Curtis, K. M., & Martins, S. L. (2006). Progestogen-only contraception and bone mineral density: a systematic review. Contraception, 73(5), 470-487. https://doi.org/10.1016/j.contraception.2005.12.010
Curtis KM, Martins SL. Progestogen-only contraception and bone mineral density: a systematic review. Contraception. 2006;73(5):470-487. doi:10.1016/j.contraception.2005.12.010
Curtis, Kathryn M., and Summer L. Martins. "Progestogen-only contraception and bone mineral density: a systematic review." Contraception, vol. 73, no. 5, 2006, pp. 470-487.
Centers for Disease Control and Prevention042twtr12
Linked to ROR, the Research Organization Registry
RRM Academy Synopsis
DMPA users usually have lower bone density that rises after stopping
Women using the birth control shot DMPA usually had lower bone density than nonusers, a systematic review of 39 studies found. In studies of women who stopped DMPA, bone density rose again afterward. Limited evidence suggested other progestogen-only methods did not change bone density.
Key Findings
From 163 articles identified, 39 met the criteria: one examined fracture and 38 examined bone mineral density (BMD). Thirty-two studies examined depot medroxyprogesterone acetate (DMPA).
Among 3758 female Army recruits, DMPA use was associated with stress fracture in non-Hispanic white women (relative risk 1.71; 95% CI 1.01–2.90), and became nonsignificant after adjusting for baseline bone density.
In adults, cross-sectional BMD deficits in DMPA users were generally within 1 SD of nonusers. Two studies of women starting DMPA found decreases of about 2–3% per year.
Among 53 DMPA users aged 12 to 18, spine BMD fell a mean 1.4% over 12 months. The 152 nonhormonal or abstinence users gained a mean 3.8%.
Among 38 adolescents who stopped DMPA, BMD matched or exceeded that of 84 nonusers by 12 months. One adult study found BMD similar to nonusers' about 30 months after stopping.
Interpretation
This systematic review looked at 39 studies on DMPA and bone density, in teens and adults, during use and after stopping. Bone density losses during DMPA use went away after women stopped using it. The authors note that only one study looked at fractures, so less is known about fracture risk itself. The findings support larger studies on how bone recovers after stopping DMPA, especially in teens whose bones are still growing.
RRM Context
DMPA is a hormonal contraceptive, part of the group of drugs called suppressive medications. This review ties its bone concerns to DMPA's low-estrogen effect. Restorative reproductive medicine starts from the cause of a painful, irregular or absent cycle. Teen years matter here, since bone mass is still being built during those years.
Our editorial summary of this paper, not the article's abstract.
Abstract
Questions have been raised about the effects of progestogen-only contraceptive use on bone health, particularly among young women who have not yet reached peak bone mass and perimenopausal women who may be starting to lose bone mass. We conducted a systematic review that evaluated the association between progestogen-only contraceptive use and fracture risk or bone mineral density (BMD). We identified 39 articles from MEDLINE and EMBASE, published through July 2005. One study reported that depot medroxyprogesterone acetate (DMPA) users were more likely to experience stress fractures than nonusers; this association was not statistically significant after controlling for baseline bone density. In cross-sectional studies, the mean BMD in DMPA users was usually below that of nonusers, but within 1 SD. In longitudinal studies, BMD generally decreased more over time among DMPA users than among nonusers, but women gained BMD upon discontinuation of DMPA. Limited evidence suggested that use of progestogen-only contraceptives other than DMPA did not affect BMD.
Bone Health › Bone Mineral Density › Peak Bone Mass · Contraception › Adverse Effects › Bone Density Effects · Therapeutics › Hormonal Agents › Progesterone and Progestins
Kathryn M Curtis, Summer L Martins
Kathy Curtis, Kate Curtis, K Curtis, S Martins
PMID 16627031 16627031 DOI 10.1016/j.contraception.2005.12.010 10.1016/j.contraception.2005.12.010 Curtis et al. 2006, Curtis 2006
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