No description available.

No description available.

No description available.

The objective of this study was to examine the link between radiographic measures of bone quality and total knee implant migration as measured by radiostereometric analysis (RSA). Two uncemented total knee arthroplasty studies (n=65) with RSA and bone mineral density (BMD) exams up to two years post surgery, and one study with cemented total knees with one year RSA data (n=18) were examined. Radiograph image texture analysis was used to characterize the bone microarchitecture, and a feasibility study was conducted to determine if a given x-ray machine could be used to obtain bone mineral density at the same time as the RSA exams. Random ForestTM ensemble classification tree statistical models classified patients into groups based on implant migration with a range of cut-points. Models based on bone texture parameters measured from the two year radiographs had a sensitivity of 87.5% and specificity of 80% when classifying patients who had more than 0.3mm maximum total point motion (MTPM) at two years using the one year exam as reference. Other cut-points were examined, with models generally having a lower specificity if the acceptable migration was smaller, and lower sensitivity if higher migrations were tolerable. In a predictive model, post-operative bone texture could be used to create a model with a sensitivity of 75% and a specificity of 80% when predicting those subjects with cemented implants who went on to more than 0.4mm total migration by one year. Bone mineral density of the proximal tibia, as determined by clinical scanners, was not found to increase the accuracy of implant migration group classification. An empirical fit to central regions of a purposed-built cross-wedge calibration phantom returned residuals of less than ±1.5% for the bone-equivalent thicknesses. The coefficient of variation of the region greyscale values in three images spread over three days is under 4%, showing the stability of the system to hold a calibration between phantom exams and patient scans. Scatter and dynamic range issues will need to be considered for an accurate calibration across the full range of areal bone mineral densities in the distal femur and proximal tibia.

Background: Phytoestrogens are diphenolic compounds found in plants with a structure and molecular weight similar to oestradiol which enables them to bind to the oestrogen receptor. Isoflavonoids occur mainly within the legume family with highest concentration in soybeans. Lignans are found in a range of plant foods and the richest known source is linseed. Few studies have been published on intake of isoflavonoids and none were located on intake of lignans in Australian women. The validity of methods designed to estimate intake can be assessed using urinary excretion of isoflavonoids and lignans as studies have found an association between intake and excretion of isoflavonoids and lignans. It has been proposed that, through their ability to act like oestrogen, phytoestrogens could decrease bone turnover and attenuate the loss of bone mineral density (BMD) at menopause. The aims of this research were to determine the pattern of intake of isoflavonoids and lignans in 500 women from food and supplements and to assess a questionnaire used to estimate intake using excretion in a sub-sample of 141 women. Associations between usual intake or excretion of isoflavonoids and lignans and biomarkers of bone health were also examined. Methods: A cross-sectional study was conducted involving 500 women aged 40-80 years participating in the Longitudinal Assessment of Ageing in Women (LAW), a 5 year study being conducted in the Betty Byrne Henderson Centre at the Royal Brisbane and Women's Hospital. Subjects were randomly selected from the electoral role and stratified into ten year age groups. Intake of isoflavonoids and lignans from food and supplements was assessed using a specially designed questionnaire containing 110 items. Values for individual items were obtained from published literature and summed to provide average daily intakes of isoflavonoids and lignans (mg/d). A sub-sample of 141 women was recruited to take part in the assessment of the association between phytoestrogen intake and excretion. Participants collected three 24-h urine samples spaced over one week. Samples were analysed using high performance liquid chromatography MS/MS for seven isoflavonoids and four lignans. Bone mineral densities (BMD) of the femur neck, total hip and lumbar spine were measured by dual energy x-ray absorptiometry. Bone formation was assessed using serum bone alkaline phosphatase (bone ALP) and osteocalcin (OC) and bone resorption was assessed using deoxypyridinoline (DPD) and urinary excretion of N-terminal cross-linking telopeptide of type-I collagen (NTX). Potential confounding factors were also evaluated. Statistical analyses were conducted using SPSS for windows (version 10). Participants were defined as consumers if they reported intake of one or more serves of soy or linseed in the prior month. Differences in socio-demographic and lifestyle characteristics between groups were assessed using ANOVA and Chi Square tests. Associations between intake and excretion of phytoestrogens were assessed using Spearman's rank-order correlations () for non-normal data. Phytoestrogen intake was categorised into four groups for the assessment of the association with markers of bone health. Associations between phytoestrogen excretion and markers of bone health were assessed using Pearson's product moment correlations for normal data (r) and Spearman's rank-order correlations for non-normal data. A value of P < 0.05 was taken as statistically significant. Results: Consumption of soy food was reported by 40% and consumption of linseed by 34% of women. Median (range) intakes among soy/linseed consumers for isoflavonoids, 3.87 (0-173) mg/d, and lignans, 2.40 (0.1-33) mg/d, were significantly higher than corresponding intakes among non consumers of 0.005 (0-2.6) and 1.57 (0.4-4.7) mg/d, respectively (P < 0.001). Soy/linseed consumers reported higher intakes of energy (P=0.043), dietary fibre (P=0.003) and polyunsaturated fat (P=0.004); and a higher level of physical activity (P=0.006), SEP (P < 0.001), education (P < 0.001) and supplement use (P < 0.001). Use of non-prescription supplements for menopause in the previous month was reported by 13% of women. A review of supplements available for treatment of menopause indicated that use of soy, red clover, black cohosh and sage could have a role in treatment of menopause symptoms. Evidence supporting the presence of oestrogenic components was available for soy and red clover isoflavonoids only. There was a significant association between intake and excretion of isoflavonoids within the total group (r=0.207, P < 0.05), with a stronger association in soy consumers (r=0.364, P < 0.01). Excretion of isoflavonoids was detected in women who did not report known intake of soy foods, suggesting isoflavonoids could be derived in small amounts from other plant foods or use of soy as an ingredient in processed foods. There was no significant association between intake and excretion of lignans, however both intake and excretion were associated with dietary fibre (r=0.303 and r=0.230, respectively, P < 0.01 for both). Bone ALP was higher among the very low isoflavonoid intake group (P=0.005) for the total sample (P=0.005) and women with BMI≤25 kg/m2 (P=0.002). Data also demonstrated an inverse association between excretion of isoflavonoids and NTX within women with BMI≤25 kg/m2 (r=-0.33, P < 0.05). There was a positive association between lignan excretion and bone ALP in the total sample (r=0.21, P < 0.05) which was strengthened in women with osteoporosis/osteopenia (r=0.41, P < 0.05) and a positive association between lignan excretion and DPD among women with BMI≤25 kg/m2 (ρ=0.28, P < 0.05) All associations remained significant after adjustment for confounding. Conclusions: Few women who chose phytoestrogen-rich foods consumed amounts similar to women with traditional soy-based diets although some achieved high intakes with supplements. Women who consumed soy or linseed foods differed in lifestyle and sociodemographic characteristics that could influence the association with disease in epidemiological studies. Results indicated that the phytoestrogen questionnaire was useful for assessment of isoflavonoids but was not acceptably precise for measurement of lignans. Findings suggest that there is an inverse association between isoflavonoid status and bone ALP and NTX although the precise mechanism of action has not been clarified. The association between lignan intake and bone is less well understood; however findings of a positive association with bone ALP indicate that further research on the lignan content of foods and the inclusion of lignans in studies is warranted.

Biochemical assays and radioabsorptiometry evaluated the relationship of mineral and bone metabolism to the systemic response to neurotrauma or orthopaedic trauma of adult males. Forty-one adult males (29.4±9.3 years) participated of which 37 had a primary diagnosis of traumatic spinal cord injury (SCI) and four were vertebral fracture controls. Biochemical abnormalities found included hyperphosphataemia, in association with low or low normal serum levels of 1,25-dihydroxyvitmain D (1,25(OH)₂D) and of parathyroid hormone (PTH), whilst patients remained normocalcaemic. These disturbances of phosphate and vitamin D metabolism and the markedly accelerated resorption of bone were strongly associated with the interval since injury and the severity of injury, but none of these relationships was correlated with the level of the injury, the sensory status of a patient or the presence of spine fracture. The disturbances of phosphate and vitamin D metabolism and the markedly accelerated resorption of bone found in this study are a mirror image of the data of patients with the heritable disorders autosomal dominant hyperphosphataemic rickets (ADHR), which results from an inactivating mutation of the gene encoding fibroblast growth factor 23 (FGF23) and autosomal recessive hypophosphataemic rickets (ARHR), which is caused by a mutation of the gene encoding dentin matrix protein-1 (DMP-1). It is potentially important that the hormone/proteolytic enzyme/extra-cellular matrix protein cascade associated with these disorders is counter-regulated by 1,25(OH)₂D, acting either directly or indirectly. The present results suggest that the serum levels of 1,25(OH)₂D of the neurotrauma patients chosen for study may have been inappropriately high with respect to the “physiological and metabolic set” of serum levels of phosphate and ionised calcium in the period corresponding to the uncoupling of the resorption and formation of bone, at least in males, prompting further investigation. The findings are consistent with a new “physiological set,” possibly involving an abnormality in the synthesis or processing of the endocrine fibroblast growth factors or other circulating phosphatonins, which may act as an additional level of regulation of the renal–bone axis, rather than renal failure. Strongly supporting this was the dynamic pattern of the biochemistry and radiological data of these neurotrauma patients and also, preliminary evidence of disturbances in circulating levels of other systemic modulators of mineral and bone metabolism. The relationships that were observed potentially may be explained by the diversity of the physiological activities of the endocrine fibroblast growth factors and the modes of actions of secreted FGF23 in bone. The findings provide an understanding of why bone loss occurs and may form the target for safe and cost effective interventions. / http://proxy.library.adelaide.edu.au/login?url= http://library.adelaide.edu.au/cgi-bin/Pwebrecon.cgi?BBID=1345019 / Thesis (Ph.D.) - University of Adelaide, School of Medicine, Discipline of Orthopaedics and Trauma, 2008

Biochemical assays and radioabsorptiometry evaluated the relationship of mineral and bone metabolism to the systemic response to neurotrauma or orthopaedic trauma of adult males. Forty-one adult males (29.4±9.3 years) participated of which 37 had a primary diagnosis of traumatic spinal cord injury (SCI) and four were vertebral fracture controls. Biochemical abnormalities found included hyperphosphataemia, in association with low or low normal serum levels of 1,25-dihydroxyvitmain D (1,25(OH)₂D) and of parathyroid hormone (PTH), whilst patients remained normocalcaemic. These disturbances of phosphate and vitamin D metabolism and the markedly accelerated resorption of bone were strongly associated with the interval since injury and the severity of injury, but none of these relationships was correlated with the level of the injury, the sensory status of a patient or the presence of spine fracture. The disturbances of phosphate and vitamin D metabolism and the markedly accelerated resorption of bone found in this study are a mirror image of the data of patients with the heritable disorders autosomal dominant hyperphosphataemic rickets (ADHR), which results from an inactivating mutation of the gene encoding fibroblast growth factor 23 (FGF23) and autosomal recessive hypophosphataemic rickets (ARHR), which is caused by a mutation of the gene encoding dentin matrix protein-1 (DMP-1). It is potentially important that the hormone/proteolytic enzyme/extra-cellular matrix protein cascade associated with these disorders is counter-regulated by 1,25(OH)₂D, acting either directly or indirectly. The present results suggest that the serum levels of 1,25(OH)₂D of the neurotrauma patients chosen for study may have been inappropriately high with respect to the “physiological and metabolic set” of serum levels of phosphate and ionised calcium in the period corresponding to the uncoupling of the resorption and formation of bone, at least in males, prompting further investigation. The findings are consistent with a new “physiological set,” possibly involving an abnormality in the synthesis or processing of the endocrine fibroblast growth factors or other circulating phosphatonins, which may act as an additional level of regulation of the renal–bone axis, rather than renal failure. Strongly supporting this was the dynamic pattern of the biochemistry and radiological data of these neurotrauma patients and also, preliminary evidence of disturbances in circulating levels of other systemic modulators of mineral and bone metabolism. The relationships that were observed potentially may be explained by the diversity of the physiological activities of the endocrine fibroblast growth factors and the modes of actions of secreted FGF23 in bone. The findings provide an understanding of why bone loss occurs and may form the target for safe and cost effective interventions. / http://proxy.library.adelaide.edu.au/login?url= http://library.adelaide.edu.au/cgi-bin/Pwebrecon.cgi?BBID=1345019 / Thesis (Ph.D.) - University of Adelaide, School of Medicine, Discipline of Orthopaedics and Trauma, 2008

Biochemical assays and radioabsorptiometry evaluated the relationship of mineral and bone metabolism to the systemic response to neurotrauma or orthopaedic trauma of adult males. Forty-one adult males (29.4±9.3 years) participated of which 37 had a primary diagnosis of traumatic spinal cord injury (SCI) and four were vertebral fracture controls. Biochemical abnormalities found included hyperphosphataemia, in association with low or low normal serum levels of 1,25-dihydroxyvitmain D (1,25(OH)₂D) and of parathyroid hormone (PTH), whilst patients remained normocalcaemic. These disturbances of phosphate and vitamin D metabolism and the markedly accelerated resorption of bone were strongly associated with the interval since injury and the severity of injury, but none of these relationships was correlated with the level of the injury, the sensory status of a patient or the presence of spine fracture. The disturbances of phosphate and vitamin D metabolism and the markedly accelerated resorption of bone found in this study are a mirror image of the data of patients with the heritable disorders autosomal dominant hyperphosphataemic rickets (ADHR), which results from an inactivating mutation of the gene encoding fibroblast growth factor 23 (FGF23) and autosomal recessive hypophosphataemic rickets (ARHR), which is caused by a mutation of the gene encoding dentin matrix protein-1 (DMP-1). It is potentially important that the hormone/proteolytic enzyme/extra-cellular matrix protein cascade associated with these disorders is counter-regulated by 1,25(OH)₂D, acting either directly or indirectly. The present results suggest that the serum levels of 1,25(OH)₂D of the neurotrauma patients chosen for study may have been inappropriately high with respect to the “physiological and metabolic set” of serum levels of phosphate and ionised calcium in the period corresponding to the uncoupling of the resorption and formation of bone, at least in males, prompting further investigation. The findings are consistent with a new “physiological set,” possibly involving an abnormality in the synthesis or processing of the endocrine fibroblast growth factors or other circulating phosphatonins, which may act as an additional level of regulation of the renal–bone axis, rather than renal failure. Strongly supporting this was the dynamic pattern of the biochemistry and radiological data of these neurotrauma patients and also, preliminary evidence of disturbances in circulating levels of other systemic modulators of mineral and bone metabolism. The relationships that were observed potentially may be explained by the diversity of the physiological activities of the endocrine fibroblast growth factors and the modes of actions of secreted FGF23 in bone. The findings provide an understanding of why bone loss occurs and may form the target for safe and cost effective interventions. / http://proxy.library.adelaide.edu.au/login?url= http://library.adelaide.edu.au/cgi-bin/Pwebrecon.cgi?BBID=1345019 / Thesis (Ph.D.) - University of Adelaide, School of Medicine, Discipline of Orthopaedics and Trauma, 2008

Biochemical assays and radioabsorptiometry evaluated the relationship of mineral and bone metabolism to the systemic response to neurotrauma or orthopaedic trauma of adult males. Forty-one adult males (29.4±9.3 years) participated of which 37 had a primary diagnosis of traumatic spinal cord injury (SCI) and four were vertebral fracture controls. Biochemical abnormalities found included hyperphosphataemia, in association with low or low normal serum levels of 1,25-dihydroxyvitmain D (1,25(OH)₂D) and of parathyroid hormone (PTH), whilst patients remained normocalcaemic. These disturbances of phosphate and vitamin D metabolism and the markedly accelerated resorption of bone were strongly associated with the interval since injury and the severity of injury, but none of these relationships was correlated with the level of the injury, the sensory status of a patient or the presence of spine fracture. The disturbances of phosphate and vitamin D metabolism and the markedly accelerated resorption of bone found in this study are a mirror image of the data of patients with the heritable disorders autosomal dominant hyperphosphataemic rickets (ADHR), which results from an inactivating mutation of the gene encoding fibroblast growth factor 23 (FGF23) and autosomal recessive hypophosphataemic rickets (ARHR), which is caused by a mutation of the gene encoding dentin matrix protein-1 (DMP-1). It is potentially important that the hormone/proteolytic enzyme/extra-cellular matrix protein cascade associated with these disorders is counter-regulated by 1,25(OH)₂D, acting either directly or indirectly. The present results suggest that the serum levels of 1,25(OH)₂D of the neurotrauma patients chosen for study may have been inappropriately high with respect to the “physiological and metabolic set” of serum levels of phosphate and ionised calcium in the period corresponding to the uncoupling of the resorption and formation of bone, at least in males, prompting further investigation. The findings are consistent with a new “physiological set,” possibly involving an abnormality in the synthesis or processing of the endocrine fibroblast growth factors or other circulating phosphatonins, which may act as an additional level of regulation of the renal–bone axis, rather than renal failure. Strongly supporting this was the dynamic pattern of the biochemistry and radiological data of these neurotrauma patients and also, preliminary evidence of disturbances in circulating levels of other systemic modulators of mineral and bone metabolism. The relationships that were observed potentially may be explained by the diversity of the physiological activities of the endocrine fibroblast growth factors and the modes of actions of secreted FGF23 in bone. The findings provide an understanding of why bone loss occurs and may form the target for safe and cost effective interventions. / http://proxy.library.adelaide.edu.au/login?url= http://library.adelaide.edu.au/cgi-bin/Pwebrecon.cgi?BBID=1345019 / Thesis (Ph.D.) - University of Adelaide, School of Medicine, Discipline of Orthopaedics and Trauma, 2008

Bone drilling is an essential part of many orthopaedic surgical procedures, including those for internal fixation and for attaching prosthetics. Drilling into bone is a fundamental skill that can be both very simple, such as drilling through long bones, or very difficult, such as drilling through the vertebral pedicles where incorrectly drilled holes can result in nerve damage, vascular damage or fractured pedicles. Also large forces experienced during bone drilling may promote crack formation and can result in drill overrun, causing considerable damage to surrounding tissues. Therefore, it is important to understand the effect of bone material quality on the bone drilling forces to select favourable drilling conditions, and improve orthopaedic procedures.