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Unlabelled: Ethnic differences in bone mineral density (BMD) between healthy adult black and white South African women were studied. Higher BMD was only noted at the femoral sites in black women. Body weight significantly impacted these findings. A lower fracture risk at all skeletal sites cannot be assumed in black South African (SA) women., Purpose: Bone mineral density (BMD) varies amongst women of different ethnicities. African-Americans have higher BMD at all skeletal sites compared with whites. On the African continent, bone density studies suggest site-specific ethnic differences in BMD. To examine the contribution of body weight and lifestyle characteristics to ethnic differences in BMD between adult black and white South African women, we assessed lumbar spine (SBMD), femoral neck (FNBMD) and total femoral BMD (FTBMD) by dual-energy X-ray absorptiometry (DXA) in 184 black and 143 white women aged between 23 and 82 years., Methods: BMDs were compared amongst pre- and postmenopausal blacks and whites before and after adjustment for covariates with significant univariate association with BMD. Volumetric bone mineral apparent density (BMAD) of the spine and femoral neck was also calculated to account for ethnic differences in bone size., Results: Before adjustment, SBMD was lower (p < 0.05), FTBMD similar and FNBMD (p < 0.01) higher in premenopausal black women. Similar SBMD, but significantly higher BMD at the femoral sites (p < 0.01), was noted in postmenopausal blacks compared with whites. Amongst anthropometric measures and lifestyle factors, only adjustment for weight significantly altered these observed ethnic differences in bone density. After adjustment for weight, SBMD remained lower in premenopausal blacks and became lower in young postmenopausal blacks. Weight adjustment eliminated all ethnic differences in proximal femoral BMD measurements, with the exception of FNBMD that remained higher in younger postmenopausal blacks. Before adjustment, calculated SBMAD was similar and FNBMAD consistently higher in blacks in all the menstrual groups. Adjustment for weight did not alter these findings., Conclusion: Most of the observed ethnic difference in BMD was explained by differences in body weight between black and white SA women. The higher femoral BMD in older blacks may explain, the lower hip fracture prevalence in black South African women. The lower SBMD in pre- and postmenopausal black women in this study suggests that factors other than BMD should be considered to explain a lower vertebral fracture prevalence in blacks, if a lower fracture prevalence does indeed exist.

Statins have been postulated to affect bone metabolism. We investigated the effects of different doses of simvastatin (1, 5, 10, and 20 mg. kg(-1). d(-1)), atorvastatin (2.5 mg. kg(-1). d(-1)), and pravastatin (10 mg. kg(-1). d(-1)) administered orally for 12 weeks to intact female Sprague-Dawley rats and the effect of 20 mg. kg(-1). d(-1) simvastatin in sham-operated and ovariectomized rats on femoral bone mineral density (BMD) and quantitative bone histomorphometry (QBH) and compared them with controls. BMD was decreased by 1 mg. kg(-1). d(-1) simvastatin (P=0.042), atorvastatin (P=0.0002), and pravastatin (P=0.002). The effect on QBH parameters differed with different doses of simvastatin (ANOVA, P=0.00012). QBH parameters of both bone formation and resorption were equivalently and markedly increased by 20 mg. kg(-1). d(-1) simvastatin in 2 separate groups of intact rats and were reflected by a relatively unchanged BMD. At lower doses, 1 mg. kg(-1). d(-1) simvastatin decreased bone formation while increasing bone resorption, as reflected by a marked decrease in BMD. Ovariectomized animals receiving 20 mg. kg(-1). d(-1) simvastatin showed no change in BMD relative to the untreated, ovariectomized controls; their increase in bone formation was smaller than in sham-operated rats receiving simvastatin, and there was no change in bone resorption. Dose-response curves of simvastatin for bone formation and resorption differed. These studies indicate that (1) statins decrease BMD in rodents, (2) high-dose simvastatin increases bone formation and resorption, (3) low-dose simvastatin decreases bone formation and increases bone resorption, (4) the effects of simvastatin on QBH differ at different dosages, (5) the effects of simvastatin seen in intact rats are not observed in ovariectomized rats, and (6) simvastatin is unable to prevent bone loss caused by ovariectomy.

Purpose: Although fragility hip fractures (HF) in the South African (SA) population are among the lowest worldwide, the incidence of HF is expected to more than double over the next few decades. Little is known about the contributors to increased hip fracture risk, including low bone mineral density (BMD), in our unique population. In addition, the ability of the recently calibrated SA Fracture Risk Assessment Tool (FRAX) to identify high fracture risk in the SA population accurately has not been validated. Methods: A retrospective, descriptive, cohort study of SA postmenopausal women and men ≥ 50 years who presented with fragility HFs was conducted. The ability of clinical risk factors (CRFs) and BMD measured by dual-energy X-ray absorptiometry (DXA), as well as calculated FRAX probability scores, to identify the known high fracture risk in SA patients were evaluated. The SA FRAX tool was used, and a high fracture risk defined if the United States (US) fixed thresholds for major osteoporotic (MOF) and/or HF risk were exceeded (≥ 20% and ≥ 3% over 10 years respectively). Results: A total of 163 patients were included. The most useful predictive CRFs were age and gender, recreational toxins in men, and a history of falls. Most were females (71%), who were older than males. DXA-BMD and FRAX-HF calculations best identified the known high fracture risk in the study cohort. FRAX-MOF calculations performed poorly. Conclusion: Fracture risk assessment tools did not identify the known high fracture risk in all of the elderly study cohort with HF. Clinicians must continue to appreciate the important role of a good clinical assessment to ensure optimal fracture risk prediction. [ABSTRACT FROM AUTHOR]

In premenopausal women, bone mineral density measurement by dual-energy X-ray absorptiometry should not be used as the sole guide for diagnosis or treatment of osteoporosis, universal screening with bone mineral density is not advised and the World Health Organization classification of bone status should not be applied. A diagnosis of premenopausal osteoporosis is reserved for those with evidence of fragility and may also be considered in women with low bone mass and an ongoing secondary cause of osteoporosis. Idiopathic osteoporosis in young women is rare. A thorough evaluation of secondary causes is indicated in all patients, with glucocorticoid treatment a common secondary cause of low bone mass and osteoporosis. Hypoestrogenism may be the primary cause of low bone mass and contribute to excessive bone loss in many conditions associated with premenopausal osteoporosis, and should be treated unless contra-indicated. The mainstay of treatment in premenopausal females with low bone mass includes risk factor reduction, advocating a healthy, active lifestyle and optimal treatment of secondary causes of bone loss. The safety of bone-specific therapy, especially long term and during pregnancy, remains uncertain. Bisphosphonates, teriparatide, denosumab and estrogen treatment increase bone density in premenopausal women with osteoporosis, but there are no study data confirming short-term fracture prevention with use of these agents. [ABSTRACT FROM AUTHOR]

Increased bone resorption is a well-described consequence of primary hyperparathyroidism (PHPT). In South Africa, little is known about the impact of PHPT on skeletal health. To determine the prevalence of decreased bone mineral density (BMD), vertebral fractures and osteitis fibrosa cystica in patients with PHPT who underwent parathyroidectomy. Retrospective study of patients who underwent parathyroidectomy for PHPT at Tygerberg Hospital in Cape Town, from January 2010 to December 2019. Clinical, biochemical and BMD parameters are described. Final analysis included 56 patients (median age 63.5 years; 80.4% female). Initial calcium, parathyroid hormone (PTH) and 25-hydroxyvitamin D (25[OH]D) levels were 2.93 mmol/l, 19.4 pmol/l and 34.0 nmol/l, respectively. Of the total cohort, 71.4% had decreased BMD. The prevalence of osteoporosis and osteopenia in postmenopausal women and men ≥ 50 years was 50.0% and 39.1% respectively; low bone mass for age in premenopausal women and men < 50 years was 20.0%. Vertebral fractures were seen in 21.2% of patients on radiography. Osteitis fibrosa cystica was present in five patients (9.6%). PTH levels were significantly elevated in patients with osteoporosis compared with those with normal BMD (36.4 vs. 16.1 pmol/l; p = 0.02). Two-thirds of patients who underwent parathyroidectomy for PHPT had decreased BMD, with osteoporosis present in 50% of postmenopausal women and older men. One in five had vertebral fractures. These findings underscore the importance of skeletal assessment in the management of PHPT. [ABSTRACT FROM AUTHOR]