Current Review; Biomarkers in Diagnosing Periprosthetic Joint Infection
Journal Title: Biomedical Journal of Scientific & Technical Research (BJSTR) - Year 2017, Vol 1, Issue 5
Abstract
Periprosthetic joint infection (PJI) is one of the most dreaded complications after total joint arthroplasty [1]. There is no gold standard for diagnosing PJI, hence, a clinician who encounters a suspected PJI case, ought to use a combination of tests. All of which, besides their expense can be invasive and even this can’t provide 100% accuracy [2]. Several biomarkers have been introduced that are potentially reliable tools for diagnosing PJI [3]. In this article, we aimed to review the current diagnostic measures of PJI with a special focus on molecular biomarkers. Synovial fluid biomarkers play an imperative role in the diagnosing PJI. Leukocyte esterase (LE), human α-defensin, human β-defensin, synovial CRP, and cathelicidin LL-37 are namely the biomarkers that have shown promising results. LE is an enzyme that is secreted by the activated neutrophils. It can be detected using colorimetric strip tests via reactions that result in a color change [4]. LE is a readily available and simple test and is now part of the minor criteria of the Musculoskeletal Infection Societydiagnostic criteria for PJI [5]. Tischler et al. [6] demonstrated that the LE strip test has a high specificity, positive, and negative predictive value for diagnosing PJI. Wetters et al. [7] investigated the accuracy of the LE test and reported a sensitivity of 92.9% to 100% and a specificity of 77.0% to 88.8%. The important point is to note that bloody samples cannot be evaluated for the LE test without being centrifuged as the presence of blood can potentially interfere with the colorimetric changes of the test strip [6]. Synovial fluid α-defensin test has shown great sensitivityand specificity for diagnosing PJI, 97% and 96% consequetively [8]. Defensins are 2-6 kDa cationic microbicidal peptides that are active against many Gram-negative and Gram-positive bacteria, fungi, and enveloped viruses [9]. Defensins in mammalians are classified into alpha, beta, and theta categories, based on their size and pattern of disulfide bonding. Alpha-defensins are particularly found in neutrophils, certain macrophage populations, and Paneth cells. Defensins are produced in response to microbial products or pro-inflammatory cytokines. The α-defensin mechanism by which microorganisms are killed and inactivated is not yet fully understood. Nevertheless, it is thought that it causes membrane disruption in microorganisms [10]. The spatially separated, charged, and hydrophobic regions, along with the polar topology of α-defensin, allows it to insert itself into the membranes; therefore, the hydrophobic regions are buried within the interior phospholipid membrane and the cationic sites interact with anionic phospholipid head groups and water. The disruption of membrane integrity and function leads to lysis of the microorganisms [11,12]. Several studies have endorsed the role of the α-defens in test in diagnosing PJI. The α-defensin test provides consistent results regardless of the organism type, Gram staining, species, or virulence of the organism [13].
Authors and Affiliations
George N. Guild, Alisina Shahi, Thomas L. Bradbury
Keywords
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- EP ID EP581020
- DOI 10.26717/BJSTR.2017.01.000453
- Views 170
- Downloads 0
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