The role of bacterial corrosion on recolonization of titanium implant surfaces: An in vitro study.

BACKGROUND: Inflammation triggered by bacterial biofilms in the surrounding tissue is a major etiological factor for peri-implantitis and subsequent implant failure. However, little is known about the direct effects of bacterial corrosion and recolonization on implant failure PURPOSE: To investigate the influence of oral commensals on bacterial corrosion and recolonization of titanium surfaces. MATERIALS AND METHODS: Streptococcus sanguinis (S. sanguinis) and Porphyromonas gingivalis (P. gingivalis), which are key bacteria in oral biofilm formation, were cultured on commercially pure titanium and titanium-aluminum-vanadium (Ti6Al4V) plates in artificial saliva/brain heart infusion medium under aerobic or anaerobic conditions. Biofilm formation was examined after 7 and 21 days by crystal violet and live/dead staining. Titanium ions released into culture supernatants were analyzed over a period of 21 days by atomic absorption spectrometry. Visual changes in surface morphology were investigated using scanning electron microscopy. Biofilm formation on sterilized, biocorroded, and recolonized implant surfaces was determined by crystal violet staining. RESULTS: S. sanguinis and P. gingivalis formed stable biofilms on the titanium samples. Bacterial corrosion led to a significant increase in titanium ion release from these titanium plates (p < 0.01), which was significantly higher under aerobic conditions on pure titanium (p ≤ 0.001). No obvious morphological surface changes, such as pitting and discoloration, were detected in the titanium samples. During early biofilm formation, the addition of titanium ions significantly decreased the number of live cells. In contrast, a significant effect on biofilm mass was only detected with P. gingivalis. Bacterial corrosion had no influence on bacterial recolonization following sterilization of titanium and Ti6Al4V surfaces. CONCLUSION: Bacterial corrosion differs between oral commensal bacteria and leads to increased titanium ion release from titanium plates. The titanium ion release did not influence biofilm formation or bacterial recolonization under in vitro conditions.

Do oral bacteria alter the regenerative potential of stem cells? A concise review.

Mesenchymal stem cells (MSCs) are widely recognized as critical players in tissue regeneration. New insights into stem cell biology provide evidence that MSCs may also contribute to host defence and inflammation. In case of tissue injury or inflammatory diseases, e.g. periodontitis, stem cells are mobilized towards the site of damage, thus coming in close proximity to bacteria and bacterial components. Specifically, in the oral cavity, complex ecosystems of commensal bacteria live in a mutually beneficial state with the host. However, the formation of polymicrobial biofilm communities with pathogenic properties may trigger an inadequate host inflammatory-immune response, leading to the disruption of tissue homoeostasis and development of disease. Because of their unique characteristics, MSCs are suggested as crucial regulators of tissue regeneration even under such harsh environmental conditions. The heterogeneous effects of bacteria on MSCs across studies imply the complexity underlying the interactions between stem cells and bacteria. Hence, a better understanding of stem cell behaviour at sites of inflammation appears to be a key strategy in developing new approaches for in situ tissue regeneration. Here, we review the literature on the effects of oral bacteria on cell proliferation, differentiation capacity and immunomodulation of dental-derived MSCs.

Dental follicle progenitor cells responses to Porphyromonas gingivalis LPS.

Periodontitis is a bacterially induced chronic inflammatory disease. Dental follicle progenitor cells (DFPCs) have been proposed as biological graft for periodontal regenerative therapies. The potential impact of bacterial toxins on DFPCs properties is still poorly understood. The aim of this study was to investigate whether DFPCs are able to sense and respond to lipopolysaccharide (LPS) from Porphyromonas gingivalis, a major periopathogenic bacterium. Specifically, we hypothesized that LPS could influence the migratory capacity and IL-6 secretion of DFPCs. DFPCs properties were compared to bone marrow mesenchymal stem cells (BMSCs), a well-studied class of adult stem cells. The analysis by flow cytometry indicated that DFPCs, similar to BMSCs, expressed low levels of both toll-like receptor (TLR) 2 and 4. The TLR4 mRNA expression was down-regulated in response to LPS in both cell populations, while on protein level TLR4 was significantly up-regulated on BMSCs. The TLR2 expression was not influenced by the LPS treatment in both DFPCs and BMSCs. The migratory efficacy of LPS-treated DFPCs was evaluated by in vitro scratch wound assays and found to be significantly increased. Furthermore, we assayed the secretion of interleukin-6 (IL-6), a potent stimulator of cell migration. Interestingly, the levels of IL-6 secretion of DFPCs and BMSCs remained unchanged after the LPS treatment. Taken together, these results suggest that DFPCs are able to sense and respond to P. gingivalis LPS. Our study provides new insights into understanding the physiological role of dental-derived progenitor cells in sites of periodontal infection.