Extracellular pH regulates bone cell function

The skeletons of land vertebrates contain a massive reserve of alkaline mineral (hydroxyapatite), which is ultimately available to buffer metabolic H+ if acid-base balance is not maintained within narrow limits. The negative impact of acidosis on the skeleton has long been known but was thought to result from passive, physicochemical dissolution of bone mineral. This brief, selective review summarizes what is now known of the direct functional responses of bone cells to extracellular pH. We discovered that bone resorption by cultured osteoclasts is stimulated directly by acid. The stimulatory effect is near-maximal at pH 7.0, whereas above pH 7.4, resorption is switched off. In bone organ cultures, H+-stimulated bone mineral release is almost entirely osteoclast-mediated, with a negligible physicochemical component. Acidification is the key requirement for osteoclasts to excavate resorption pits in all species studied to date, and extracellular H+ may thus be regarded as the long-sought osteoclast activation factor. Acid-activated osteoclasts can be stimulated further by agents such as parathyroid hormone, 1,25-dihydroxycholecalciferol, and receptor activator of nuclear factor kappaB ligand. Osteoclasts may respond to pH changes via H+-sensing ion channels such as transient receptor potential vanilloid 1, a nociceptor that is also activated by capsaicin. Acidosis also exerts a powerful, reciprocal inhibitory effect on the mineralization of bone matrix by cultured osteoblasts. This is caused by increased hydroxyapatite solubility at low pH, together with selective inhibition of alkaline phosphatase, which is required for mineralization. Diets or drugs that shift acid-base balance in the alkaline direction may provide useful treatments for bone loss disorders.     

Acid-base imbalance and the skeleton

Summary Humans generally consume a diet that generates metabolic acids leading to a reduction in the concentration of systemic bicarbonate and a fall in pH. In vitro experiments indicate that this metabolic acidosis causes a release of calcium from bone that initially is simply due to physicochemical dissolution of the mineral. On a more chronic basis metabolic acidosis alters bone cell function; there is an increase in osteoclastic bone resorption and a decrease in osteoblastic bone formation. Concomitant with the dissolution and resorption of the bone mineral there is buffering of the addition protons by bone leading to restoration of the systemic pH. Interestingly respiratory acidosis, caused by an increase in the partial pressure of carbon dioxide induces far less bone dissolution and resorption and the additional hydrogen ions are not buffered by bone. As we age we are less able to excrete these metabolic acids due to the normal decline in renal function. We hypothesize that a slight, but significant, metabolic acidosis leads to greater loss of bone mineral and increase potential to fracture. Received: 13 September 2001, Accepted: 20 September 2001     

Lycopene I--effect on osteoclasts: lycopene inhibits basal and parathyroid hormone-stimulated osteoclast formation and mineral resorption mediated by reactive oxygen species in rat bone marrow cultures

Osteoclasts have been shown to produce reactive oxygen species (ROS) that can stimulate bone resorption. We explored the hypothesis that lycopene, the antioxidant carotenoid from tomatoes, can inhibit mineral resorption by inhibiting osteoclast formation and the production of ROS. Cells from bone marrow prepared from rat femur were plated into 16-well calcium phosphate-coated Osteologic Multi-test Slides and cultured in alpha-minimal essential medium supplemented with dexamethasone, beta-glycerophosphate, and ascorbic acid. The cells were treated with varying doses of lycopene in the absence or presence of parathyroid hormone (PTH) at the start of culture and at each medium change (i.e., every 48 hours). On day 8, mineral resorption pits were quantitated. Similar, parallel experiments were carried out in 12-well plastic dishes to assess tartrate-resistant acid phosphatase (TRAP) activity. Results showed that lycopene inhibited TRAP + formation of multinucleated cells in both vehicle- and PTH-treated cultures. Osteoclasts reduced nitroblue tetrazolium (NBT) to purple-colored formazan, indicating the presence of ROS in these cells. The formazan-staining cells were decreased by treatment with 10(-5) M lycopene, indicating that lycopene inhibited the formation of ROS-secreting osteoclasts. In conclusion, we have shown that lycopene inhibits basal and PTH-stimulated osteoclastic mineral resorption and formation of TRAP + multinucleated osteoclasts, as well as the ROS produced by osteoclasts. These findings are novel and may be important in the pathogenesis, treatment, and prevention of osteoporosis.     

Nutrition Society Medal lecture. The role of the skeleton in acid-base homeostasis

Nutritional strategies for optimising bone health throughout the life cycle are extremely important, since a dietary approach is more popular amongst osteoporosis sufferers than drug intervention, and long-term drug treatment compliance is relatively poor. As an exogenous factor, nutrition is amenable to change and has relevant public health implications. With the growing increase in life expectancy, hip fractures are predicted to rise dramatically in the next decade, and hence there is an urgent need for the implementation of public health strategies to target prevention of poor skeletal health on a population-wide basis. The role that the skeleton plays in acid-base homeostasis has been gaining increasing prominence in the literature; with theoretical considerations of the role alkaline bone mineral may play in the defence against acidosis dating as far back as the late 19th century. Natural, pathological and experimental states of acid loading and/or acidosis have been associated with hypercalciuria and negative Ca balance and, more recently, the detrimental effects of 'acid' from the diet on bone mineral have been demonstrated. At the cellular level, a reduction in extracellular pH has been shown to have a direct enhancement on osteoclastic activity, with the result of increased resorption pit formation in bone. A number of observational, experimental, clinical and intervention studies over the last decade have suggested a positive link between fruit and vegetable consumption and the skeleton. Further research is required, particularly with regard to the influence of dietary manipulation using alkali-forming foods on fracture prevention. Should the findings prove conclusive, a 'fruit and vegetable' approach to bone health maintenance may provide a very sensible (and natural) alternative therapy for osteoporosis treatment, which is likely to have numerous additional health-related benefits.     

水溶性大豆异黄酮对破骨细胞分化和功能的影响

目的:研究水溶性大豆异黄酮(WSSI)对1,25-二羟基维生素D3诱导兔骨髓细胞分化形成破骨细胞样细胞以及兔成熟破骨细胞骨吸收功能的影响。方法:通过TRAP染色对骨髓细胞诱导分化形成的TRAP阳性多核巨细胞计数;用显微摄影结合计算机图像分析测定骨吸收造成的陷窝数目及表面积,以评价破骨细胞活性;用扫描电镜观察骨吸收陷窝的形态。结果:浓度为20.0、4.0、2.0和0.4μg/ml的水溶性大豆异黄酮既能抑制破骨细胞样细胞的形成(P<0.001),还能抑制成熟破骨细胞的骨吸收功能(P<0.001),具体表现在随着浓度的升高骨吸收陷窝数目及表面积减少。结论:WSSI可以明显抑制破骨细胞样细胞的形成和成熟破骨细胞的骨吸收功能。     

Effects of oligofructose-enriched inulin on intestinal absorption of calcium and magnesium and bone turnover markers in postmenopausal women

Deficiency of oestrogen at menopause decreases intestinal Ca absorption, contributing to a negative Ca balance and bone loss. Mg deficiency has also been associated with bone loss. The purpose of the present investigation was to test the hypothesis that treatment with a spray-dried mixture of chicory oligofructose and long-chain inulin (Synergy1; SYN1) would increase the absorption of both Ca and Mg and alter markers of bone turnover. Fifteen postmenopausal women (72.2 (SD 6.4) years) were treated with SYN1 or placebo for 6 weeks using a double-blind, placebo-controlled, cross-over design. Fractional Ca and Mg absorption were measured using dual-tracer stable isotopes before and after treatment. Bone turnover markers were measured at baseline, 3 and 6 weeks. Fractional absorption of Ca and Mg increased following SYN1 compared with placebo (P < 0.05). Bone resorption (by urinary deoxypyridinoline cross-links) was greater than baseline at 6 weeks of active treatment (P < 0.05). Bone formation (by serum osteocalcin) showed an upward trend at 3 weeks and an increase following 6 weeks of SYN1 (P < 0.05). Closer examination revealed a variation in response, with two-thirds of the subjects showing increased absorption with SYN1. Post hoc analyses demonstrated that positive responders had significantly lower lumbar spine bone mineral density than non-responders (dual X-ray absorptiometry 0.887 +/- 0.102 v. 1.104 +/- 0.121 g/cm2; P < 0.01), and changes in bone turnover markers occurred only in responders. These results suggest that 6 weeks of SYN1 can improve mineral absorption and impact markers of bone turnover in postmenopausal women. Further research is needed to determine why a greater response was found in women with lower initial spine bone mineral density.     

Energy regulation by the skeleton

Bones of the skeleton are constantly remodeled through bone resorption by cells called osteoclasts and bone formation by cells called osteoblasts. Both cell types are under multi-hormone control. New research findings demonstrate that bone formation by osteoblasts is negatively regulated by the hormone leptin, which is secreted by adipocytes and acts through the leptin receptor in the central nervous system and ultimately through the sympathetic nervous system. Leptin deficiency leads to increased osteoblast activity and increased bone mass. Reciprocally, expression of the Esp gene, exclusive to osteoblasts, regulates glucose homeostasis and adiposity through controlling the osteoblastic secretion of the hormone-like substance osteocalcin. An undercarboxylated form of osteocalcin acts as a regulator of insulin in the pancreas and adiponectin in the adipocyte to modulate energy metabolism. Osteocalcin deficiency in knockout mice leads to decreased insulin and adiponectin secretion, insulin resistance, higher serum glucose levels and increased adiposity.     

Diet, evolution and aging

Theoretically, we humans should be better adapted physiologically to the diet our ancestors were exposed to during millions of years of hominid evolution than to the diet we have been eating since the agricultural revolution a mere 10,000 years ago, and since industrialization only 200 years ago. Among the many health problems resulting from this mismatch between our genetically determined nutritional requirements and our current diet, some might be a consequence in part of the deficiency of potassium alkali salts (K-base), which are amply present in the plant foods that our ancestors ate in abundance, and the exchange of those salts for sodium chloride (NaCl), which has been incorporated copiously into the contemporary diet, which at the same time is meager in K-base-rich plant foods. Deficiency of K-base in the diet increases the net systemic acid load imposed by the diet. We know that clinically-recognized chronic metabolic acidosis has deleterious effects on the body, including growth retardation in children, decreased muscle and bone mass in adults, and kidney stone formation, and that correction of acidosis can ameliorate those conditions. Is it possible that a lifetime of eating diets that deliver evolutionarily superphysiologic loads of acid to the body contribute to the decrease in bone and muscle mass, and growth hormone secretion, which occur normally with age? That is, are contemporary humans suffering from the consequences of chronic, diet-induced low-grade systemic metabolic acidosis? Our group has shown that contemporary net acid-producing diets do indeed characteristically produce a low-grade systemic metabolic acidosis in otherwise healthy adult subjects, and that the degree of acidosis increases with age, in relation to the normally occurring age-related decline in renal functional capacity. We also found that neutralization of the diet net acid load with dietary supplements of potassium bicarbonate (KHCO3) improved calcium and phosphorus balances, reduced bone resorption rates, improved nitrogen balance, and mitigated the normally occurring age-related decline in growth hormone secretion--all without restricting dietary NaCl. Moreover, we found that co-administration of an alkalinizing salt of potassium (potassium citrate) with NaCl prevented NaCl from increasing urinary calcium excretion and bone resorption, as occurred with NaCl administration alone. Earlier studies estimated dietary acid load from the amount of animal protein in the diet, inasmuch as protein metabolism yields sulfuric acid as an end-product. In cross-cultural epidemiologic studies, Abelow found that hip fracture incidence in older women correlated with animal protein intake, and they suggested a causal relation to the acid load from protein. Those studies did not consider the effect of potential sources of base in the diet. We considered that estimating the net acid load of the diet (i. e., acid minus base) would require considering also the intake of plant foods, many of which are rich sources of K-base, or more precisely base precursors, substances like organic anions that the body metabolizes to bicarbonate. In following up the findings of Abelow et al., we found that plant food intake tended to be protective against hip fracture, and that hip fracture incidence among countries correlated inversely with the ratio of plant-to-animal food intake. These findings were confirmed in a more homogeneous population of white elderly women residents of the U.S. These findings support affirmative answers to the questions we asked above. Can we provide dietary guidelines for controlling dietary net acid loads to minimize or eliminate diet-induced and age-amplified chronic low-grade metabolic acidosis and its pathophysiological sequelae. We discuss the use of algorithms to predict the diet net acid and provide nutritionists and clinicians with relatively simple and reliable methods for determining and controlling the net acid load of the diet. A more difficult question is what level of acidosis is acceptable. We argue that any level of acidosis may be unacceptable from an evolutionarily perspective, and indeed, that a low-grade metabolic alkalosis may be the optimal acid-base state for humans.     

中枢性性早熟女童GnRHa治疗后骨代谢指标变化的临床研究

目的 探讨中枢性性早熟(CPP)女童GnRHa治疗后骨代谢指标的动态变化情况和临床意义,为临床治疗提供科学依据。方法 选取2015年10月-2016年6月在昆明市儿童医院接受GnRHa治疗的36例中枢性性早熟女童和36例健康女童作为对照,检测治疗前和治疗后6、12、18、24个月两组女童常见的血清骨营养指标、骨形成和骨吸收标志物水平,比较组间和不同时点各指标的差异。结果 研究结束,观察组失访5例(失访率13.89%),对照组失访4例(失访率11.11%)。血Ca、P、25-(OH)D₃、β-CTX4Ⅲ项指标治疗后各时点与治疗前差异无统计学意义(P>0.05),各时点组间比较差异无统计学意义(P＞0.05),血E2、N-MID OC、P1NP、BALP4Ⅲ项指标治疗后逐渐下降,且各时点组间比较差异有统计学意义(P<0.05)。结论 GnRHa治疗的最初12月内,患儿雌激素水平下降较明显。GnRHa对成骨细胞的作用较破骨细胞明显     

The effects of zinc and calcium deficiencies on the rate of bone resorption in the rat

An effect of zinc deficiency on bone resorption was assessed in rats, by measuring the rate of resorption in rapidly growing animals and a pathologically increased resorption secondary to calcium deficiency. Bone resorption was quantitated by the loss of ³H-tetracycline from previously labeled bone. There was no effect of zinc deficiency on bone resorption in either normally growing or calcium deficient animals. Calcium deficiency alleviated the effect of zinc deficiency on body weight. In calcium deficient animals, bone zinc concentration was almost double that of calcium supplemented animals, suggesting a partial substitution of zinc for calcium in bone mineral.     

Effects of mushroom, Pleurotus eryngii, extracts on bone metabolism

We performed the present study to investigate whether Pleurotus eryngii extracts (PEX) play a role in bone metabolism. PEX treatment showed increase in the alkaline phosphatase activity of the osteoblasts and in the osteocalcin mRNA expression from primary osteoblasts. PEX also increased the expression of the Runx2 gene, and the secretion of osteoprotegerin from the osteoblasts showed marked increases after treatment with PEX. In addition, PEX treatment decreased the number of tartrate-resistant acid phosphatase (TRAP)-positive multinucleated cells and resorption areas. In vivo studies, using rats with ovariectomy-induced osteoporosis revealed that PEX alleviated the decrease in the trabecular bond mineral density.     

Bone and gastric bypass surgery: effects of dietary calcium and vitamin D

OBJECTIVE: To examine bone mass and metabolism in women who had previously undergone Roux-en-Y gastric bypass (RYGB) and determine the effect of supplementation with calcium (Ca) and vitamin D. RESEARCH METHODS AND PROCEDURES: Bone mineral density and bone mineral content (BMC) were examined in 44 RYGB women (> or = 3 years post-surgery; 31% weight loss; BMI, 34 kg/m(2)) and compared with age- and weight-matched control (CNT) women (n = 65). In a separate analysis, RYGB women who presented with low bone mass (n = 13) were supplemented to a total 1.2 g Ca/d and 8 microg vitamin D/d over 6 months and compared with an unsupplemented CNT group (n = 13). Bone mass and turnover and serum parathyroid hormone (PTH) and 25-hydroxyvitamin D were measured. RESULTS: Bone mass did not differ between premenopausal RYGB and CNT women (42 +/- 5 years), whereas postmenopausal RYGB women (55 +/- 7 years) had higher bone mineral density and BMC at the lumbar spine and lower BMC at the femoral neck. Before and after dietary supplementation, bone mass was similar, and serum PTH and markers of bone resorption were higher (p < 0.001) in RYGB compared with CNT women and did not change significantly after supplementation. DISCUSSION: Postmenopausal RYGB women show evidence of secondary hyperparathyroidism, elevated bone resorption, and patterns of bone loss (reduced femoral neck and higher lumbar spine) similar to other subjects with hyperparathyroidism. Although a modest increase in Ca or vitamin D does not suppress PTH or bone resorption, it is possible that greater dietary supplementation may be beneficial.     

Glucocorticoid-induced osteoporosis

Chronic glucocorticoid treatment is the most frequent cause of secondary osteoporosis. The direct inhibitory effect of glucocorticoids on osteoblasts results in decreased bone formation. Increased osteoclastic bone resorption due to low concentrations of gonadal steroid hormones and glucocorticoid-induced direct suppression of intestinal calcium absorption also contribute to the decrease of bone mass in these patients. Bone loss is rapid, particularly in the first months of glucocorticoid therapy. Bone mineral density of the lumbar spine and proximal femur should be measured in patients who are starting chronic therapy with glucocorticoids. Although glucocorticoid-induced osteoporosis is a severe and nowadays partially preventable disorder, osteoporosis prophylaxis is only rarely prescribed to these patients. Recent randomized, controlled trials proved the therapeutic effects of hormone replacement therapy, as well as of bisphosphonates and active vitamin D analogs in primary and secondary prevention of glucocorticoid-induced osteoporosis.     

Effects of local and overall vibration on bone mineral density and phosphorus and calcium metabolism]

The authors studies bone mineral density (BMD) was studied by ultrasound densitometry of the calcaneus on an Achilles + device (Lunar, USA) and phosphorus and calcium metabolism in patients with vibration disease. The patients' age ranged from 41 to 61 years. A control group comprised 88 healthy males of the same age. Long-term exposure to systemic and local vibration causes a reduction in the mineral density of bony tissue in the presence of slightly enhanced bone resorption.     

Estrogen Receptor 1 (ESR1) and the Wnt/β-Catenin Pathway Mediate the Effect of the Coumarin Derivative Umbelliferon on Bone Mineralization

Bone physiology is regulated by osteoblast and osteoclast activities, both involved in the bone remodeling process, through deposition and resorption mechanisms, respectively. The imbalance between these two phenomena contributes to the onset of bone diseases. Among these, osteoporosis is the most common metabolic bone disorder. The therapies currently used for its treatment include antiresorptive and anabolic agents associated with side effects. Therefore, alternative therapeutic approaches, including natural molecules such as coumarin and their derivatives, have recently shown positive results. Thus, our proposal was to investigate the effect of the coumarin derivative umbelliferon (UF) using an interesting model of human osteoblasts (hOBs) isolated from osteoporotic patients. UF significantly improved the activity of osteoporotic-patient-derived hOBs via estrogen receptor 1 (ESR1) and the downstream activation of β-catenin pathway. Additionally, hOBs were co-cultured in microgravity with human osteoclasts (hOCs) using a 3D system bioreactor, able to reproduce the bone remodeling unit in bone loss conditions in vitro. Notably, UF exerted its anabolic role by reducing the multinucleated cells. Overall, our study confirms the potential efficacy of UF in bone health, and identified, for the first time, a prospective alternative natural compound useful to prevent/treat bone loss diseases such as osteoporosis.     

Inhalation of diesel engine exhaust increases bone mineral concentrations in growing rats

Experiments were conducted to determine whether diesel engine exhaust affects bone metabolism in growing rats. The rats were assigned to three groups: those exposed to total diesel engine exhaust with 5.63 mg/m³ particulate matter, 4.10 ppm nitrogen dioxide, 8.10 ppm nitrogen monoxide; those exposed to filtered exhaust without particulate matter; and those exposed to clean air. Dosing experiments were performed for 3 months beginning at birth (6 h/day for 5 days/week). Bone mineral content (BMC) values in lumbar vertebral bone were significantly increased in both groups exposed to diesel exhaust (P<0.01) compared to that of rats exposed to clean air. Bone mineral density (BMD) values were also significantly increased in both exposed groups, total exhaust (P<0.01) and filtered exhaust (P<0.001), compared to that of rats exposed to clean air. BMD values in the mid-femur were also significantly greater in animals exposed to diesel exhaust, total exhaust (P<0.05), and filtered exhaust (P<0.01), compared to that of those exposed to clean air. Urinary excretion of deoxypyridinolines, a biochemical marker for bone resorption, was significantly reduced in animals exposed to total diesel exhaust and filtered exhaust (P<0.001, P<0.01) compared to control. There was also a significant difference between the two exposure groups of diesel exhaust (P<0.05). Since these effects were not inhibited by filtration, the gaseous phase of the exhaust was considered more responsible than particulate matter for reducing bone resorption.     

Skeletal unloading and dietary copper depletion are detrimental to bone quality of mature rats

This study was designed to examine the skeletal response to copper depletion and mechanical unloading in mature animals. In a 2 x 2 experimental design, 5.5-mo-old male Sprague-Dawley rats (n = 36) consumed either the control (AIN-93M) or Cu-depletion ((-)Cu) diet beginning 21 d before suspension and throughout the remainder of the study. Half of the rats in each dietary treatment group were either tail-suspended (TS) or kept ambulatory (AMB) for 28 d. Lower bone mineral densities (BMD) of 5th lumbar vertebra (L5) (P < 0.05) and femur were observed with (-)Cu and TS, but no differences were noted in the BMD of the humerus. Mechanical strength in the femur and vertebra decreased in response to TS, but were unaffected by copper depletion. Urinary deoxypyridinoline, an index of bone resorption, was significantly greater in TS rats, but unaltered by (-)Cu. No changes in serum or bone alkaline phosphatase activity, an indicator of bone formation, were observed. Our findings suggest that TS and (-)Cu decreased BMD in unloaded femur and vertebra but had no effect on normally loaded humerus. Bone loss with TS appeared to be related to accelerated bone resorption. Alterations in bone metabolism and bone mechanical properties in the mature skeleton resulting from (-)Cu warrant further investigation.     

Experimental evidence for the effects of calcium and vitamin D on bone: a review

Animal models fed low calcium diets demonstrate a negative calcium balance and gross bone loss while the combination of calcium deficiency and oophorectomy enhances overall bone loss. Following oophorectomy the dietary calcium intake required to remain in balance increases some 5 fold, estimated to be approximately 1.3% dietary calcium. In the context of vitamin D and dietary calcium depletion, osteomalacia occurs only when low dietary calcium levels are combined with low vitamin D levels and osteoporosis occurs with either a low level of dietary calcium with adequate vitamin D status or when vitamin D status is low in the presence of adequate dietary calcium intake. Maximum bone architecture and strength is only achieved when an adequate vitamin D status is combined with sufficient dietary calcium to achieve a positive calcium balance. This anabolic effect occurs without a change to intestinal calcium absorption, suggesting dietary calcium and vitamin D have activities in addition to promoting a positive calcium balance. Each of the major bone cell types, osteoblasts, osteoclasts and osteocytes are capable of metabolizing 25 hydroxyvitamin D (25D) to 1,25 dihydroxyvitamin D (1,25D) to elicit biological activities including reduction of bone resorption by osteoclasts and to enhance maturation and mineralization by osteoblasts and osteocytes. Each of these activities is consistent with the actions of adequate circulating levels of 25D observed in vivo.     

Change in maternal bone mineral density during pregnancy and relationship between the density and foetus growth--a prospective study

In order to study change in maternal bone mineral density during pregnancy and its relationships with bone metabolism and maternal perinatal factors including foetus growth, bone mineral density and bone metabolic markers were measured in 45 pregnant women aged 26-35 years. Specifically, bone mineral density was measured twice, first at 8-20 weeks of gestation and secondly within two weeks postpartum by ultrasonic bone densitometry, while bone metabolic markers were assessed at 8-20 and 26-30 weeks of gestation and at one week postpartum. Bone mineral density and metabolic markers were also examined in 35 non-pregnant controls, twice with a six-month interval. The results of the measurements and subsequent examinations based thereon were as follows: 1. Stiffness as an index of bone density decreased significantly during pregnancy (mean: -4.3%), with wide variation among individuals (-20%-(+)11%). Stiffness in controls did not show any significant change within the 6 months. 2. During pregnancy, bone alkaline phosphatase and osteocalcin levels were significantly lower while urinary hydroxyproline levels (H.P/Cre) were significantly higher than in controls. Significant negative correlations were found between change rate in stiffness and HP/Cre measured at second trimester and postpartum. These results indicate that bone formation is reduced while bone resorption is increased during pregnancy, and that stiffness index reflects the extent of bone resorption. 3. Pre-pregnancy BMI and weight gain during pregnancy could not be linked with change in bone mineral density. 4. The women with greater bone density demonstrated a greater extent of loss postpartum. 5. Postpartum bone mineral density showed a significant, positive correlation with baby birth weight and height. Higher preservation of maternal bone mass is important not only for the mother's health but also for the baby's. Ultrasonic bone densitometry was found to be useful for measuring bone mineral density because it could detect small changes during pregnancy reflecting bone metabolism.