Abstract
Orthopedic implant-related infections remain a major problem even nowadays. Bacterial resistance through biofilm formation, in addition to the limited treatment options available, has resulted in an increased effort to better understand pathophysiology mechanisms. We performed a review of the literature in order to identify major biofilm formation pathways through which possible treatment strategies could arise.
Highlights
Orthopedic devices are in common practice worldwide for a wide number of procedures, including, among others, fracture treatment and total joint replacements (TJR)
Biofilms complicate prosthetic joint implants at a rate of 1%-2% in primary joint replacement and in a percentage of 3%-5% in revision surgeries, even though rates as high as 20% have been referred [3]. The bone allografts, another common biomaterial in orthopedic procedures, have infection rates ranging from 4% to 12% [4]
The major bacteria responsible for periprosthetic infections are Staphylococcus (S.) epidermidis and S. aureus in 70% of all cases [5] while other bacteria are responsible for 22% of the infections [6]
Summary
Orthopedic devices are in common practice worldwide for a wide number of procedures, including, among others, fracture treatment and total joint replacements (TJR). The reversible phase ends with bonding the bacteria to the ECM components through the microbial surface components recognizing adhesive matrix molecules (MSCRAMMs) [15] Those adhesins recognize molecules of the ECM, especially fibronectin (FN) and fibrinogen (Fg), with the first one having been proved to multiply the adherent ability of S. aureus due to fibronectin-binding protein A (FnBPA) and FnBPB binding proteins [16]. Colonies that produce it can host neighboring colonies with species that cannot do so inside the same biofilm [29] These colonies communicate through interstitial voids (water channels) in which nutrients, signaling molecules, and extracellular DNA circulate [30]. S. aureus biofilms have been well-studied for their resistance to antibiotics and the host's immune system Those bacteria avoid phagocytosis by destroying local macrophages and polynuclear cells (PNC). The fact that QS regulates biofilm's resistance has gained attention as a possible new treatment strategy through QS interference, using hamamelitannin and vancomycin-releasing hydroxypropyl-β-cyclodextrin-functionalized cellulose gauzes [50]
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