Related Experiment Video
Updated: Jun 24, 2026
Inducing Apical Periodontitis in Mice
Published on: August 6, 2019
Does an untreated peri-implant dehiscence defect affect the progression of peri-implantitis?: A preclinical in vivo
Young Woo Song1, Jin-Young Park2, Ji-Yeong Na2
1Department of Periodontology, Dental Hospital, Veterans Health Service Medical Center, Seoul, South Korea.
Objective:
To investigate the early impact of plaque accumulation in a buccal dehiscence defect on peri-implant marginal bone resorption.
Materials And Methods:
In six male Mongrel dogs, four dental implants were placed in the posterior maxilla on both sides (two implants per side). Based on the group allocation, each implant was randomly assigned to one of the following four groups to decide whether buccal dehiscence defect was prepared and whether silk ligation was applied at 8 weeks post-implant placement for peri-implantitis induction: UC (no defect without ligation); UD (defect without ligation); LC (no defect with ligation); and LD (defect with ligation) groups. Eight weeks after disease induction, the outcomes from radiographic and histologic analyses were statistically analyzed (p < .05).
Results:
Based on radiographs, the exposed area of implant threads was smallest in group UC (p < .0083). Based on histology, both the distances from the implant platform to the first bone-to-implant contact point and to the bone crest were significantly longer in the LD group (p < .0083). In the UD group, some spontaneous bone fill occurred from the base of the defect at 8 weeks after implant placement. The apical extension of inflammatory cell infiltrate was significantly more prominent in the LD and LC groups compared to the UC group (p < .0083).
Conclusion:
Plaque accumulated on the exposed implant surface had a negative impact on maintaining the peri-implant marginal bone level, especially when there was a dehiscence defect around the implant.
