Presence of ROS in Inflammatory Environment of Peri-Implantitis Tissue: In Vitro and In Vivo Human Evidence

Abstract

Analyses of composition, distribution of cellular and extracellular matrix components, and molecular analysis of mitochondria related genes of bone loss in the presence of inflammatory environment in humans was the aim of the present project. As a human model we chose peri-implantitis. Morphological analyses were performed by means classical histological, immunohistochemical, and SEM (scanning electron miscroscopy) test. Gene expression analysis was performed to evaluate epithelium maturation, collagen fiber production, and genes related to mitochondrial activity. It was found that a well-defined keratinocyte epithelium was present on the top of all specimens; a distinct basal lamina was present, as well as desmosomes and autophagic processes related to the maturation of keratinocytes. Under this epithelium, a full inflammatory cell infiltrate was present for about 60% of the represented by plasma cells. Collagen type I fibers were present mainly in the form of fragmented cord tissue without cells. A different distribution of blood vessels was also present from the apical to the most coronal portion of the specimens. High levels of genes related to oxidative stress were present, as well as the activation of genes related to the loss of ability of osteogenic commitment of Mesenchymal stem cells into osteoblasts. Our study suggests that peri-implantitis lesions exhibit a well defined biological organization not only in terms of inflammatory cells but also on vessel and extracellular matrix components even if no difference in the epithelium is evident, and that the presence of reactive oxygen species (ROS) related to the inflammatory environment influences the correct commitment of Mesenchymal stem cells.

Evaluation of Gingival Tissue Pathological Changes in Human Peri-implantitis: Histological, Immunohistochemical and Ultrastructural Study

“…It should also be noted that excessive collagenization was detected in the connective tissue in all cases of peri-implantitis as demonstrated by transmission electron microscope. Our results are in agreement with Mijiritsky et al (14) who demonstrated bundles of collagen fibers in the connective tissue underneath the epithelium in cases of periimplantitis. This finding could be mediated by cytokine pathway that is initiated by particles of implant material and then resulted in collagen production (26) .…”

“…Our present results are consistent with those of Mijiritsky et al (14) who reported an inflammatory infiltrate underneath the epithelium with collagen fibers in peri-implantitis tissue as well as a differ- ent distribution of blood vessels throughout the connective tissue. In contrast to our findings, some other studies have demonstrated an inflammatory infiltrate that was of T-cell dominated one in both normal gingival and peri-implantitis tissues (15,16) .…”

Evaluation of the anti-oxidative and ROS scavenging properties of biomaterials coated with epigallocatechin gallate for tissue engineering

“…Excessive ROS cause apoptosis and activation of inflammatory signaling cascades, leading to incomplete recovery of damaged tissue [ 1 , 2 ]. For example, the high level of ROS surrounding dental implants results in uncontrolled inflammation with bone loss, and elevation of ROS during autologous or allogenic hematopoietic stem cell transplantation (HSCT) can result in serious toxic problems [3][4][5] . It has been reported that pro-oxidant methemoglobin (Fe 3 + ) released from lysed blood cells and H 2 O 2 derived from the lysis of epithelial or immune cells during surgical incision of implantation process are associated with ROS-mediated failure of tissue engineering approaches [ 6 , 7 ].…”

Effect of Oxidative Stress on Bone Remodeling in Periprosthetic Osteolysis

“…Wear particles can be generated from the surface of the implant, but also from the contact point of modular implants [62]. The range and size of particles wear debris are heterogeneous: smaller particles are generated during repeated rolling movements and by sliding and rotational motion on bearing surface by adhesion and abrasion, while larger particles originate from surface fatigue [63]. The size of wear particles isolated from periprosthetic tissue has a range of 0.1 to 1000 µm, but the majority belongs to the range of 0.1 to 10 µm.…”