Authors
Eun-Bin Bae, Ahana Goswami, Jun Yaung, Soo Yeon Kim, Sherry S Baik, Kaylyn A Yu, Chan Park, Jung-Bo Huh, Jae-Young Kim, Christine Y Hong, Sol Kim, Reuben H Kim
Published in
Clinical oral implants research. Oct 20, 2026. Epub Oct 20, 2026.
Abstract
Medication-related osteonecrosis of the jaw (MRONJ) is a debilitating condition associated with antiresorptive agents (ARAs) and can occur around well-osseointegrated dental implants. Although implant presence-triggered osteonecrosis (IPTO) has been primarily linked to bacteria-related peri-implantitis, whether occlusal trauma contributes to IPTO remains unclear. Therefore, this study developed a novel premature occlusal contact (POC) mouse implant model to evaluate the effect of occlusal trauma on MRONJ development around osseointegrated implants.
Eighteen mice underwent bilateral maxillary first molar extraction followed by immediate implant placement. After a 3-week healing period to allow osseointegration, mice were randomized to receive intravenous zoledronic acid (ZOL, 125 μg/kg) or saline vehicle (Veh) twice weekly (n = 9 per group). One week later, POC was induced in a split-mouth design by applying composite resin to one implant, whereas the contralateral implant served as a control. After 5 weeks of occlusal loading, mice were euthanized for μCT and histological analyses.
μCT analysis revealed that POC reduced radiographic bone-to-implant contact (rBIC) in both Veh- and ZOL-treated mice. POC significantly increased empty lacunae around the implant neck in Veh-treated mice, whereas in ZOL-treated mice, POC induced extensive circumferential bone necrosis around the implant, accompanied by increased macrophage infiltration. No significant differences in peptidoglycan (PGN)-positive signals were observed among the experimental groups.
These findings suggest that POC contributes to peri-implant osteonecrosis under ZOL treatment, supporting occlusal trauma as an important local factor in MRONJ development around osseointegrated dental implants.
PMID:
42902500
Bibliographic data and abstract were imported from PubMed on 21 Oct 2026.
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