The physiological relevance of calcitonin in osteoclast function [ 2002 - 2004 ]

Research Grant

Researchers: Prof Jeffrey Zajac (Principal investigator) ,  A/Pr Rachel Davey ,  Prof David Findlay

Brief description Throughout adult life, bone tissue is continuously remodelled. The two main processes involved in bone remodelling, are bone formation and bone breakdown. Bone formation is controlled by cells known as osteoblasts and bone breakdown is controlled by cells known as osteoclasts. Under normal circumstances these two processes are tightly coupled. Excessive breakdown of bone, causes these two processes to become unbalanced and results in bone loss. This is the basis of many bone diseases such as osteoporosis, a condition in which the bones become fragile and therefore more susceptible to fracture. 1 in 2 women and 1 in 5 men aged 70 years and older suffer from osteoporosis in Australia. Despite this, the mechanisms which control osteoclast breakdown of bone are not well understood. Our laboratory is interested in how hormones affect osteoclast action. We plan to examine the role of the hormone calcitonin, thought to be important inhibitor of osteoclastic bone breakdown. This will be achieved by studying transgenic mice in which the receptor for calcitonin is specifically removed from osteoclasts. This will allow us to precisely determine the role of calcitonin in osteoclast function. Current treatment for osteoporosis involves the administration of drugs which inhibit bone breakdown. This project will increase our understanding of how calcitonin acts to regulate the function of osteoclasts. We believe that this research is of great importance as osteoporosis is becoming more prevalent as the population ages.

Funding Amount $AUD 437,640.00

Funding Scheme NHMRC Project Grants

Notes Standard Project Grant