(1) Abstract: 

This review constructs an osteoimmune cell atlas of peri-implantitis by integrating transcriptomics, single-cell RNA sequencing, spatial transcriptomics, flow cytometry, and immunohistochemistry. It describes expanded and activated neutrophils, macrophages, T cells, B cells/plasma cells, and stromal and vascular populations, proposes NF-κB-, CXCL13-, NETosis-, and RANKL-related mechanisms, and highlights knowledge gaps including NLRP3 and type I interferon signaling.

(2) Background: 

Peri-implantitis is a chronic inflammatory disease of peri-implant tissues characterized by progressive bone loss. It differs from periodontitis in inflammatory infiltrate extent, osteoimmune features, and tissue destruction rate. Traditional histopathology, immunohistochemistry, and bulk transcriptomics cannot fully resolve cellular heterogeneity and spatial organization. Single-cell and spatial transcriptomics provide new opportunities for atlas construction.

(3) Main Content: 

The review is organized by cell type: neutrophils show CXCR2+ subsets and NETosis-related activity; macrophages include M1-like, M2-like, CD300E+, CD163L1+, and C1QA+ subsets with lineage commitment skewed toward inflammation and osteoclastogenesis; T cells show enhanced CD4+ activation, Th17/Treg imbalance, and impaired Treg function; B cells/plasma cells expand and form CXCL13-associated adaptive immune niches. Less-studied populations including dendritic cells, NK cells, and mast cells are also discussed, along with NF-κB, NLRP3, CXCL13, and RANKL molecular circuits.

(4) Study Design: 

A narrative scoping review. It integrates bulk transcriptomics, single-cell RNA sequencing, spatial transcriptomics, flow cytometry, and immunohistochemistry, explicitly distinguishing direct evidence from human peri-implantitis tissues from indirect evidence derived from animal models, periodontitis studies, bioinformatic deconvolution, or ligand-receptor analyses; the latter are regarded as hypothesis-generating rather than functional validation.

(5) Results: 

Peri-implantitis lesions display a highly structured osteoimmune ecosystem with gradient inflammatory infiltration toward the implant interface and CD38+ endothelial immune-vascular hubs. Neutrophils expand with disease-specific states, macrophage lineage commitment skews toward inflammation and osteoclastogenesis, Th17/Treg balance is disturbed, and B cells/plasma cells expand into CXCL13-associated adaptive immune niches. Fibroblast-neutrophil and endothelial-immune communication circuits sustain chronic inflammation.

(6) Future Directions: 

Longitudinal human studies, subcellular-resolution spatial multiomics, and ex vivo functional validation models are needed; osteal macrophages and efferocytosis, direct NLRP3 inflammasome evidence, type I interferon signaling, and RANKL cellular source hierarchies require clarification; protein-level validation should be integrated to distinguish causal from secondary mechanisms and to systematically dissect immune-stromal-vascular interaction networks.

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