Objective To establish an experimental peri-implantitis model and investigate the effects of titanium ions(TI) on inflammatory response and bone remodeling in peri-implantitis(PI).

Methods Thirty-two SD(Sprague-Dawley) rats were randomly divided into four groups: healthy implant group(HI group), HI+TI group, PI group and PI+TI group. Micro-implants were implanted in the maxillary first molar region of the rats, and after a 4-week healing period, ligation was performed to induce inflammation in the PI group and PI+Ti group, followed by local injection of titanium ion solution(10 μg/mL) for a 4-week intervention. Gingival tissue morphology was observed; bone resorption was measured using micro-computed tomography(Micro-CT); inflammatory infiltration and osteoclast count were assessed using hematoxylin-eosin(HE) staining and tartrate-resistant acid phosphatase(TRAP) staining; matrix metalloproteinase-8(MMP-8) and tumor necrosis factor-α(TNF-α) expressions were detected by immunohistochemistry(IHC); and the mRNA expressions of interleukin-1β(IL-1β), tumor necrosis factor-α(TNF-α), receptor activator of nuclear factor κB(RANKL), and osteoprotegerin(OPG) were detected by real-time quantitative PCR(RT-qPCR).

Results Compared with the HI group and the HI+TI group, the PI group and the PI+TI group showed gingival redness and swelling, and increased bone resorption(P < 0.05). Compared with the PI group, the PI+Ti group exhibited significantly higher numbers of osteoclasts, as well as significantly increased positive expressions of MMP-8 and TNF-α(all P < 0.05). Compared with the PI group, the PI+TI group showed upregulated mRNA expression levels of IL-1β, TNF-α, and RANKL, and an increased RANKL/OPG ratio(P < 0.05).

Conclusion Titanium ions can synergistically exacerbate peri-implant inflammatory infiltration and bone resorption in the inflammatory microenvironment. This mechanism may be related to the upregulation of inflammatory factors such as TNF-α, IL-1β, and RANKL, as well as the promotion of activation of bone resorption-related signaling pathways.