Abstract
A projected increased use of total joint arthroplasties will naturally result in a related increase in the number of prosthetic joint infections (PJIs). Suppression of the local peri-implant immune response counters efforts to eradicate bacteria, allowing the formation of biofilms and compromising preventive measures taken in the operating room. For these reasons, the prevention of PJI should focus concurrently on the following targets: (i) identifying at-risk patients; (ii) reducing “bacterial load” perioperatively; (iii) creating an antibacterial/antibiofilm environment at the site of surgery; and (iv) stimulating the local immune response. Despite considerable recent progress made in experimental and clinical research, a large discrepancy persists between proposed and clinically implemented preventative strategies. The ultimate anti-infective strategy lies in an optimal combination of all preventative approaches into a single “clinical pack”, applied rigorously in all settings involving prosthetic joint implantation. In addition, “anti-infective” implants might be a choice in patients who have an increased risk for PJI. However, further progress in the prevention of PJI is not imaginable without a close commitment to using quality improvement tools in combination with continual data mining, reflecting the efficacy of the preventative strategy in a particular clinical setting.
Highlights
Prosthetic joint infection (PJI) is a disastrous complication of modern orthopedic surgery, frequently leading to prolonged morbidity and even to increased mortality [1,2,3]
PJI may be a manifestation of host–bacteria interactions that differ from those traditionally assumed to result from intraoperative colonization of implant surfaces
* high-volume surgeons working in the best operating rooms; ATB: antibiotic; BMI: body mass index; MA: meta-analysis; methicillin-resistant S. aureus (MRSA): methicillin-resistant Staphylococcus aureus; PJI: prosthetic joint infection; postop.: postoperatively; preop.: preoperatively; surgical site infections (SSIs): surgical site infection; SR: systematic review; total joint arthroplasty (TJA): total joint infection; TNF: tumor necrosis factor
Summary
Prosthetic joint infection (PJI) is a disastrous complication of modern orthopedic surgery, frequently leading to prolonged morbidity and even to increased mortality [1,2,3]. And delayed PJIs are associated with direct contamination at the time of surgery, awrheearsesaoscilate/dhwemitahtodgireencotucsonPtJaIsmairneaatisosnocaitatehde twimithe obflosoudrgdeerlyi,vwerhyeorefains fleacttei/vheemagaetnotgse. OOnnccee fifirrmmllyy aattttaacchheedd ttoo tthhee ssuurrffaaccee ooff aann iimmppllaanntt,, tthhee mmiiccrroooorrggaanniissmmss iinniittiiaattee bbiiooffiillmm ffoorrmmaattiioonn,, wwhhiicchh iiss ththeecrceraetaiotinonofoaf “aba“cbtearcitaelrtiaislsuties”su[2e3”].[T23h]e. Intracellular bacteria including Staphylococci spp. can live in cytoplasm (cytoplasmic vacuoles) [28], and some pathogens can even invade the intranuclear environment [29]. Despite this intracellular umbrella, these bacteria cannot escape from the cells of innate immunity and can, for instance, be identified through a specific sensing mechanism of inflammasomes [30,31]. Details on host–intracellular pathogen interactions have been given elsewhere [33,34]
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