Emeritus Faculty, Acad Council, Medicine - Endocrinology, Gerontology, & Metabolism
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RETIRED in 2008, do not conduct research
To determine the effect of alendronate (ALN) and teriparatide on trabecular bone score (TBS) in patients with glucocorticoid-induced osteoporosis.Patients with chronic glucocorticoid therapy-induced osteoporosis (median 7.5 mg/day prednisone equivalent for ?90 days) were randomized to receive oral ALN 10 mg/day (n?=?214) or subcutaneous teriparatide 20 ?g/day (n?=?214) for 36 months; 118 patients in the ALN group and 123 patients in the teriparatide group completed treatment. Dual x-ray absorptiometry (DXA) results for 53 patients receiving ALN and 56 patients receiving teriparatide who had DXA scans with adequate resolution to perform TBS analysis and completed 36 months of therapy were blindly analyzed for TBS at baseline and 3, 6, 12, 18, 24, and 36 months.In teriparatide-treated patients, TBS was significantly increased at 18 months compared to baseline, and by 36 months had increased 3.7% (P?0.05). In ALN-treated patients, there was not a significant change in TBS compared to baseline at any time point. Changes in lumbar spine bone mineral density (BMD) measured by DXA in the subgroup with TBS data were similar to BMD results in the overall study population. At 36 months, increases in lumbar spine BMD were 5.5% and 10.3% in patients treated with ALN and teriparatide, respectively.In patients with glucocorticoid-induced osteoporosis, both ALN and teriparatide increased lumbar spine BMD. However, trabecular bone score significantly increased with teriparatide but did not significantly change with ALN. The pathogenesis of glucocorticoid-induced osteoporosis is predominantly reduced bone formation. TBS may represent a sensitive measure to discriminate treatment effects of an anabolic versus an antiresorptive drug in glucocorticoid-induced osteoporosis.
View details for DOI 10.1002/art.39726
View details for Web of Science ID 000383498800010
View details for PubMedID 27111239
To examine the relationship between severity grade for radiography, triple-phase technetium 99m nuclear medicine bone scanning, magnetic resonance (MR) imaging, and computed tomography (CT); clinical severity; and recovery time from a tibial stress injury (TSI), as well as to evaluate interassessor grading reliability.This protocol was approved by the Griffith University Human Research Ethics Committee, the Stanford University Panel on Human Subjects in Medical Research, the U.S. Army Human Subjects Research Review Board, and the Australian Defense Human Research Ethics Committee. Informed consent was obtained from all subjects. Forty subjects (17 men, 23 women; mean age, 26.2 years ± 6.9 [standard deviation]) with TSI were enrolled. Subjects were examined acutely with standard anteroposterior and lateral radiography, nuclear medicine scanning, MR imaging, and CT. Each modality was graded by four blinded clinicians. Mixed-effects models were used to examine associations between image severity, clinical severity, and time to healing, with adjustments for image modality and assessor. Grading reliability was evaluated with the Cronbach ? coefficient.Image assessment reliability was high for all grading systems except radiography, which was moderate (? = 0.565-0.895). Clinical severity was negatively associated with MR imaging severity (P ? .001). There was no significant relationship between time to healing and severity score for any imaging modality, although a positive trend existed for MR imaging (P = .07).TSI clinical severity was negatively related to MR imaging severity. Radiographic, bone scan, and CT severity were not related to time to healing, but there was a positive trend for MR imaging.
View details for DOI 10.1148/radiol.12102426
View details for Web of Science ID 000304416900023
View details for PubMedID 22623695
Tibial stress fractures increasingly affect athletes and military recruits, with few known effective management options. Electrical stimulation enhances regular fracture healing, but the effect on stress fractures has not been definitively tested.Capacitively coupled electric field stimulation will accelerate tibial stress fracture healing.Randomized controlled trial; Level of evidence, 1.Twenty men and 24 women with acute posteromedial tibial stress fractures were referred from local clinicians. Subjects were randomly assigned active or placebo capacitively coupled electric field stimulation to be applied for 15 hours per day until healed, given supplemental calcium, and instructed to rest from provocative training. Healing was confirmed when hopping to 10 cm for 30 seconds could be achieved without pain.No difference in time to healing was detected between treatment and placebo groups. Women in the treatment group healed more slowly than did the men (P = .05). Superior treatment compliance was associated with reduced time to healing (P = .003). Rest noncompliance was associated with increased time to healing (P = .05).Whole-group analysis did not detect an effect of capacitively coupled electric field stimulation on tibial stress fracture healing; however, greater device use and less weightbearing loading enhanced the effectiveness of the active device. More severe stress fractures healed more quickly with capacitively coupled electric field stimulation.Although the use of capacitively coupled electric field stimulation for tibial stress fracture healing may not be efficacious for all, it may be indicated for the more severely injured or elite athlete/recruit whose incentive to return to activity may motivate superior compliance.
View details for DOI 10.1177/0363546507310076
View details for Web of Science ID 000253374000016
View details for PubMedID 18055921
We examined the association between endogenous sex hormones (estradiol, estrone, testosterone, and SHBG) and coronary heart disease (CHD) in white male twins. Stored plasma samples were available for 566 participants of the National Heart, Lung, and Blood Institute Twin Study, a longitudinal study of cardiovascular disease in male twins. Twenty-eight of these individuals were lost to follow-up, and outcome data were missing. Of the remaining 538 participants, 78 had CHD at baseline, and 154 subsequently developed CHD over 20 yr of follow-up. We observed no differences in mean unadjusted or age- and body mass index-adjusted log-transformed sex hormone concentrations for participants with and without CHD (all P > 0.08). Quartile and median split analyses revealed no significant association between any of the sex hormones and either prevalent or incident CHD. The discordant monozygotic twins showed no significant case-control group difference in estradiol, estrone, testosterone, and SHBG (all P > 0.3). The positive and negative concordant twin pairs had similar values for each of the sex hormones (all P > 0.3). We observed no relationship between endogenous sex hormone concentrations and prevalent or incident CHD in this sample of male twins.
View details for PubMedID 15001617
To examine the relationships between disordered eating, menstrual irregularity, and low bone mineral density (BMD) in young female runners.Subjects were 91 competitive female distance runners aged 18-26 yr. Disordered eating was measured by the Eating Disorder Inventory (EDI). Menstrual irregularity was defined as oligo/amenorrhea (0-9 menses per year). BMD was measured by dual x-ray absorptiometry.An elevated score on the EDI (highest quartile) was associated with oligo/amenorrhea, after adjusting for percent body fat, age, miles run per week, age at menarche, and dietary fat, (OR [95% CI]: 4.6 [1.1-18.6]). Oligo/amenorrheic runners had lower BMD than eumenorrheic runners at the spine (-5%), hip (-6%), and whole body (-3%), even after accounting for weight, percent body fat, EDI score, and age at menarche. Eumenorrheic runners with elevated EDI scores had lower BMD than eumenorrheic runners with normal EDI scores at the spine (-11%), with trends at the hip (-5%), and whole body (-5%), after adjusting for differences in weight and percent body fat. Runners with both an elevated EDI score and oligo/amenorrhea had no further reduction in BMD than runners with only one of these risk factors.In young competitive female distance runners, (i) disordered eating is strongly related to menstrual irregularity, (ii) menstrual irregularity is associated with low BMD, and (iii) disordered eating is associated with low BMD in the absence of menstrual irregularity.
View details for DOI 10.1249/01.MSS.0000064935.68277.E7
View details for PubMedID 12750578
Antiresorptive treatments for postmenopausal osteoporosis have been studied extensively, but due to the volume of published data and lack of head-to-head trials, it is difficult to evaluate and compare their fracture reduction efficacy. The objective of this review is to summarize the results from clinical trials that have fracture as an endpoint and to discuss the factors in study design and populations that can affect the interpretation of the results. Although there are numerous observational studies suggesting that estrogen and hormone replacement therapies may reduce the risk of vertebral and nonvertebral fractures, there is no large, prospective, randomized, placebo-controlled, double-blind clinical trial demonstrating fracture efficacy. The effects of raloxifene, alendronate, risedronate, and salmon calcitonin on increasing bone mineral density (BMD) and decreasing fracture risk have been shown in randomized, placebo-controlled, double-blind clinical trials of postmenopausal women with osteoporosis. Although the increases in lumbar spine BMD vary greatly in these trials, the decrease in relative risk of vertebral fractures is similar among therapies. However, nonvertebral fracture efficacy has not been consistently demonstrated. Combined administration of two antiresorptive therapies results in greater BMD increases, but the effects on fracture risk are unknown. Direct comparisons of clinical trial results should be considered carefully, given the differences in study design and populations. Differences in study design that may influence the efficacy of fracture risk reduction include calcium and vitamin D supplementation, primary fracture endpoints, definition of vertebral deformity or fracture, discontinuation rates, and statistical power. Factors in the study population that may influence fracture efficacy include the age of the population and the proportion of subjects with prevalent fractures. The use of surrogate endpoints such as BMD to predict fracture risk should be approached with caution, as the relationship between BMD changes and fracture risk reduction with antiresorptive therapies is uncertain. Consideration of these results from clinical trials can contribute to clinical judgment in selecting the best treatment option for postmenopausal osteoporosis.
View details for Web of Science ID 000173900600002
View details for PubMedID 11844743
Bone mass at any time of life reflects the totality of events that have impinged on the skeleton to that point. For adults, these events include those that have influenced the acquisition of bone during years of growth, resulting in the achievement of skeletal maturity, or "peak bone mass," as well as those that have subsequently influenced bone losses. For each limb of this trajectory, physical activity has been implicated as a powerful and independent factor. This article reviews current evidence regarding the relation of habitual physical activity to bone acquisition and maintenance, the skeletal consequences of exercise training, and the clinical value of exercise for patients with skeletal frailty.
View details for Web of Science ID 000167685100007
View details for PubMedID 11285991
View details for Web of Science ID A1994BB55L00011
Although age-related bone loss due to remodeling is basically a normal, predictable phenomenon, it is one that may be accelerated, at times quite dramatically, by dietary factors, hormonal insufficiency, or lack of exercise. Recent data regarding the long-term prophylactic efficacy of calcium supplementation, estrogen replacement therapy, and exercise are evaluated.
View details for Web of Science ID A1989U131700016
View details for PubMedID 2538489