Peri-implantitis and systemic inflammation: the evidence is still thin

For periodontitis, the link with systemic inflammation has become part of the clinical conversation. For peri-implantitis the same story is often told by analogy. This systematic review, published in the Journal of Periodontal Research by a Santiago de Compostela–Loma Linda group, asks whether the analogy holds up.

The authors searched MEDLINE, Embase, Scopus and Web of Science from inception to December 2025, with an update in April 2026, following PRISMA guidelines. They included observational studies comparing systemic inflammatory biomarkers or systemic diseases in people with and without peri-implantitis, and interventional studies testing whether treating peri-implantitis changes systemic inflammatory burden. Random-effects meta-analyses used standardised mean differences (Hedges' g). Particular attention went to methodological limits and residual confounding.

Of 2,399 records screened, 21 studies were included: 14 observational studies on inflammatory biomarkers, three randomised trials on the systemic effect of treatment, and four observational studies on systemic diseases. Conventional C-reactive protein (CRP) was significantly higher in patients with peri-implantitis than in healthy implant controls (Hedges' g = 3.73; 95% CI 0.63–6.83), but heterogeneity was extreme (I² = 99%). High-sensitivity CRP, the more precise marker, showed no significant difference (g = −0.29; I² = 2%), and neither did IL-6, TNF-α, IL-10 or IL-1β. Evidence on systemic diseases was too sparse and heterogeneous to pool. After peri-implantitis treatment, the interventional studies suggested modest and mostly short-term reductions in selected biomarkers, without consistent improvements in systemic metabolic outcomes.

The authors read their own numbers with caution. The only positive pooled signal rests on highly heterogeneous data and disappears with high-sensitivity CRP. Most studies did not adequately control for the obvious confounder, previous or concurrent periodontitis, nor for shared metabolic and inflammatory risk factors. It therefore remains open whether peri-implantitis is an independent source of systemic inflammation or simply the visible expression of a susceptible host.

Clinical relevance: peri-implantitis should be treated for the sake of the implant and the surrounding tissues. On current evidence, it is not appropriate to promise patients systemic benefits from that treatment. Well-designed longitudinal and interventional studies are needed before any such claim can be made.