Peri-implant Inflammation Defined by the Implant-Abutment Interface

TLDR

An implant‑abutment interface at the alveolar bone crest is linked to sustained peri‑implant inflammation, but it is unclear whether inflammation magnitude depends on interface position. The study compared inflammatory cell distribution and density around implants with different interface positions. The authors evaluated these differences by measuring inflammatory cell distribution and density across supracrestal, crestal, and subcrestal interfaces. Neutrophil accumulation peaked at or just above the interface and increased with deeper (subcrestal) interfaces, with greater densities correlating with bone loss, indicating that interface depth governs peri‑implant inflammation and bone loss.

Abstract

An implant-abutment interface at the alveolar bone crest is associated with sustained peri-implant inflammation; however, whether magnitude of inflammation is proportionally dependent upon interface position remains unknown. This study compared the distribution and density of inflammatory cells surrounding implants with a supracrestal, crestal, or subcrestal implant-abutment interface. All implants developed a similar pattern of peri-implant inflammation: neutrophilic polymorphonuclear leukocytes (neutrophils) maximally accumulated at or immediately coronal to the interface. However, peri-implant neutrophil accrual increased progressively as the implant-abutment interface depth increased, i.e., subcrestal interfaces promoted a significantly greater maximum density of neutrophils than did supracrestal interfaces (10,512 ± 691 vs. 2398 ± 1077 neutrophils/mm 2 ). Moreover, inflammatory cell accumulation below the original bone crest was significantly correlated with bone loss. Thus, the implant-abutment interface dictates the intensity and location of peri-implant inflammatory cell accumulation, a potential contributing component in the extent of implant-associated alveolar bone loss.