Teodor Paul Chioașcă

Background: Patients with diabetes mellitus exhibit increased susceptibility to peri-implant inflammation and implant failure due to systemic metabolic dysfunction, impaired immunity, and delayed tissue healing. The oral microbiome is increasingly recognized as a key intermediary in these pathogenic processes. Aims: This review aims to systematically evaluate the available literature examining the relationships among the oral microbiome, biomaterial biocompatibility, and inflammatory changes in peri-prosthetic tissues in insulin-dependent diabetic patients. Methods: A systematic search of PubMed and Scopus databases identified studies published between January 2000 and July 2025. Eligible studies (25 in total) included clinical, histological, microbiological, or immunohistochemical investigations involving diabetic patients rehabilitated with dental implants or prostheses. Study selection and reporting followed PRISMA 2020 guidelines. Results: Diabetic cohorts showed consistent microbial alterations, including a higher relative abundance of periopathogenic species (P. gingivalis, T. forsythia, and F. nucleatum), lower microbial diversity, and greater biofilm-forming potential. Histological analyses frequently described increased inflammatory infiltrates, higher cytokine expression, and reduced soft-tissue integration. Biomaterial surface characteristics were also associated with differences in microbial adhesion, while hyperglycemia was linked to microbial and host-response patterns suggestive of greater pathogenicity and inflammation. Collectively, these findings suggest that diabetes-associated dysbiosis may be associated with increased peri-implant inflammatory changes and altered peri-implant homeostasis. Conclusions: The oral microbiome may be involved in inflammatory activity and biocompatibility at the tissue–implant interface in diabetic patients. A better understanding of host–microbe–material interactions may support risk assessment and help inform future personalized management strategies, such as targeted antimicrobial approaches, probiotic modulation, and biomaterial surface optimization, although these implications should be interpreted cautiously given the predominantly observational and heterogeneous nature of the available evidence.

Inflammatory bowel diseases (IBDs) encompass Crohn’s disease and ulcerative colitis. They represent idiopathic and chronic inflammatory conditions. Mucosal immune dysfunction and compromised gastrointestinal barrier integrity are implicated in the pathophysiological mechanisms of inflammatory bowel diseases. Recent studies have identified endothelial dysfunction as a pivotal mediator in IBD pathogenesis. Through multiple cellular and molecular interactions, endothelial dysfunction orchestrates inflammatory responses. Objectives: This systematic review examines contemporary evidence (2019–2025), emphasising the role of endothelial dysfunction in intestinal inflammation mechanisms, focusing on vascular-epithelial crosstalk, molecular signalling pathways, and therapeutic implications. Methods and results: A comprehensive literature search was conducted using PubMed, Google Scholar, Europe PMC and DOAJ databases, focusing on peer-reviewed articles published between 2019 and 2025. Following the database search and screening process, a total of 53 studies met the eligible criteria and were included in the final analysis. Keywords included “endothelial dysfunction,” “inflammatory bowel disease,” “gut-vascular barrier,” “nitric oxide,” and “intestinal inflammation.” Contemporary research demonstrates that endothelial dysfunction in IBD manifests through decreased nitric oxide bioavailability, enhanced oxidative stress, aberrant cytokine networks, pathological angiogenesis, and compromised gut-vascular barrier integrity. The emerging concept of dual barrier dysfunction highlights the interdependent relationship between epithelial and endothelial barriers in maintaining intestinal homeostasis. Conclusions: Offering novel therapeutic targets for precision medicine approaches, endothelial dysfunction represents a central driver in the pathophysiological mechanism in IBD. Understanding vascular-epithelial interactions provides fundamental insights for developing targeted interventions to restore intestinal barrier function and resolve chronic inflammation.