NLRP3 and AIM2 inflammasomes expression is modified by LPS and titanium ions increasing the release of active IL-1ß in alveolar bone-derived MSCs.

Periodontitis and peri-implantitis are inflammatory diseases of infectious etiology that lead to the destruction of the supporting tissues located around teeth or implants. Although both pathologies share several characteristics, it is also known that they show important differences which could be due to the release of particles and metal ions from the implant surface. The activation of the inflammasome pathway is one of the main triggers of the inflammatory process. The inflammatory process in patients who suffer periodontitis or peri-implantitis has been mainly studied on cells of the immune system; however, it is also important to consider other cell types with high relevance in the regulation of the inflammatory response. In that context, mesenchymal stromal cells (MSCs) play an essential role in the regulation of inflammation due to their ability to modulate the immune response. This study shows that the induction of NLRP3 and absent in melanoma 2 (AIM2) inflammasome pathways mediated by bacterial components increases the secretion of active IL-1ß and the pyroptotic process on human alveolar bone-derived mesenchymal stromal cells (hABSCs). Interestingly, when bacterial components are combined with titanium ions, NLRP3 expression is further increased while AIM2 expression is reduced. Furthermore, decrease of NLRP3 or AIM2 expression in hABSCs partially reverses the negative effect observed on the progression of the inflammatory process as well as on cell survival. In summary, our data suggest that the progression of the inflammatory process in peri-implantitis could be more acute due to the combined action of organic and inorganic components.

Is the degree of physiological bone remodeling a predictive factor for peri-implantitis?

BACKGROUND: The amount of initial physiological bone remodeling (IPBR) after implant placement varies and the ways it may play a role in peri-implantitis development remains unknown. The aim of this retrospective study was to investigate the association between the amount of IPBR during the first year of implant placement and incidence of peri-implantitis as well as the pattern of progressive bone loss. METHODS: Clinical and radiographic documentation of implants at the time of implant placement (T0), 1 year ± 6 months after crown placement (T1), and at a ≥2-year follow-up from implant placement (T2) were retrospectively collected. IPBR was defined as the bone loss occurring from implant placement to the end of the bone remodeling (T1). Cases were grouped into those diagnosed with (test) or without peri-implantitis (PIm) (control). Linear regression model under generalized estimation equation approach was estimated to assess correlation between marginal bone loss (MBL) rates in both periods (T1-T0) and (T2-T1). Receiver operating characteristics curve was estimated to explore an optimal cut-off point of T1-T0 MBL to discriminate between PIm and no-PIm implants. RESULTS: A total of 45 patients receiving 57 implants without PIm and 40 with PIm were included. There were no associations between PIm and IPBR (p > 0.05), nor between BML of (T2-T1) and (T1-T0). However, arch and total follow-up showed significant influence on the probability of PIm. Splinted implants showed an MBL rate of 0.60-mm/year higher than non-splinted implants (p < 0.001) from T1 to T2. CONCLUSION: No statistically significant association was found between IPBR and incidence of peri-implantitis.

The correlation between history of periodontitis according to staging and grading and the prevalence/severity of peri-implantitis in patients enrolled in maintenance therapy.

BACKGROUND: The aim of this study was to determine if a previous history of periodontitis according to the preset definitions of the 2017 World Workshop is correlated with increased implant failure, and occurrence and severity of peri-implantitis (PI). METHODS: A retrospective analysis of patients with a history of periodontitis who received nonsurgical and, if indicated, surgical corrective therapy prior to implant placement was performed. Periodontitis stage and grade were determined for each included patient based on data from the time of initiation of active periodontal therapy. Cox Proportional Hazard Frailty models were built to analyze the correlation between stage and grade of periodontitis at baseline with implant failure, as well as occurrence and severity of PI. RESULTS: Ninety-nine patients with a history of periodontitis receiving 221 implants were followed for a mean duration of 10.6 ± 4.5 years after implant placement. Six implants (2.7%) failed and a higher rate of implant failure due to PI was found for Grade C patients (P < 0.05), whereas only an increased trend was seen for Stages III and IV compared with I and II. Grading significantly influenced the risk of marginal bone loss (MBL) >25% of the implant length (P = 0.022) in PI-affected implants. However, a direct correlation between higher-level stage and grade and PI prevalence was not recorded. CONCLUSION: No statistically significant association between periodontitis stage or grade and the prevalence of PI was found. However, when PI was diagnosed, there was a relationship between periodontitis grade and severity of PI or the occurrence of implant failure.