Influences of standardized clinical probing on peri-implant soft tissue seal in a situation of peri-implant mucositis: A histomorphometric study in dogs.

BACKGROUND: Clinical probing is commonly recommended to evaluate peri-implant conditions. In a situation of peri-implant mucositis or peri-implantitis, the peri-implant seal healing from the disruption of soft tissue caused by probing has not yet been studied. This study aimed to investigate soft tissue healing after standardized clinical probing around osseointegrated implants with peri-implant mucositis in a dog model. METHODS: Three transmucosal implants in each hemi-mandible of six dogs randomly assigned to the peri-implant healthy group or peri-implant mucositis group were probed randomly in the mesial or distal site as probing groups (PH or PM), the cross-sectional opposite sites as unprobed control groups. Histomorphometric measurements of implant shoulder (IS)-most coronal level of alveolar bone contact to the implant surface (BCI), apical termination of the junctional epithelium (aJE)-BCI, mucosal margin (MM)-BCI, and MM-aJE were performed at 1 day, 1 week, and 2 weeks after probing. Apoptosis, proliferation, proinflammatory cytokines, and matrix metalloproteinases (MMPs) of peri-implant soft tissue were estimated by immunofluorescent analysis. RESULTS: In the PM group, apical migration of junctional epithelium was revealed by significantly decreased aJE-BCI from 1 day to 2 weeks in comparison to unprobed sites (p < 0.05), while no significant differences were found in the PH group. Immunofluorescent analysis showed higher levels of interleukin-1ß (IL-1ß), IL-6, tumor necrosis factor-α (TNF-α), MMP-1, and MMP-8, together with exaggerated apoptosis and proliferation of peri-implant soft tissue in the PM group. CONCLUSION: Within the limitations, standardized clinical probing might lead to apical migration of the junctional epithelium in a situation of peri-implant mucositis.

Asperuloside Prevents Peri-Implantitis via Suppression of NF-κB and ERK1/2 on Rats.

Peri-implantitis is characterized by inflammatory cell infiltration and hyperactivation of the osteoclasts surrounding dental implants which can result in bone resorption and ultimately implant failure. Therefore, coordinating the activity of inflammatory response and bone-resorbing osteoclasts is crucial for the prevention of peri-implantitis. Asperuloside (ASP), an iridoid glycoside, has significant anti-inflammatory activities, suggesting the great potential in attenuating peri-implantitis bone resorption. A ligature-induced peri-implantitis model in the maxilla of rats was established, and the effects of ASP on preventing peri-implantitis were evaluated after four weeks of ligation using micro-CT and histological staining. RT-PCR, western blotting, tartrate-resistant acid phosphatase (TRAP), and immunofluorescent staining were conducted on osteoclasts to confirm the mechanisms of ASP on osteoclastogenesis. The results show that ASP could lead to attenuation of alveolar bone resorption in peri-implantitis by inhibiting osteoclast formation and decreasing pro-inflammatory cytokine levels in vivo. Furthermore, ASP could inhibit osteoclastogenesis by downregulating expression levels of transcription factors nuclear factor of activated T-cell (NFATc1) via restraining the activations of nuclear factor kappa beta (NF-κB) and the phosphorylation of extracellular signal-related kinase 1/2 (ERK1/2). In conclusion, ASP could significantly attenuate bone resorption in peri-implantitis via inhibition of osteoclastogenesis by suppressing NF-κB and ERK1/2 signaling pathways activations.

The mechanically activated p38/MMP-2 signaling pathway promotes bone marrow mesenchymal stem cell migration in rats.

OBJECTIVE: The aim of the present study was to investigate the effect of static strain on bone marrow mesenchymal stem cell (BMMSC) migration and whether the p38/matrix metalloproteinase-2 (MMP-2) axis plays a role in induction of BMMSC migration under mechanical strain. DESIGN: Both in vivo and in vitro investigations were performed. Twelve adult male Sprague-Dawley rats were randomly divided into 2 groups (n=6 per group). Rats in the experimental group underwent right mandibular distraction osteogenesis, whereas rats in the control group were subjected to osteotomy in the mandible without distraction. Immunohistochemistry and immunofluorescence were performed to evaluate phospho-p38 (p-p38) and Nestin expression. BMMSCs were isolated from rat mandibles. BMMSCs in the experimental group were subjected to static mechanical strain for 2h, whereas those in the control group underwent no strain. The biological roles of static strain and the p38/MMP-2 axis in BMMSC migration were evaluated by Transwell assays and western blotting by inhibiting p38 phosphorylation. RESULTS: There were significantly more Nestin+ cells in the bone calluses of the experimental group than in those of the control group. In addition, Nestin+/p-p38+ cell numbers were significantly higher in the experimental group than in the control group, indicating that static strain activated p38 signaling in BMMSCs in vivo. In accordance with in vivo results, static strain in vitro stimulated phosphorylation of p38 in BMMSCs. Furthermore, expression of MMP-2 was elevated in BMMSCs under static strain compared with the control, and strain-induced MMP-2 expression was abolished by inhibition of p38 phosphorylation in BMMSCs. Moreover, Transwell assay results showed that static strain promoted BMMSC migration, which was abolished by inhibition of p38 phosphorylation. CONCLUSIONS: The present study demonstrated that static strain can promote the migration ability of BMMSCs via p38/MMP-2 signaling. To the best of our knowledge, this study is the first report demonstrating that the p38/MMP-2 axis governs BMMSC migration under static mechanical strain.