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Biomedical subjects

S Poupon

Publications and source records attributed to S Poupon.

3 recordsLinked to original sources

Fractal analysis of radiographic trabecular bone texture and bone mineral density: two complementary parameters related to osteoporotic fractures.

Trabecular bone microarchitecture and bone mineral density (BMD) are two main factors related to osteoporotic fractures. Currently, however, microarchitecture is not evaluated. We have developed and validated a trabecular bone texture analysis from radiographic images. The objective was to determine if the fractal analysis of texture was able to distinguish osteoporotic fracture groups from control groups, either in vertebrae, hip, or wrist fractures, and to determine if this indicator and BMD were independent and complementary. In this cross-sectional unicenter case-control population study in postmenopausal women, 107 fracture cases were enrolled and age-matched with 197 control cases. This population comprised 40 vertebral fractures (with 70 controls), 30 hip fractures (55 controls), and 37 wrist fractures (62 controls). Hip and lumbar spine BMD were measured by double-energy X-ray absorptiometry. Fractal analysis of texture was performed on calcaneus radiographs and the result was expressed as the H parameter (H = 2-fractal dimension). The H parameter showed a lower value (0.679 +/- 0.053 SD) in fracture cases versus control cases (0.696 +/- 0.030; p = 0.007), the statistical significance persisting after adjustment for age and for lumbar spine (LS) or hip BMD. This result was confirmed in vertebral fractures (p = 0.0001) and hip fractures (p = 0.003) but not wrist fractures (p = 0.07). We determined the threshold between high and low H values and then the odds ratios (OR) of fracture for low H for BMD < or = -2.5 SD in T score and for the combinations of both parameters. The OR of fracture for low H was 1.6 (95% CI, 1.1-2.6). For LS BMD < or = -2.5 SD the OR of 6.1 (3.4-10.8) shifted to 9.0 (4.0-20.4) when we added low H and for hip BMD it shifted from 5.6 (3.3-9.4) to 8.1 (4.0-16.8). In vertebral, hip, and wrist fracture cases the results were also significant. These data have shown that the fractal analysis of texture on calcaneus radiographs can distinguish osteoporotic fracture groups from control groups. This analysis and BMD provide independent and complementary information. These data suggest that we can improve the fracture risk evaluation by adding information related to microarchitecture, derived from analysis of conventional radiographic images.

Absorptiometry, Photon↗

Long-term corticosteroid therapy induces mild changes in trabecular bone texture.

The relative roles of bone mineral density (BMD) decrease and of microarchitectural changes in corticosteroid-induced osteoporosis (CIOP) are debated. Our objective has been to evaluate both bone microarchitecture (by a fractal analysis of texture on radiographs) and BMD in corticosteroid (CS)-treated patients. In this study, 60 patients from a rheumatology unit with a mean age of 60.6+/-14.8 years taking CS therapy for more than 6 months and a cumulative dose of prednisone over 1 g and 57 controls among age-matched patients and hospital staff were recruited. Bone diseases and bone-modifying drugs (except calcium, vitamin D, and hormonal replacement therapy [HRT]) were considered as exclusion criteria. A fractal analysis of trabecular bone texture was performed on calcaneus radiographs after an oriented analysis in 18 directions. The fractal analysis was based on the fractional Brownian motion model. Results were expressed by H parameter (H = 2 - fractal dimension) in each direction, Hmean being the average of 18 directions, Hmini the minimum, and Hmaxi the maximum. BMD was measured by double-energy X-ray absorptiometry (DEXA) at the femoral neck (FN) and lumbar spine (LS). The odds ratios (OR) were calculated for a variation of 1 SD. The mean duration and dose of CS therapy was 5.6+/-6.6 years and 16.9+/-19.7 g. CS therapy was significantly correlated to a decrease in FN or LSBMD: OR = 1.95, 95% confidence interval (CI, 1.29-2.97) and OR = 3.19 (CI, 1.80-5.66), respectively. The Hmean and Hmaxi were significantly lower in the cases than in the controls: P = 0.03 and P = 0.02; OR = 1.67 (CI, 1.10-2.54) and OR = 1.75 (CI, 1.05-2.37). A similar trend was observed with Hmini but the difference did not reach the level of statistical significance: P = 0.06, OR = 1.57 (CI, 1.05-2.37). This study was repeated among cases and controls who had never taken HRT (respectively, n = 40 and n = 39). The results were similar. Among patients taking CS therapy, the presence of nontraumatic fractures was inversely related to BMD values but not to texture parameters. These data have shown that long-term CS therapy induces both BMD decrease and trabecular bone texture changes. The effect of CS therapy was much stronger on BMD than on the fractal H parameter. These results are in accordance with previous studies showing a lower effect of CS therapy on bone microarchitecture than on bone mass. These results can be contrasted with those observed in women with postmenopausal osteoporosis and vertebral crush fractures in which the variations in the fractal parameters are more significant than the BMD variations.

Adrenal Cortex Hormones↗

Glucocorticoid-induced osteoporosis: is the bone density decrease the only explanation?

BACKGROUND: Glucocorticoids may increase bone fragility via mechanisms independent from their bone mass reducing effect. OBJECTIVE: To study relationships between osteoporotic fractures and bone mineral density in patients on long-term glucocorticoid therapy. PATIENTS AND METHODS: We studied 121 women with a mean age of 60.4 +/- 14.3 years on long-term glucocorticoid therapy (cumulative dose > or = 1 g of prednisone equivalent, duration > or = 6 months) for rheumatoid arthritis (n = 38), polymyalgia rheumatica or giant cell arteritis (n = 26), connective tissue disease (n = 15), asthma (n = 14), another inflammatory joint disease (n = 14), or another condition (n = 14). The control group was composed of 125 subjects who had the same mean age and met the same exclusion criteria as the case group. Bone mineral density was measured at the lumbar spine and femoral neck using a Hologic QDR 4500 unit. In subjects with back pain, radiographs of the thoracic and lumbar spine were obtained to look for fractures. RESULTS: The odds ratio for a bone mineral density decrease of one standard deviation at the femoral neck was 1.68 (1.20-2.35) in patients with a cumulative glucocorticoid dose of 10 g of prednisone equivalent and 1.67 (1.22-2.29) in those with a glucocorticoid therapy duration of 2 years. Sixty-eight fractures were recorded in 56 patients (46% of the overall patient group). Even after adjustment on age, glucocorticoid therapy duration, and dose, mean bone mineral density values at the lumbar spine and femoral neck were significantly lower in the subgroup of patients with fractures than in the subgroup without fractures. Sensitivity and specificity of bone mineral density at the femoral neck and/or lumbar spine for the diagnosis of vertebral fracture and/or peripheral fracture were 73% and 51%, respectively. In the stepwise logistic regression model, factors explaining the presence of fractures were as follows, in hierarchical order: age; absence of calcium/vitamin D supplementation, femoral neck T-score, and glucocorticoid dose. CONCLUSION: Our data are compelling evidence that bone mineral density is a major determinant of the fracture risk in patients with glucocorticoid-induced osteoporosis.

Bone Density↗