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.

Highlights

  • IntroductionIf the system is prolonged or inefficient, it changes to the chronic state of inflammation often associated with loss of tissues such as bone

  • Inflammation is the immune response i to foreign pathogens

  • Epithelium organization in the peri-implantitis specimens was evaluated by means of immunohistochemistry against keratin

Read more

Summary

Introduction

If the system is prolonged or inefficient, it changes to the chronic state of inflammation often associated with loss of tissues such as bone. During this stage, high levels of ROS are present in the tissue since it acts as both a signaling molecule and a mediator of inflammation. In chronically inflamed bone tissue is not rare to find adipocytes instead of osteocytes causing ROS bone loss In light of this consideration, in the present study we analyzed a human bone loss model related to a chronic state of inflammation: peri-implantitis. In this work we focused our attention on ROS physiology in severe peri-implantitis

Methods
Results
Discussion
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call