Regulation Of Bone Formation And Resorption By Osteoblastic EphrinB2/EphB4 Signalling
Funder
National Health and Medical Research Council
Funding Amount
$648,479.00
Summary
Skeletal strength is maintained by balanced cycles of bone resorption and bone formation. Cells that live inside the bone matrix, osteocytes, are thought to co-ordinate this. We have found that two proteins, EphrinB2 and EphB4, exist on the surface of osteocytes and regulate bone formation and resorption. This project investigates how they do this, and whether interfering with or enhancing their signals could be used to increase bone strength in osteoporosis.
gp130 is a protein expressed in all cells in the body; this project will analyse the influence of gp130 within the cells that form bone, the cells that destroy bone, and the cells that form a communication network within the bone matrix. Understanding the way this protein works will help us to understand how current therapies for osteoporosis work, and will help us to design new therapies.
Furin: Carving-up Vital Substrates For Bone Remodelling And Homeostasis
Funder
National Health and Medical Research Council
Funding Amount
$815,972.00
Summary
Osteoporosis, or porous bone, is a disease characterized by low bone mass and structural deterioration of bone tissue, leading to bone fragility and an increased susceptibility to fractures. It is caused by an imbalance between the cells that are constantly reabsorbing and reforming bone. The proposed project will address furin as a novel regulator of bone remodelling.
Relationship Of The Anabolic And Catabolic Responses In Healing A Critical Sized Defect In Rats
Funder
National Health and Medical Research Council
Funding Amount
$329,750.00
Summary
Delayed bone healing after trauma is a large clinical problem. Figures suggest up to 60,000 fractures result in a delay in healing in Australia per year. Bone healing can also fail to occur in other circumstances, such as after an operation. Research effort into new approaches to solving these problems is clearly justified. We believe that in some situations, bone healing fails due to the body's healing response, the anabolic response, being insufficient. In some other situations, the body's bon ....Delayed bone healing after trauma is a large clinical problem. Figures suggest up to 60,000 fractures result in a delay in healing in Australia per year. Bone healing can also fail to occur in other circumstances, such as after an operation. Research effort into new approaches to solving these problems is clearly justified. We believe that in some situations, bone healing fails due to the body's healing response, the anabolic response, being insufficient. In some other situations, the body's bone resorbing response, the catabolic response, may be too high and prevent healing from occurring. In normal bone healing, there is a balance between the anabolic and catabolic response. In disordered bone healing, these responses are out of balance. Several reasonably new treatments are available which can increase the anabolic response or decrease the catabolic response. We have preliminary results showing that with these agents we can bring these elements into better control, and thus drive bone healing. We have optimised an animal model where both the anabolic and catabolic responses can be controlled. In this project, we explore the optimisation of the timing and magnitude of anabolic and catabolic responses in bone healing.Read moreRead less
Targeting Histone Deacetylases 1 And 5 To Reduce Inflammation And Bone Loss In Periodontitis.
Funder
National Health and Medical Research Council
Funding Amount
$536,745.00
Summary
Bone loss and tooth loosening are serious complications in periodontitis. Despite the prevalence of this disease current treatments do not directly stop the bone loss. Our recent laboratory studies show inhibiting histone deacetylase (HDAC) activity with very low doses of inhibitors can effectively suppress this bone loss in periodontitis. This project aims to investigate specific targeting inhibitors of HDAC 1 and HDAC 5 to treat periodontitis by enhancing bone formation and reducing bone loss.
Skeletal structure is continually modified throughout life to take into account dietary, hormonal and physical changes. This is brought about by three major cell types which either form bone, destroy bone, or sense mechanical and hormonal influences on the skeleton. My work seeks to understand the way these cells are controlled and how they control each other. In this way, I will identify new ways of treating osteoporosis, arthritis, skeletal birth defects and cancer-induced bone disease.
IL-6 Classic And Trans-signalling In Bone Physiology And Pathology
Funder
National Health and Medical Research Council
Funding Amount
$731,372.00
Summary
This project seeks to determine whether it is possible to prevent bone loss associated with osteoporosis and inflammatory bowel disease by blocking interleukin 6. Two different methods of blockade will be tested, with the hope that one of these methods will have less side effects.