Three-dimensional power Doppler sonographic visualization of synovial vasculature: an 'in vivo' model to study angiogenesis in rheumatoid arthritis
© The Author(s) 2004
Received: 16 January 2004
Published: 25 February 2004
Joint damage in rheumatoid arthritis (RA) is caused by a tumor-like proliferation of synovial cells, which is accompanied by an increase in vasculature (angiogenesis) to support the metabolic requirements. Technological improvements such as three-dimensional (3D) power Doppler sonography have made possible the assessment of a whole blood vessel tree in a region of interest (ROI).
Because 3D power Doppler sonography plays an important role in obstetrics and oncology for assessing the vascular system, we used it to visualize intra-articular synovial new blood vessel formation in painful and swollen joints of patients with RA.
Inflamed wrist, knee or finger joints in 21 patients with active RA were investigated by ultrasound. Vascularity near and inside the joint capsule was visualized by power Doppler mode. The online 3D power Doppler function, provided by the ATL/HDI 5000 vascular software, was used to generate a 3D image of the periarticular and intra-articular blood vessels.
In 21 patients with RA who showed power Doppler signals in 2D mode, the 3D function revealed a blood vessel tree branching out from periarticular small blood vessels into the joint capsule. Until now it was possible to obtain good 3D imaging of synovial vasculature in the wrist (15 patients), knee (three patients), and finger joints (MCP II and PIP III) (three patients).
This is the first report on 3D power Doppler imaging of synovial angiogenesis. In comparison with 2D power Doppler, 3D mode reveals more and very small blood vessels in connection with the whole blood vessel tree, and provides a new opportunity to study the architecture and morphological structure of synovial vasculature in various joint disorders and under different conditions. Thus 3D power Doppler sonography may be used as an 'in vivo' model to study the mechanisms between inflammation and angiogenesis in rheumatoid joint damage.