Dental implant surfaces treated with phosphoric acid can modulate cytokine production by blood MN cells

Abstract

The study characterizes dental implant surfaces treated with phosphoric acid to assess the effects of acid treatment on blood cells and correlate them with cytokine levels. The implant surfaces examined were divided into untreated metal surface (US; n = 50), metal surface treated with phosphoric acid (ATS; n = 50) and cement surface (CS; n = 50) groups. The samples were characterized by scanning electron microscopy (SEM) and rheometry. The implants were incubated with human blood mononuclear cells for 24 h, with surface rinsing in the ATS treatment. Cell viability was determined by colorimetric methods and cytokines in the culture supernatant were quantified using flow cytometry. In the ATS group, the surface porosity and contact surface were increased and plaques were observed on the surface. The blood flow and viscosity curves were similar among the treatments, and the high cell viability rates indicate the biocompatibility of the materials used. An increase in the levels of IL-2, IL-4, IL-6, IL-10 and TNF-α was observed in the ATS and CS groups. There were positive correlations between IL-10 and IL-2 levels and between IL-10 and IL-4 levels in the culture supernatant of the ATS group. The results suggest that implant surface treatment with phosphoric acid activates the production of inflammatory cytokines. The increased cytokine levels can modulate the immune response, thereby improving biofunctional processes and promoting the success of dental implants.

Immunological Aspects of Dental Implant Rejection

“…IL-17, which immune reaction is mediated by Th17 cells, is another kind of proinflammatory molecule that takes part in excessive inflammatory actions [ 63 ] such as macrophage and neutrophil recruitment and some other proinflammatory mechanisms' stimulation [ 42 ]. Levels of IL-17 are high in patients with peri-implantitis, which proved that this cytokine augments local inflammation [ 42 , 59 , 60 , 64 ].…”

“…Moreover, the vast quantity of IL-6 production and also inflammatory response is correlated to the great tissue trauma [ 10 ]. Levels of IL-6 are high in failed implants in comparison to healthy implants [ 11 , 51 , 53 , 55 , 60 , 68 – 71 ]. However, Severino et al concluded that there was no significant difference when comparing the levels of IL-6 between healthy and peri-implantitis conditions [ 64 ].…”

“…IL-2 is a cytokine that has a crucial role in promoting cell proliferation. Its increase not only exhibits improved fixation and roughness because of the acid treatment but also is helpful in the biological acceptance of the implant [ 60 ]. Moreover, one study showed that the upregulation of IL-2 might cause failure in implants [ 60 ].…”

“…Its increase not only exhibits improved fixation and roughness because of the acid treatment but also is helpful in the biological acceptance of the implant [ 60 ]. Moreover, one study showed that the upregulation of IL-2 might cause failure in implants [ 60 ]. Mannose-binding lectin level is another factor, which can contribute in inflammation [ 73 ] but no study investigated its role, and further studies are needed.…”

“…The primary function of this cytokine is the elimination and limitation of inflammatory reactions. Therefore, IL-10 is a critical immune modulator [ 74 ] and plays a positive role in vivo regulation, dampens acute inflammatory feedbacks, and produces a negative feedback loop that decreases the inflammatory mediators' release [ 60 ]. It suppresses macrophage and Th17 responses by inhibiting the production of proinflammatory cytokines like IL-6 and TNF- α [ 75 ].…”