Relationship of ultrasonographic findings with synovial angiogenesis modulators in different forms of knee arthritides.
Angiogenesis is controlled by a variety of angiogenesis stimulators and inhibitors. The increased power Doppler (PD) signals determined by ultrasonography is an indirect marker of synovial vascularity in arthritis. We aimed to investigate relationship between ultrasonographic findings and synovial angiogenesis modulators. Thirteen Behcet's disease (BD), 15 spondyloarthropathy, 21 rheumatoid arthritis (RA), and 15 osteoarthritis (OA) patients with knee arthritis were included. Cumulative effusion, synovial hypertrophy, and PD signal scores were calculated in arthritic joints. In synovial fluid samples, angiogenesis inhibitors (angiostatin, thrombospondin-1, and endostatin) and stimulators [bFGF (basic fibroblast growth factor), angiopoietin-1] were studied. The comparisons between groups were made by Kruskal-Wallis test, and correlation analysis was calculated with Pearson and Spearman tests. Effusion scores were significantly higher in inflammatory arthritis than in OA. Synovial hypertrophy scores were higher in RA and spondylarthritis than in OA and BD. PD scores were not different between the groups. Synovial angiostatin and bFGF levels were significantly higher in patients with inflammatory arthritis than in OA. Cumulative effusion scores were positively correlated with angiopoietin-1, angiostatin, and bFGF and negatively correlated with thrombospondin-1 levels. Synovial hypertrophy scores were positively correlated with angiostatin and bFGF levels and negatively correlated with thrombospondin-1. No correlation was found between PD scores and modulators of angiogenesis. In large joints like knee, detecting PD signals alone was not sufficient to assess the angiogenesis. However, cumulative activity scores were positively correlated with angiogenesis stimulators. Therefore, when investigating the angiogenesis, PD technique should be added to gray-scale examinations.
Division of Rheumatology, Gulhane School of Medicine, 06018, Etlik, Ankara, Turkey.
Mahmut
M
Gok
Hakan
H
Erdem
Feride
F
Gogus
Sedat
S
Yilmaz
Omer
O
Karadag
Ismail
I
Simsek
Rahsan Ilikci
RI
Sagkan
Mutlu
M
Saglam
Ugur
U
Musabak
Ayhan
A
Dinc
Salih
S
Pay
D000328:Adult; D043925:Angiogenesis Inducing Agents / Q000494:pharmacology; D020533:Angiogenesis Inhibitors / Q000494:pharmacology; D042683:Angiopoietin-1 / Q000494:pharmacology; D043168:Angiostatins / Q000494:pharmacology; D001172:Arthritis, Rheumatoid / Q000000981:diagnostic imaging*; D001528:Behcet Syndrome / Q000000981:diagnostic imaging*; D043169:Endostatins / Q000494:pharmacology; D005260:Female; D016222:Fibroblast Growth Factor 2 / Q000494:pharmacology; D006801:Humans; D007719:Knee Joint / Q000000981:diagnostic imaging*; D008297:Male; D008875:Middle Aged; D020370:Osteoarthritis, Knee / Q000000981:diagnostic imaging*; D025242:Spondylarthropathies / Q000000981:diagnostic imaging*; D013582:Synovial Fluid / Q000187:drug effects*; D019700:Thrombospondin 1 / Q000494:pharmacology; D014463:Ultrasonography
D043925:Angiogenesis Inducing Agents; D020533:Angiogenesis Inhibitors; D042683:Angiopoietin-1; D043169:Endostatins; D019700:Thrombospondin 1; D016222:Fibroblast Growth Factor 2; D043168:Angiostatins