Our osteoporosis research

Our osteoporosis research

Members of Garvan’s Bone Biology Division. L-R: Professor Peter Croucher, Dr Michelle McDonald, Professor Tuan Nguyen, Professor John Eisman AO and Dr Paul Baldock

Researchers in Garvan’s Bone Biology Division have been world leaders in osteoporosis and bone biology research for more than 40 years, beginning with the Dubbo Osteoporosis Project, the world’s longest running epidemiological study in both men and women to identify and predict risk and adverse outcomes for osteoporosis, including premature mortality.

Garvan researchers were the first to identify a gene associated with fracture, initiating the field of osteoporosis genetics. Discovering that our genes significantly control bone mass has led to studies worldwide to identify new genetic pathways that control our skeleton. These international collaborations include the Genetics Factors of Osteoporosis Consortium and the Wellcome Trust Origins of Bone and Cartilage Disease (OBCD) Program.

Our osteoporosis research takes advantage of the latest developments in genomics research and personalised medicine. This will help deliver new treatments that will prevent the onset of osteoporosis and improve the lives of Australians living with the disease. You can support our goal to prevent, treat and cure osteoporosis.

Key areas of investigation

Dr Michelle McDonald
Dr Michelle McDonald

Anti-Sclerostins repairing lost bone

A healthy skeleton is constantly undergoing bone remodelling, resorbing (dissolving and reabsorbing back into the body) damaged bone and creating new bone in a tightly regulated balance. Osteoporosis is caused when the balance is disrupted, mainly by the ageing process, and the rate of bone resorption exceeds the rate of bone formation.

‘Anti-sclerostin antibody (anti-SOST), a novel bone anabolic agent (a drug that increases the growth and mineralisation of bone) is now in advanced clinical development for the treatment of osteoporosis.’ Dr Michelle McDonald

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Prof John Eisman AO
Prof John Eisman AO

Genetics of bone quality

Clinically, osteoporosis is defined primarily using a measurement of bone density. However, the majority of individuals who suffer osteoporotic fractures do not have osteoporotic bone density. So while reduced bone density is an important cause of fracture, it is clearly not the sole causative factor.

‘We have already identified new genes that increase and decrease the quality of bone, but believe there are many more to be found. This information on the genes involved in bone quality will provides major insights into basic bone biology, help predict the risk of having a fracture and potentially identify novel targets for treatment.’ Professor John Eisman

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Prof Tuan Nguyen
Prof Tuan Nguyen

Co-Existing diseases (Comorbidities)

People with osteoporosis are commonly found to have co-existing diseases (comorbidities), including diabetes, obesity, cardiovascular diseases, osteoarthritis and neurological disorders. On average, a person with osteoporosis has three co-diseases, the presence of which contributes to worsen the person’s bone health.

‘Knowing the relationship between comorbidities, we will then go on to develop a predictive model that uses this ‘comorbidities network’ to determine a person’s risk of fracture. We expect that this project will provide an insight into the origins of osteoporosis and its related conditions.’ Professor Tuan Nguyen

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Prof Peter Croucher
Prof Peter Croucher

Cancer metastasis in bone

Garvan researchers are also investigating bone diseases, including osteoporosis, resulting from common cancers that grow in bone, or spread to bone such as breast and prostate cancer. Research has shown that advanced breast and prostate cancers, which have travelled to the bone, and myeloma (a cancer which forms in the bone marrow) have dramatic effects on the skeleton, breaking it down or causing bone to form where it shouldn’t.

‘Our research has shown that the bone’s own dynamic process of building up and breaking down can send signals to cancer cells inside it, to stay dormant or become active. This has led us to think in a whole new way about treating bone metastasis.’ Professor Peter Croucher

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National and International Collaborations

  • Amgen/UCB, Thousand Oaks, USA
  • Anzac Institute, Sydney, Australia
  • Canadian Multicentre Osteoporosis Study, Vancouver, Canada
  • Children’s Hospital Westmead, Sydney, Australia
  • Decode Genetics, Reykjavik, Iceland
  • Erasmus Medical Centre, Rotterdam, Netherlands
  • Imperial College London, UK
  • Maastricht University Medical Centre, Netherlands
  • Novartis Pharma, Basel, Switzerland
  • Pham Ngoc Thach University of Medicine, Ho Chi Minh City, Vietnamn
  • Prince of Wales Hospital, Sydney, Australia
  • Royal North Shore Hospital, Sydney, Australian
  • Ton Duc Thang University, Ho Chi Minh City, Vietnamn
  • University of Calgary, Alberta, Canada
  • University of Connecticut, USA
  • University of Maryland, Baltimore, USA
  • University of Melbourne, Australia
  • University of New South Wales, Sydney, Australia
  • University of Notre Dame, Sydney, Australia
  • University of Oslo, Norway
  • University of Sydney, Australia
  • University of Toronto, Canada
  • University of Tromso, Norway
  • Wellcome Trust Sanger Institute, Hinxton, Cambridge, UK.