RESUMO
AIM: To investigate the influence of diabetes mellitus (DM) in a murine model of peri-implantitis (PI). MATERIALS AND METHODS: Twenty-seven 4-week-old C57BL/6J male mice had their first and second maxillary left molars extracted. Eight weeks later, one machined implant was placed in each mouse. Four weeks after osseointegration, the mice were divided into three groups: (a) control (C), (b) PI and (c) DM + PI. DM was induced by streptozotocin (STZ) administration. After DM induction, PI was induced using ligatures for 2 weeks. The hemimaxillae were collected for micro-CT and histological analyses. The primary outcomes consisted of linear (mm) and volumetric (mm3) bone loss. Secondary outcomes were based on histological analysis and included inflammatory infiltrate, osteoclastic activity, matrix organization, composition and remodelling. Data are presented as means ± SEM. Statistical analyses were performed using one-way ANOVA, followed by Tukey's test. RESULTS: Gingival tissue oedema was detected in the PI and DM + PI groups. Micro-CT showed significantly increased linear and volumetric bone loss in the DM + PI group compared to the C and PI groups. H&E staining showed greater inflammatory response and bone resorption in the PI and DM + PI groups than in the C group. The DM + PI group had significantly higher osteoclast numbers than the C and PI groups. Picrosirius red stained less for types I and III collagen in the PI and DM + PI groups than in the C group. There was a significant increase in monocyte/macrophage (CD-11b) counts and matrix metalloproteinases (MMP-2 and MMP-8) marker levels and a significant decrease in the matrix metalloproteinases inhibition marker (TIMP-2) levels in the DM + PI group compared to the C and PI groups. CONCLUSIONS: DM exacerbates PI-induced soft-tissue inflammation, matrix degradation and bone loss.
RESUMO
Dental implants are increasing in prevalence as desirable options for replacing missing teeth. Unfortunately, implants come with complications, and animal models are crucial to studying the pathophysiology of complications. Current murine model experiments can be lengthy, with 8 weeks of extraction socket healing before implant placement. Therefore, we aimed to investigate the efficacy of decreasing extraction healing time from 8 to 4 weeks in a dental implant mouse model. Thirty-one 3-week-old C57BL/6J male mice underwent maxillary first and second molar extractions followed by 8 (control) or 4 (test) weeks of extraction socket healing before implant placement. Mice were euthanized after 4 weeks of implant osseointegration. Samples were analyzed via microcomputerized tomography and histology. When mice received implants 4 weeks after extractions, there was no statistical difference in initial bone crest remodeling or surrounding bone volume compared to those after 8 weeks of healing. Histologically, the hard and soft tissues surrounding both groups of implants displayed similar alveolar bone levels, inflammatory infiltrate, osteoclast count, and collagen organization. A 4-week extraction healing period can be utilized without concern for osseointegration in a murine implant model and is a viable experimental alternative to the previous eight weeks of healing. While small animal implant models are less directly applicable to humans, advancements in experimental methods will ultimately benefit patients receiving dental implants through improved prevention and treatment of complications. Subsequent research could investigate occlusal effects or whether healing time affects prognosis after induction of peri-implantitis.