Ankylosing spondylitis: The link between blood vessels and bone damage
Disease - Ankylosing spondylitis, rheumatoid arthritis, osteoporosis
Lead applicant - Dr Amy Naylor
Organisation - University of Birmingham
Type of grant - Career Development Fellowship
Status of grant - Active
Amount of the original award - £574,685.87
Start date - 1 January 2018
Reference - 21743
Public Summary
What are the aims of this research?
In inflammatory arthritis, it is known that bone damage can continue even when inflammation is well controlled. Currently, drugs are targeted to treat the inflammation, but not the bone damage. The research will look at two genes involved in controlling inflammation and bone damage.
Why is this research important?
Before new drugs can be developed, understanding of the processes involved in bone damage and inflammation needs to be improved. It is known that specific types of blood vessel in the bone are involved in these processes, and are present at sites of bone formation. The two genes that will be studied as part of this research allow interaction between the cells that make bone, and the fine blood vessels within the bone.
The researchers have shown that mice lacking these two genes show increased inflammation, bone formation and bone damage. However, the intensity of inflammation does not correspond with the amount of bone damage, which is the same as is seen in patients with inflammatory arthritis, making it representative. In this project, the researchers will study the bones and blood vessels within the bone of mice where either one of the genes is absent, and will then be able to determine exactly what each gene does.
How will the findings benefit patients?
There are currently no drugs available that reverse bone damage in arthritis. In order to develop new treatments, and prevent or reverse bone damage in arthritis, understanding of the processes taking place must first be improved. Ultimately, the aim is to target abnormalities in bone blood vessels to prevent bone damage and maintain joint function.