Quantitative Computed Tomography of Vertebral Spongiosa: A Sensitive Method for Detecting Early Bone Loss After Oophorectomy

Genant, Harry K.; Cann, Christopher E.; Ettinger, Bruce; Gordan, Gilbert S.

doi:10.1097/00003086-200003000-00002

Cited by 70 publications

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“…Based on these studies, it appears that there is a clear threshold for this relationship in cortical bone, but perhaps not in trabecular bone; or at least that the relationship between serum estradiol levels and cortical bone plateaus at much lower estradiol levels ( Figure 1A) than the relationship between serum estradiol levels and trabecular bone ( Figure 1B). These recent findings are, in fact, entirely consistent with earlier data using QCT which found that a 4-fold higher dose of estrogen was required to prevent trabecular as compared to cortical bone loss in women following oophorectomy [26] (Figure 2). Thus, there likely is a threshold below which the male or female skeleton develops estrogen deficiency, but this threshold appears to be much higher for trabecular as compared to cortical bone (i.e., it take more estrogen to prevent decreases in trabecular bone and less estrogen to prevent decreases in cortical bone).…”

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confidence: 90%

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Estrogen and bone: Insights from estrogen-resistant, aromatase-deficient, and normal men

Khosla

2008

Bone

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Findings from estrogen-resistant and aromatase-deficient men have provided important insights into the role of estrogen in the male skeleton during growth. Importantly, as reported elsewhere in this issue, these data also suggested dose-response relationships between estrogen and bone turnover. In addition, studies in these unusual patients have stimulated research on defining the role of estrogen in regulating bone metabolism in normal adult and aging men, providing further insights into estrogen regulation of bone metabolism not only in men, but also in women.1994 represents perhaps a watershed year in our thinking regarding sex steroids and the male skeleton. Prior to that, it was generally assumed that, similar to the critical role of estrogen in regulating bone metabolism in women [1], testosterone was the dominant (and perhaps only) sex steroid governing the maturation and maintenance of the male skeleton. However, a landmark case report published by Smith and colleagues [2] in the fall of 1994 forced a reevaluation of this longstanding dogma. The patient described in that report was a 28 year old male who initially presented to an orthopedic surgeon for evaluation of genu valgum ("knock knees"). As part of his evaluation, he had X-rays performed, which surprisingly showed unfused epiphyses. He was also very tall (6 ft 8 inches) and by history, had continued linear growth into adulthood. Pubertal development was otherwise normal, and through a series of astute studies, the investigators demonstrated elevated estradiol levels and homozygous mutations in his estrogen receptor (ER)α gene, which resulted in a non-functional ER. He also had markedly elevated values for bone turnover (resorption and formation) markers and osteopenia, with a spine bone mineral density (BMD) that was 3.1 SD below the mean for agematched normal women and more than 2 SD below the mean for 15 year old boys (the patient's bone age).This was truly a remarkable patient who focused attention away from testosterone and firmly on estrogen as perhaps critical for the development of the male skeleton. Thus, despite normal testosterone levels, by virtue of his complete resistance to estrogen, this patient had unfused epiphyses, no clear growth spurt but rather slow linear longitudinal growth into his late 20's, elevated bone turnover, and at least as assessed by dual energy X-ray absorptiometery, osteopenia. The inescapable conclusion was that even in males, estrogen was necessary for epiphyseal fusion, the pubertal growth spurt, and the acquisition of bone mass.Subsequent to this report, Carani et al. [3] and Bilezikian et al. [4] described two patients with a skeletal phenotype very similar to that of the ER-resistant male. However, in these patients, Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers

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confidence: 90%

“…Note that while cortical bone loss is prevented at an estrogen dose of 0.15 mg/d (panel A), four times this estrogen dose (0.6 mg/d) is required to prevent trabecular bone loss (panel B). Adapted from Genant et al [26], with permission.…”

mentioning

confidence: 99%

Estrogen and bone: Insights from estrogen-resistant, aromatase-deficient, and normal men

Khosla

2008

Bone

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“…Similar results were found by Maillefert et al who reported falls in bone density of 3% at 6 months, rising to 7% by 18 months. 19 This loss of bone density approximates to values seen in women following oopherectomy or post-menopause 20 and compares to a loss of 0.5% per year in normal age matched men. 21 In addition to bone density the risk of fracture relates to other factors including body mass, exercise and diet.…”

Section: Discussionmentioning

confidence: 61%

Bone loss associated with the use of LHRH agonists in prostate cancer

Peters¹,

Fairney

Kyd

et al. 2001

Prostate Cancer Prostatic Dis

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Hypogonadism is a recognised cause of osteoporosis in men. When patients with advanced prostate cancer are treated with luteinising hormone releasing hormone (LHRH) agonist analogues their circulating testosterone levels decline and these patients may develop fractures.We have undertaken a cross-sectional study on a cohort of patients treated with goserelin (n ¼ 41) and compared their bone density and bone turnover with patients with prostate cancer not on goserelin and elderly patients living in the community.There was no difference in bone density between the patients on treatment and those living in the community and there was a similar incidence of osteoporosis (50 and 42%, respectively). The bone marker measurements were higher in the treated patients: urine N-telopeptide (NTX) 80.1 (9) (mean (s.e.)) BCE/mmol, compared to 30.1 (2.9), P < 0.001 in elderly patients; and bone alkaline phosphatase 41.9 (6.1) u/l in treated patients and 20.7 (1.5) in untreated prostate cancer patients, P < 0.002. Patients on treatment with radionuclide scan evidence of metastases did not have higher bone marker values than those with negative scans.As increased bone turnover and low bone density are associated with enhanced risk of osteoporotic fractures, we suggest that patients on LHRH agonist analogues should receive advice and possibly anti-bone resorptive treatment with bisphosphonates to prevent further bone loss and fractures. Prostate Cancer and Prostatic Diseases (2001) 4, 161-166.

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“…There was a strong variation in the bone annual loss rate in the study cohort with different age and clinical implications. Overall, the trabecular bone has a 3-10 fold bone loss rate compared to the cortical bone [76,95,[97][98][99].…”

Section: Comparing the Bone Loss Rate Between The Trabecular And Cortmentioning

confidence: 99%

Application of quantitative computed tomography for assessment of trabecular bone mineral density, microarchitecture and mechanical property

et al. 2016

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a b s t r a c t a r t i c l e i n f oOsteoporosis is a common metabolic bone disease, causing increased skeletal fragility characterized by a low bone mass and trabecular microarchitectural deterioration. Assessment of the bone mineral density (BMD) is the primary determinant of skeletal fragility. Computed tomography (CT)-based trabecular microarchitectural and mechanical assessments are important methods to evaluate the skeletal strength. In this review, we focus the feasibility of QCT BMD measurement using a calibration phantom or phantomless. The application of QCT could extend the bone mineral density assessment to all patients who underwent a heart, lung, whole-body, and as well as all routine clinical implications of CT scan.

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Quantitative Computed Tomography of Vertebral Spongiosa: A Sensitive Method for Detecting Early Bone Loss After Oophorectomy

Cited by 70 publications

References 0 publications

Estrogen and bone: Insights from estrogen-resistant, aromatase-deficient, and normal men

Estrogen and bone: Insights from estrogen-resistant, aromatase-deficient, and normal men

Bone loss associated with the use of LHRH agonists in prostate cancer

Application of quantitative computed tomography for assessment of trabecular bone mineral density, microarchitecture and mechanical property

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