Clinical Significance of Gelatinases in Septic Arthritis of Native and Replaced Knees

Abstract

We hypothesized that more gelatinases appear in effusions of septic arthritis than aseptic arthritis. This study examined the laboratory variables of inflammation and the levels of gelatinase A and B (matrix metalloproteinases-2 and -9) in 75 effusions from the knees of 37 patients with inflammatory arthritis and compared them with effusions of septic and aseptic arthritis. Gelatin zymography revealed that the levels of the latent matrix metalloproteinase-9 were higher in 24 effusions of septic arthritis than in 51 effusions of aseptic arthritis. The latent matrix metalloproteinase-9 levels of septic arthritis also correlated with the neutrophil counts in effusions. Significantly more activated matrix metalloproteinases-2 and -9 appeared in effusions of septic arthritis in native and replaced knees than in effusions of aseptic arthritis. A high matrix metalloproteinase-9 level and the appearance of activated matrix metalloproteinases-2 and -9 may distinguish septic from aseptic arthritis, even in cases with a low neutrophil count in the replaced knee. Joint aspiration may not only reduce the bacteria counts, endotoxins, and proinflammatory cytokines, but also decrease the amount of matrix metalloproteinases in effusions that attack the extracellular matrix of native and artificial joints.

Expression levels of matrix metalloproteinase (MMP)-9 and its specific inhibitor TIMP-1, in septic and aseptic arthritis of the knee

“…These observations suggest enhanced expression and activation of MMP-9 in septic knee arthritis compared with the aseptic, which is consistent with previous studies [2,4,7,20]. Chu et al also showed by gelatin zymography that levels of latent MMP-9 and activated MMP-2 and MMP-9 were higher in effusions of septic arthritis than in effusions of aseptic arthritis [4]. Chu et al also showed by gelatin zymography that levels of latent MMP-9 and activated MMP-2 and MMP-9 were higher in effusions of septic arthritis than in effusions of aseptic arthritis [4].…”

“…These observations suggest enhanced expression and activation of MMP-9 in septic knee arthritis compared with the aseptic, which is consistent with previous studies [2,4,7,20]. These observations suggest enhanced expression and activation of MMP-9 in septic knee arthritis compared with the aseptic, which is consistent with previous studies [2,4,7,20].…”

“…However, in cases of septic arthritis, considerable enzymic activity occurs following saturation of endogenous inhibitory capacity due to a larger expression and activation of MMPs that is induced by bacteria or certain bacterial components [4,20]. The inflammatory cascade is activated in both septic and aseptic inflammatory knee arthritis.…”

Effects of nonsteroidal anti-inflammatory drugs on the expression of urokinase plasminogen activator and inhibitor and gelatinases in the early osteoarthritic knee of humans

“…In general, the levels of latent and activated MMP-2 in all NSAIDs treated media at 24 h were unaltered in all tissue cultures (Figs. [3][4][5]. Significantly suppressive effects almost appeared from day 2, and persisted through to day 4; however, the decreases of proMMP-2 in celecoxib-treated meniscal cultures and activated MMP-2 in celecoxib-treated chondral cultures could not exhibit significant differences.…”

“…Gelatinases (type IV collagenases) can be divided into gelatinase-A (MMP-2) and gelatinase-B (MMP-9) and their expressions increase in pathologic chondral, meniscal and synovial lesions of OA, which is likewise believed to play an important role in OA pathophysiology [2]. In fact, increased expression of gelatinases in arthritic effusions easily reflected the inflammatory condition of joints [3][4][5][6], and nonsteroidal antiinflammatory drugs (NSAIDs) may down-regulate the MMPs in synovial fluids of gouty arthritis [3]. Recently, the vital contribution of inflammation in cartilage destruction has been pointed out [7,8] and synovial inflammation has been implicated as a central component of OA pathogenesis [1].…”