The osteoimmune cell atlas of peri‐implantitis: A narrative scoping review

Background/Aim Peri‐implantitis represents a complex osteoimmune disorder characterized by dysregulated cellular ecosystems that drive chronic inflammation and accelerated peri‐implant bone loss. Materials and Methods This article was designed as a narrative scoping review to map and integrate the available evidence from transcriptomics, single‐cell RNA sequencing (scRNA‐seq), spatial transcriptomics, flow cytometry, and immunohistochemistry to construct a comprehensive cellular atlas of peri‐implantitis. Key Findings Current evidence suggests that peri‐implantitis lesions contain expanded and activated neutrophil, macrophage, T‐cell, and B‐lineage compartments, together with stromal and vascular cell populations that may contribute to inflammatory amplification and osteoclastogenic signaling. Reported features include CXCR2 + neutrophil subsets with NETosis‐associated activity, inflammatory macrophage states, altered Th17/Treg‐related immune responses, and expanded B‐cell/plasma‐cell compartments forming organized adaptive immune niches. Proposed molecular mechanisms include NF‐κB‐related inflammatory activation, CXCL13‐associated adaptive immune organization, NETosis‐related pathways, and RANKL‐mediated osteoclastogenic signaling. However, several of these pathways remain incompletely validated in human peri‐implantitis tissue. Critical knowledge gaps include limited direct evidence for NLRP3 inflammasome activation, uncharacterized type I interferon signaling, unresolved hierarchies of cellular RANKL sources, and limited functional data for rare immune populations. Conclusions The peri‐implantitis osteoimmune microenvironment constitutes a highly organized, self‐reinforcing inflammatory ecosystem. Progress toward precision therapeutic strategies requires spatial multiomics at subcellular resolution, longitudinal human studies, and functional ex vivo validation models to interrogate the self‐sustaining circuits identified here.