These studies also show that both synovial C3a and C3b levels significantly correlated with histologic severity of arthritis, but do not correlate with systemic blood inflammatory markers (ESR or CRP levels) or blood plasma C3a and C3b levels, suggesting no link between systemic and local factors of complement factors produced by the joint, which is expected as the joint space is an isolated environment7. This evidence concerns the gene C3 and arthritic joint disease.