Temporal kinetics of serum amyloid A (SAA) concentration and identification of SAA isoforms in blood and synovial fluid of horses with experimentally induced septic arthritis, non-septic synovitis, and systemic inflammation.

Abstract

Prompt diagnosis of equine septic arthritis is crucial for successful treatment. Serum amyloid A (SAA) has been suggested as a reliable biomarker. However, we previously found that synovial fluid SAA increases in nonaffected joints of horses with septic arthritis. We hypothesized that systemic SAA may leak into the nonaffected joints. If this is the case, we also hypothesized that locally produced joint SAA isoforms may be better candidates for septic arthritis biomarkers. Thus, our objectives were 1) to evaluate the temporal kinetics of systemic and synovial fluid SAA in horses with septic arthritis (n = 5), non-septic synovitis (n = 5), and systemic inflammation (n = 5), examining both affected and contralateral joints; and 2) investigate putative locally produced joint SAA isoforms and detect amino-acid differences between them. We confirmed that SAA increases significantly in synovial fluid in nonaffected joints of horses with systemic inflammation (≤352 mg/L), as well as in contralateral nonaffected joins in horses with septic arthritis (≤1,830 mg/L) compared to baseline at time 0 (<0.2 mg/L). We also identified a putative locally produced joint SAA peptide in synovial fluid (FGDSGHGAADSR) that differed in 1 amino acid from 2 systemic peptides found both in plasma and synovial fluid. The putative joint SAA isoform was present in joints of horses with both septic arthritis and systemic inflammation (ion intensities 10⁴-10⁶). Thus, the increase of synovial fluid SAA may be both due to the leakage of SAA from serum into joints and local production of joint SAA isoforms.