Changes in Bone Density With Lactation

Sowers, MaryFran; Corton, Genie; Shapiro, Brahm; Jannausch, Mary; Crutchfield, Mary; Smith, Morgan; Randolph, John F.; Hollis, Bruce W.

doi:10.1001/jama.1993.03500240074029

Cited by 310 publications

(179 citation statements)

References 50 publications

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“…Since our study was focused on recovery one year postpartum, the impact of pregnancy on bone mass was not determined. In adolescent mothers followed up for a year postpartum, BMC and BMD loss and recovery follow a pattern similar to that observed in adult women (1,2,(20)(21)(22)(23)(24)(25) . To our knowledge, there are no papers reporting that BMC in lactating adolescents ,16 years of age is lower than that of 16-17-year-old adolescents due to the fact that the former may not be completely physiologically mature, as described in teenage pregnancies with respect to linear growth (47) .…”

Section: Discussionsupporting

confidence: 67%

Changes in bone mineral density of adolescent mothers during the 12-month postpartum period

Malpeli¹,

Mansur²,

Santiago³

et al. 2009

Public Health Nutr.

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Objective: Bone mineral density (BMD) loss has been described in adult women in the 12-month postpartum period. However, little is known about the precise BMD pattern in adolescent mothers. The present study aimed to evaluate BMD in Argentinean adolescent mothers followed up during the 12-month postpartum period. Design: Analytical, prospective clinical trial. BMD and body composition were determined by dual-energy X-ray absorptiometry; bone mineral content (BMC) and BMD were measured in the lumbar spine (L2-L4), femoral neck (FN), femur trochanter (TR), total hip (TH) and total body. Changes in BMD and BMC were analysed using ANOVA for pairwise comparisons. Other comparisons were performed with the paired-sample t test and Wilcoxon test; Pearson's correlation coefficient was used to analyse the relationship among continuous variables. Setting: La Plata, Argentina. Subjects: Adolescent mothers (n 35; 17 years old or less) were recruited within 15 d after delivery. Studies and follow-up were performed at 15 d and 3, 6 and 12 months postpartum. Results: BMD and BMC losses at 3 and 6 months and recovery at 12 months fitted a quadratic curve (ANOVA) at the three sites studied (FN, TH, TR), in total-body BMD (P 5 0?000) and BMC (P 5 0?038). At hip sites, BMD loss occurred at 3 months (FN, P 5 0?000; TR, P 5 0?000; TH, P 5 0?000) and 6 months (FN, P 5 0?000; TR, P 5 0?000; TH, P 5 0?000) compared with basal values. Percentage BMD loss immediately after delivery up to 6 months was about 5 %. Conclusions: Adolescents showed significant BMD and BMC losses at 6 months postpartum, with an almost total recovery at 12 months in all sites studied.

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Section: Discussionsupporting

confidence: 67%

Changes in bone mineral density of adolescent mothers during the 12-month postpartum period

Malpeli¹,

Mansur²,

Santiago³

et al. 2009

Public Health Nutr.

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“…(7,(19)(20)(21)(22)(23)(24)(25)(26)(27)(28) The reasons for the reversibility at the central skeleton are not clear.…”

Section: Journal Of Bone and Mineral Researchmentioning

confidence: 99%

“…(7,17,18) Bone loss during breastfeeding in humans is reported, but whether the microstructural deterioration is reversible after cessation of breastfeeding in human subjects is uncertain. (19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29) As trabecular bone loss, trabecular thinning, and perforation proceed rapidly after estrogen deficiency, the resulting bone fragility is attributed to deterioration in trabecular bone.…”

Section: Introductionmentioning

confidence: 99%

Irreversible Deterioration of Cortical and Trabecular Microstructure Associated With Breastfeeding

Bjørnerem

Ghasem‐Zadeh

Wang

et al. 2016

Journal of Bone and Mineral Research

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Estrogen deficiency associated with menopause is accompanied by an increase in the rate of bone remodeling and the appearance of a remodeling imbalance; each of the greater number of remodeling transactions deposits less bone than was resorbed, resulting in microstructural deterioration. The newly deposited bone is also less completely mineralized than the older bone resorbed. We examined whether breastfeeding, an estrogen-deficient state, compromises bone microstructure and matrix mineral density. Distal tibial and distal radial microarchitecture were quantified using high-resolution peripheral quantitative computed tomography in 58 women before, during, and after breastfeeding and in 48 controls during follow-up of 1 to 5 years. Five months of exclusive breastfeeding increased cortical porosity by 0.6% (95% confidence interval [CI] 0.3-0.9), reduced matrix mineralization density by 0.26% (95% CI 0.12-0.41) (both p < 0.01), reduced trabecular number by 0.22 per mm (95% CI 0.15-0.28), and increased trabecular separation by 0.07 mm (95% CI 0.05-0.08) (all p < 0.001). Relative to prebreastfeeding, at a median of 2.6 years (range 1 to 4.8) after cessation of breastfeeding, cortical porosity remained 0.58 SD (95% CI 0.48-0.68) higher, matrix mineralization density remained 1.28 SD (95% CI 1.07-1.49) lower, and trabeculae were 1.33 SD (95% CI 1.15-1.50) fewer and 1.06 SD (95% CI 0.91-1.22) more greatly separated (all p < 0.001). All deficits were greater than in controls. The results were similar at distal radius. Bone microstructure may be irreversibly deteriorated after cessation of breastfeeding at appendicular sites. Studies are needed to establish whether this deterioration compromises bone strength and increases fracture risk later in life.

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“…Mulheres com período de lactação de pelo menos 6 meses apresentam diminuição da densidade mineral óssea de 5,1% em coluna lombar e 4,8% em colo femural, quando se comparam os valores basais aos de 6 meses pós-parto (16). Por outro lado, mulheres que amamentam por menos de 1 mês não apresentam perda de massa óssea apreciável no sexto mês pós-parto.…”

Section: Discussionunclassified

Osteogenesis imperfecta no adulto e resposta ao alendronato

Donangelo

Coelho

Farias

2001

Arq Bras Endocrinol Metab

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A Osteogênese Imperfecta (OI) é um distúrbio hereditário do tecido conjuntivo, devido a um defeito qualitativo ou quantitativo do colágeno tipo I. Osteopenia, fraturas recorrentes e deformidades ósseas são as principais características da doença. Alguns pacientes também apresentam escleras azuladas. Os bisfosfonatos parecem constituir terapêu-tica eficiente em crianças, mas há poucos dados sobre o uso dessas drogas em adultos com OI. Descrevemos o caso de uma paciente de trinta anos com OI e múltiplas fraturas até a puberdade. Durante a primeira gestação as dores ósseas retornaram, piorando após o parto. Os marcadores bioquímicos sugeriam altas taxas de remodelação óssea, sendo iniciado alendronato sódico 10mg ao dia. Em poucos meses houve melhora das dores ósseas. Após o primeiro ano, a densidade mineral óssea aumentou em 10,8% na coluna lombar (CL) e 2,3% no colo femural (CF). No final do terceiro ano, o ganho total foi de 21,7% em CL e 10,9% em CF. Nossos dados sugerem que o alendronato seja boa opção terapêutica em adultos com Osteogenesis Imperfecta. ABSTRACTOsteogenesis imperfecta (OI) is a heritable disorder of connective tissue, due to a qualitative or quantitative abnormalities of type I collagen. Osteopenia, recurrent fractures and skeletal deformities are the hallmarks of the disease. Some patients also have blue sclera. Bisphosphonates appear to be an effective therapy in children but data on the efficacy of these drugs in adults with OI is limited. We describe a case of a thirty-year-old woman with OI and multiple fractures until puberty. During her first pregnancy bone pains relapsed, and worsened in the post-partum period. Bone markers suggested high bone turnover and the patient was started on alendronate 10mg per day. In a few months bone pain became less intense. Bone mass increased 10.8% at lumbar spine (LS) and 2.3% at femoral neck (FN) after one year, and 21.7% at LS and 10.9% at FN after three years of treatment. Our observations suggest that oral alendronate may be a good therapeutic option for adults with OI. A patogênese em praticamente todas as formas gira em torno de anormalidades quantitativas ou qualitativas da proteína mais abundante do osso, o colágeno tipo I. Mutações em um dos dois genes para as cadeias de procolágeno tipo I (COL1A1 e COL1A2) são responsáveis por defeito na sua biossíntese (1). apresentação de caso

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Changes in Bone Density With Lactation

Cited by 310 publications

References 50 publications

Changes in bone mineral density of adolescent mothers during the 12-month postpartum period

Changes in bone mineral density of adolescent mothers during the 12-month postpartum period

Irreversible Deterioration of Cortical and Trabecular Microstructure Associated With Breastfeeding

Osteogenesis imperfecta no adulto e resposta ao alendronato

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