Infection is still the major complication of orthopedic implants and projections based on the actual trend indicate that total hip and knee arthroplasties and their consequent infection burden are destined to greatly increase. Staphylococcus aureus and Staphylococcus epidermidis are the leading etiologic agents of orthopedic implant infection. Here we report on epidemiology of implant-related Staphylococcus infections in orthopedics, also referring to our experience, and focus on the crucial role of bacterial adhesins and on their ability to direct the pathogenesis process. Bacteria initiate implant infection by adhering to biomaterials. In the early steps of infection, adhesins mediate the specific interaction between microbial cells and the extracellular matrix proteins filming biomaterial surface. Then adhesin-mediated anchorage allows bacteria to cling to the biomaterial surface and to produce a biofilm that favors their ability to resist antibiotics. With the aim to prevent implant-related infections, anti-infective and infection-resistant biomaterials are being developed. The research for novel therapeutic strategies is incited by the emergence of antibiotic-resistant bacteria. Vaccines against the adhesins or antisense molecules against virulence genes can open a future in combating implant infections.

Staphylococcus aureus and Staphylococcus epidermidis are the most important etiological agents of biofilm associated-infections on indwelling medical devices. Biofilm infections may also develop independently of indwelling devices, e.g., in native valve endocarditis, bone tissue, and open wounds. After attachment to tissue or indwelling medical devices that have been conditioned with host plasma proteins, staphylococcal biofilms grow, and produce a specific environment which provides the conditions for cell–cell interaction and formation of multicellular communities. Bacteria living in biofilms express a variety of macromolecules, including exopolysaccharides, proteins, extracellular eDNA, and other polymers. The S. aureus surface protein C and G (SasC and SasG), clumping factor B (ClfB), serine aspartate repeat protein (SdrC), the biofilm-associated protein (Bap), and the fibronectin/fibrinogen-binding proteins (FnBPA and FnBPB) are individually implicated in biofilm matrix formation. In S. epidermidis, a protein named accumulation-associated protein (Aap) contributes to both the primary attachment phase and the establishment of intercellular connections by forming fibrils on the cell surface. In S. epidermidis, proteinaceous biofilm formation can also be mediated by the extracellular matrix binding protein (Embp) and S. epidermidis surface protein C (SesC). Additionally, multifunctional proteins such as extracellular adherence protein (Eap) and extracellular matrix protein binding protein (Emp) of S. aureus and the iron-regulated surface determinant protein C (IsdC) of S. lugdunensis can promote biofilm formation in iron-depleted conditions. This multitude of proteins intervene at different stages of biofilm formation with certain proteins contributing to biofilm accumulation and others mediating primary attachment to surfaces. This review examines the contribution of proteins to biofilm formation in Staphylococci. The potential to develop vaccines to prevent protein-dependent biofilm formation during staphylococcal infection is discussed.

Neutrophils, complement system and skin collectively represent the main elements of the innate immune system, the first line of defence of the host against many common microorganisms. Bacterial pathogens have evolved strategies to counteract all these defence activities. Specifically, Staphylococcus aureus, a major human pathogen, secretes a variety of immune evasion molecules including proteases, which cleave components of the innate immune system or disrupt the integrity of extracellular matrix and intercellular connections of tissues. Additionally, S. aureus secretes proteins that can activate host zymogens which, in turn, target specific defence components. Secreted proteins can also inhibit the anti-bacterial function of neutrophils or complement system proteases, potentiating S. aureus chances of survival. Here, we review the current understanding of these proteases and modulators of host proteases in the functioning of innate immunity and describe the importance of these mechanisms in the pathology of staphylococcal diseases.

The use of indwelling medical devices has constantly increased in recent years and has revolutionized the quality of life of patients affected by different diseases. However, despite the improvement of hygiene conditions in hospitals, implant-associated infections remain a common and serious complication in prosthetic surgery, mainly in the orthopedic field, where infection often leads to implant failure. Staphylococcus aureus is the most common cause of biomaterial-centered infection. Upon binding to the medical devices, these bacteria proliferate and develop dense communities encased in a protective matrix called biofilm. Biofilm formation has been proposed as occurring in several stages—(1) attachment; (2) proliferation; (3) dispersal—and involves a variety of host and staphylococcal proteinaceous and non-proteinaceous factors. Moreover, biofilm formation is strictly regulated by several control systems. Biofilms enable staphylococci to avoid antimicrobial activity and host immune response and are a source of persistent bacteremia as well as of localized tissue destruction. While considerable information is available on staphylococcal biofilm formation on medical implants and important results have been achieved on the treatment of biofilms, preclinical and clinical applications need to be further investigated. Thus, the purpose of this review is to gather current studies about the mechanism of infection of indwelling medical devices by S. aureus with a special focus on the biochemical factors involved in biofilm formation and regulation. We also provide a summary of the current therapeutic strategies to combat biomaterial-associated infections and highlight the need to further explore biofilm physiology and conduct research for innovative anti-biofilm approaches.

Staphylococcus aureus is a versatile and harmful human pathogen in both hospital- and community-acquired infections. S. aureus can initiate host infection by adhering to components of the extracellular matrix. Adherence is mediated by a variety of protein adhesins of the microbial surface component recognizing adhesive matrix molecule (MSCRAMM) family. In this article, we describe these MSCRAMMs in terms of structural organization and ligand-binding capacity and discuss their role as a possible target for immunotherapy.

This study compared the solubility and the pH of different root canal sealers in vitro. BioRoot™RCS, TotalFill BC Sealer, MTA Fillapex, SealapexTM, AH Plus, EasySeal, Pulp Canal Sealer™ and N2 were tested. Similar specimens were prepared using ring molds with an internal diameter of 20 ± 0,1 mm and a height of 1,5 ± 0,1 mm and digitally weighted to register the mass of each specimen before and after immersion in distilled water. Solubility was determined after 24 hours and statistically analysed using a one-way ANOVA test and post-hoc Tukey test. The pH value was measured by a digital pH meter after 3 and 24 hours from manipulation. BioRoot™RCS and TotalFill BC Sealer showed significantly higher solubility (P<0.05). All the remnant root canal sealers fulfilled the requirements of solubility of the International Standard Organization 6876 demonstrating a weight loss of less than 3%. BioRoot™RCS and Totalfill BC Sealer exhibited high alkaline pH over time (P<0.05); the alkalinity of the other tested cements was significantly lower. The prolonged alkalinity of bioceramic sealer matched the increase in solubility. This may encourage their biological and antimicrobial effects, but the ongoing solubility may impact their ability to prevent apical leakage. Key words:pH, root canal sealers, solubility.