change in two different bone turnover markers by the serum progesterone level used as a threshold for ovulation. (a) shows the bone formation marker bone-specific alkaline phosphatase (BAP) in serum, (b) depicts changes in the bone resorption marker Pyridinoline (PYD) extracted with HPLC from urine and normalized to creatinine reprinted from [77]. Permissions provided.
Figure 5
Figure 5
The 2-year-change of trabecular lumbar spine bone mineral density documented by Quantitative Computed Tomography (QCT) is shown by rate of ovulatory cycles in 28 women with complete ovulation data out of the 44 women studied prospectively in the ongoing PEKNO-Trial. Assessed by a commercially available ovulation monitor device, ovulation-likelihood was verified by luteal phase serum sampling. The graph illustrates the significant linear relationship (r = 0.7; P < .05) observed between the percentage of ovulatory cycles and BMD loss in pre- and perimenopausal women. This figure is from a presentation on the interim analysis by T. Wimmer and V. Seifert-Klauss to the Congress of the German Menopause Society (Deutsche Menopausen Gesellschaft) in Hamburg, November 6th 2009 (unpublished). The authors provide permission.

Similar articles

See all similar articles

Cited by 15 articles

See all "Cited by" articles

References

    1. Albright F, Bloomberg E, Smith PH. Postmenopausal osteoporosis. Transactions of the Association of American Physicians. 1940;55:298–305.
    1. Baxter S, Prior JC. The Estrogen Errors: Why Progesterone is Better For Women’s Health. Westport, Conn, USA: Praeger Publishers; 2009.
    1. Aitken J, Hart DM, Lindsay R. Oestrogen replacement therapy for prevention of osteoporosis after oophorectomy. British Medical Journal. 1973;3(5879):515–518. - PMC - PubMed
    1. Recker RR, Saville PD, Heaney RP. Effect of estrogens and calcium carbonate on bone loss in postmenopausal women. Annals of Internal Medicine. 1977;87(6):649–655. - PubMed
    1. Anderson GL, Limacher M, Assaf AR, et al. Effects of conjugated equine estrogen in postmenopausal women with hysterectomy: the women's health initiative randomized controlled trial. Journal of the American Medical Association. 2004;291(14):1701–1712. - PubMed

LinkOut - more resources

Feedback