The present data suggest that the increased levels of the selected PICF-derived biomarkers of periodontal tissue inflammation, matrix degradation/regulation, and alveolar bone turnover/resorption combined with site-specific microbial profiles may be associated with peri-implantitis and could have potential as predictors of peri-implant diseases.

Objectives The presence of titanium (Ti) particles around dental implants has been reported in the literature for decades. The prospective presence of Ti debris on soft tissues surrounding dental implants has not been systematically investigated and remains to be explored. Hence, this review aimed to evaluate the origin, presence, characteristics, and location of Ti particles in relation to dental implants. Material and methods Literature searches were conducted by two reviewers independently based on the PRISMA guidelines. The systematic review identified studies on Ti particles derived from dental implants. We evaluated several parameters, including anatomical location, and the suspected methods of Ti particles release. Results The search resulted in 141 articles, of which 26 were eligible and included in the systematic review of the literature. The investigations reported Ti and metal‐like particles in the soft (i.e., epithelial cells, connective tissue, and inflammatory cells) and hard (bone crest and bone marrow) tissues around the dental implants. Shape and size of the particles varied. The current literature reported a size range from 100 nm to 54 µm identified by multiple particles identification methods. Conclusion Ti particles surrounding peri‐implant tissues are a common finding. Peri‐implantitis sites presented a higher number of particles compared to healthy implants. The particles were mostly around the implants and inside epithelial cells, connective tissue, macrophages, and bone. Various mechanisms were described as causes of Ti release, including friction during implant insertion, corrosion of the implant surface, friction at the implant–abutment interface, implantoplasty, and several methods used for implant surface detoxification.

Aim To explore the M1/M2 status of macrophage polarization from healthy, gingivitis, and periodontitis patient samples. Materials and methods Gingival biopsies were collected from 42 individuals (14 gingivitis, 18 periodontitis, and 10 healthy samples) receiving periodontal therapy. Histomorphology analysis was performed with haematoxylin and eosin staining. Immunofluorescence was performed using a combination of CD68 (macrophages), iNOS (M1), and CD206 (M2) in order to acquire changes in macrophage polarization at a single‐cell resolution. Macrophages were quantified under microscopy using narrow wavelength filters to detect Alexa 488, Alexa 568, Alexa 633 fluorophores, and Hoechst 33342 to identify cellular DNA content. Results Gingivitis and periodontitis samples showed higher levels of macrophages compared with healthy samples. Unexpectedly, periodontitis samples displayed lower levels of macrophages dispersed in the stromal tissues compared with gingivitis samples; however, it remained higher than healthy tissues. The polarization of macrophages appears to be reduced in periodontitis and showed similar levels to those observed in healthy tissues. Conclusions Our study found that gingivitis and periodontitis differ from each other by the levels of macrophage infiltrate, but not by changes in macrophage polarization.

Within the limitations of the present study, the C/I ratio of implant-supported restorations has an effect on peri-implant marginal bone level. Within the range of 0.6/1 to 2.36/1, the higher the C/I ratio, the less the peri-implant MBL.

Periodontitis is a chronic infectious disease driven by dysbiosis, an imbalance between commensal bacteria and the host organism. Periodontitis is a leading cause of tooth loss in adults and occurs in about 50% of the US population. In addition to the clinical challenges associated with treating periodontitis, the progression and chronic nature of this disease seriously affect human health. Emerging evidence suggests that periodontitis is associated with mechanisms beyond bacteria-induced protein and tissue degradation. Here, we hypothesize that bacteria are able to induce epigenetic modifications in oral epithelial cells mediated by histone modifications. In this study, we found that dysbiosis in vivo led to epigenetic modifications, including acetylation of histones and downregulation of DNA methyltransferase 1. In addition, in vitro exposure of oral epithelial cells to lipopolysaccharides resulted in histone modifications, activation of transcriptional coactivators, such as p300/CBP, and accumulation of nuclear factor-κB (NF-κB). Given that oral epithelial cells are the first line of defense for the periodontium against bacteria, we also evaluated whether activation of pathogen recognition receptors induced histone modifications. We found that activation of the Toll-like receptors 1, 2, and 4 and the nucleotide-binding oligomerization domain protein 1 induced histone acetylation in oral epithelial cells. Our findings corroborate the emerging concept that epigenetic modifications play a role in the development of periodontitis.