Peri-implantitis and systemic inflammation – exploring the association

BACKGROUND: Periodontitis and peri-implantitis represent persistent oral sources of systemic inflammation, potentially influencing systemic biomarkers such as C-reactive protein (CRP) and various inflammatory cytokines. While the periodontal inflamed surface area (PISA) is used to quantify periodontal inflammation, no equivalent measure currently exists for peri-implantitis. In addition, strategies for the prevention and treatment of peri-implant diseases have been explored to reduce the local inflammatory burden. The research presented here aimed to investigate the association between peri-implantitis and systemic inflammation, develop and validate a novel peri-implant inflammatory index (dental-implant inflamed surface area, DISA), and explore preventive and therapeutic approaches to reduce the local inflammation burden. METHODS: A comprehensive multi-method research programme was conducted: 1. Systematic review of the association between peri-implantitis and systemic inflammatory markers. 2. Development and validation of the DISA index, enabling quantification of peri-implant inflammation. 3. Longitudinal assessment of DISA–CRP correlations and post-treatment changes. 4. Observational analysis of PISA–CRP associations. 5. In vitro study of titanium implant surface modification to prevent bacterial accumulation, biofilm formation and reduce local inflammation. 6. Systematic review of the impact of peri-implantitis treatment-adjunctive photodynamic therapy (PDT) on local clinical parameters. RESULTS: Evidence supports a link between peri-implantitis and elevated systemic inflammation. PISA was positively associated with CRP, and subsequently, the DISA score was developed, validated, and shown to correlate with CRP. In vitro study has demonstrated a reduction in signalling molecules following titanium implant surface modification. In addition, a systematic review suggests that PDT is a promising treatment strategy for managing peri-implant diseases. CONCLUSION: This thesis provides new evidence connecting peri-implantitis to systemic inflammation, introduces DISA as the peri-implant-specific inflammatory burden score. Preventive (titanium surface modification) and therapeutic (PDT) strategies for peri-implant diseases could potentially reduce the local inflammatory burden. Further validation of DISA in diverse cohorts and evaluation of its prognostic potential in systemic disease contexts are warranted.