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Research Topic : Bone Development
Field of Research : Endocrinology
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  • Funded Activity

    Monitoring Bone Loss And Response To Therapy Through Bone Material And Structural Composition

    Funder
    National Health and Medical Research Council
    Funding Amount
    $696,111.00
    Summary
    Millions of scripts are filled for treatment of osteoporosis. However, there is no way of knowing if these drugs are right for these individuals, if it improves bone strength or are actually doing harm. Bone density measurement is of limited value. We have developed a new analysis method that measures changes in bone structure that tell us if the treatment is or is not working so alternative treatment can be used. The aim of this study is to test this new method.
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    Funded Activity

    Does Teriparatide Reverse Osteonecrosis Of The Jaw In Patients With Cancer? A Randomised, Controlled Trial

    Funder
    National Health and Medical Research Council
    Funding Amount
    $137,700.00
    Summary
    Osteonecrosis of the jaw (ONJ) is a debilitating bone condition involving damage and suboptimal healing of bone involving the jaw. This has been associated with bisphosphonate therapy, which is commonly used for the treatment of both cancer and osteoporosis. My research aims to investigate the role of recombinant parathyroid hormone in the stimulation of bone formation and healing and, thus, its potential to reverse ONJ.
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    Funded Activity

    Regulation Of Bone Resorption And Formation In Health And Disease

    Funder
    National Health and Medical Research Council
    Funding Amount
    $5,596,183.00
    Summary
    Bone is continually being formed and broken down, and these two processes are critical forthe maintenance of a normal skeleton. These processes are dependent upon communication between the bone building and degrading cells, and the hormones growth factors and cytokines that are present in the circulation or produced in bone. The tightly regulated processes of bone formation and degradation need to remain equal, and are essential for the achievement and maintenance of skeletal strength and form. .... Bone is continually being formed and broken down, and these two processes are critical forthe maintenance of a normal skeleton. These processes are dependent upon communication between the bone building and degrading cells, and the hormones growth factors and cytokines that are present in the circulation or produced in bone. The tightly regulated processes of bone formation and degradation need to remain equal, and are essential for the achievement and maintenance of skeletal strength and form. Osteoporosis results from an excess of bone breakdown over formation, and our Program aims to identify the factors that regulate these processes, and develop new therapies that can modify them. We will also determine what it is about bone cell properties that make some cancers, especially those of breast and prostate, particularly prone to spread to bone.
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    Funded Activity

    The Effect Of Androgen Replacement Therapy On Bone And Muscle Health In Men With Chronic Kidney Disease

    Funder
    National Health and Medical Research Council
    Funding Amount
    $122,714.00
    Summary
    Low testosterone (T) levels are common in men with poor kidney function. Low T is known to cause reduced energy, decreased strength and low libido. Normal T is also needed for healthy bones and muscles. Men with kidney disease are already at risk of fractures, poor strength and quality of life. However, there are few studies that look at replacing T to men with kidney failure. We will investigate how low T affects bone and muscle and assess how giving T can benefit bone, muscle and function.
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    Funded Activity

    Bone Loss During And After Menopause In Twins

    Funder
    National Health and Medical Research Council
    Funding Amount
    $895,242.00
    Summary
    Menopause is one of the important risk factors for bone loss, structural decay and bone fragility. We aim to quantify the biochemical, microstructural and biomechanical basis of loss of bone strength during and after menopause. A cohort of 324 pairs of female-female twins aged 25 to 75 years old will be followed up for up to 9 years. Defining the structural basis of bone fragility provides a rational means to identifying women at risk for fracture.
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    Funded Activity

    Interaction Between PTH And Y2 Bone Anabolic Pathways

    Funder
    National Health and Medical Research Council
    Funding Amount
    $731,311.00
    Summary
    Osteoporosis is a costly condition that affects more than 150 million people worldwide and fills more hospital beds than any other disease*. People who have osteoporotic fractures experience a diminished quality of life and a reduced life expectancy. Although there are currently a number of therapies in use to reduce further loss of bone in osteoporotic patients, there is only one to replace lost bone, parathyroid hormone. For clinical and economic reasons, there is a need for additional bone-bu .... Osteoporosis is a costly condition that affects more than 150 million people worldwide and fills more hospital beds than any other disease*. People who have osteoporotic fractures experience a diminished quality of life and a reduced life expectancy. Although there are currently a number of therapies in use to reduce further loss of bone in osteoporotic patients, there is only one to replace lost bone, parathyroid hormone. For clinical and economic reasons, there is a need for additional bone-building therapies. Like all tissues, the nervous system affects skeletal function. We recently discovered a powerful control pathway by which the nervous system regulates bone formation. This project will test whether altering the function of this neural pathway can increase bone formation and whether it can work together with parathyroid hormone therapy to produce an enhanced bone formation response greater than either therapy alone. This research is important because of the need for new osteoporosis therapies to repair weakened bones. The knowledge gained from this study has the potential to provide a very important and useful contribution to skeletal health and thus aged health worldwide. *The Burden of Brittle Bones: Costing Osteoporosis in Australia. A report prepared by Access Economics Pty. Ltd. September 2001
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    Funded Activity

    Hypothalamic Signalling In Cortical And Trabecular Bone Anabolic Activity

    Funder
    National Health and Medical Research Council
    Funding Amount
    $472,770.00
    Summary
    Osteoporosis is a disease associated with an exponential rise in the number of fractures in the elderly. These fractures are so common that around 1 in 3 women and 1in four men will be affected. They cause pain, disability that can be permanent disability and are associated with premature death. Current treatments are able to effectively increase bone strength in osteoporotic patients but can not return bone strength to normal. Some new treatments can restore bone strength to some extent but the .... Osteoporosis is a disease associated with an exponential rise in the number of fractures in the elderly. These fractures are so common that around 1 in 3 women and 1in four men will be affected. They cause pain, disability that can be permanent disability and are associated with premature death. Current treatments are able to effectively increase bone strength in osteoporotic patients but can not return bone strength to normal. Some new treatments can restore bone strength to some extent but these are limited by expense and safety concerns. We have discovered a pathway in the brain that reduces bone formation and by blocking this pathway we can achieve doubling of the amount of bone in key bone sites. This occurs due to a marked increase in the amount of new bone formed. In fact, genetic manipulation of this pathway was able to double the speed at which bone is made by the skeleton. Excitingly, these increases in bone were possible in adult mice, suggesting such changes could be potential therapy for human patients. However, in order to be able to harness this pathway we must understand what molecules within the brain are responsible for the signals that reach the bone. Our proposal aims to identify the nerve signalling molecule(s) and the receptor for these signals within the brain that initiates the increase in bone formation. This project ultimately aims to identify a target for new therapies that could cause this beneficial effect by administration of a simple treatment, preferably by mouth in adult humans.
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    Funded Activity

    GENETIC PREDICTION OF FRACTURE IN A RISK-STRATIFIED POPULATION

    Funder
    National Health and Medical Research Council
    Funding Amount
    $363,000.00
    Summary
    Osteoporosis is a condition characterised by excessive bone loss and impaired bone quality, which ultimately results in fracture with minimal trauma. Osteoporosis affects 27% of women and 11% of men aged 60 years or above in the community, and costs Australia around $7 billion each year. Individuals with low bone mineral density (BMD) have a significantly higher risk of fracture than those with normal BMD. In the long-term (14-year) Dubbo Osteoporosis Epidemiology Study, more than half of indivi .... Osteoporosis is a condition characterised by excessive bone loss and impaired bone quality, which ultimately results in fracture with minimal trauma. Osteoporosis affects 27% of women and 11% of men aged 60 years or above in the community, and costs Australia around $7 billion each year. Individuals with low bone mineral density (BMD) have a significantly higher risk of fracture than those with normal BMD. In the long-term (14-year) Dubbo Osteoporosis Epidemiology Study, more than half of individuals with osteoporosis (e.g., low BMD) did not sustain a fracture, while approximately 60% of fracture cases had BMD above the high risk levels. Thus, BMD alone is not a good discriminant of fracture versus non-fracture cases. It is widely known that the liability to fracture is determined in part by genes. Previous studies, including from our group, have suggested a number of candidate genes that are associated with fracture risk. The fundamental issue that this study is concerned is that how and whether genetic markers could be used to facilitate case finding. It is proposed that common variations of certain genes are associated with fracture risk independent of BMD. That is, they can identify individuals at relatively high and low fracture risk after stratification for BMD. Hence, some markers may identify those individuals likely (and unlikely) to fracture even with low (osteoporotic) BMD. Similarly, some, possibly the same, markers may identify individuals at high risk of fracture despite relatively good (ie non-osteoporotic) BMD. It is further proposed that no single gene will achieve this outcome, but rather a small set of such gene polymorphisms will provide clinically useful risk information. This effect is entirely analogous to the use of clinical risk indicators (eg, age, weight, sex, family history, etc) to assess the risk of future fracture.
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    Funded Activity

    The Effects Of Zoledronic Acid On Bone Architecture In Premenopausal Women With Breast Cancer Receiving Adjuvant Combined Ovarian Suppression And Aromatase Inhibitor Therapy: A Randomised Controlled Trial.

    Funder
    National Health and Medical Research Council
    Funding Amount
    $122,714.00
    Summary
    In premenopausal women, a new treatment method that reduces oestrogen levels to almost zero significantly reduces the risk of breast cancer recurrence. However, this is likely to cause substantial bone loss leading to fractures. Using a new imaging technique (HR-pQCT), the effects of profound oestrogen deprivation on bone structure in premenopausal women will be studied. The ability of zoledronic acid, a drug that reduces bone loss, to prevent these adverse bone effects will also be examined.
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    Funded Activity

    Determinants Of Bone Fragility

    Funder
    National Health and Medical Research Council
    Funding Amount
    $138,241.00
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