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The worldwide number of dental implants and orthopedic prostheses is steadily increasing. Orthopedic implant loosening, in the absence of infection, is mostly attributable to the generation of wear debris. Dental peri-implantitis is characterized by a multifactorial etiology and is the main cause of implant failure. It consists of a peri-implant inflammatory lesion that often results in loss of supporting bone. Disease management includes cleaning the surrounding flora by hand instruments, ultrasonic tips, lasers, or chemical agents. We recently published a paper indicating that US scaling of titanium (Ti) implants releases particles that provoke an inflammatory response and osteolysis. Here we show that a strong inflammatory response occurs; however, very few of the titanium particles are phagocytosed by the macrophages. We then measured a dramatic Ti particle-induced stimulation of IL1β, IL6, and TNFα secretion by these macrophages using multiplex immunoassay. The particle-induced expression profile, examined by FACS, also indicated an M1 macrophage polarization. To assess how the secreted cytokines contributed to the paracrine exacerbation of the inflammatory response and to osteoclastogenesis, we treated macrophage/preosteoclast cultures with neutralizing antibodies against IL1β, IL6, or TNFα. We found that anti-TNFα antibodies attenuated the overall expression of both the inflammatory cytokines and osteoclastogenesis. On the other hand, anti-IL1β antibodies affected osteoclastogenesis but not the paracrine expression of inflammatory cytokines, whereas anti-IL6 antibodies did the opposite. We then tested these neutralizing antibodies using our mouse calvarial model of Ti particle-induced osteolysis and microCT analysis. Here, all neutralizing antibodies, administered by intraperitoneal injection, completely abrogated the particle-induced osteolysis. This suggests that blockage of paracrine inflammatory stimulation and osteoclastogenesis are similarly effective in preventing bone resorption induced by Ti particles. Blocking both the inflammation and osteoclastogenesis by anti-TNFα antibodies, incorporated locally into a slow-release membrane, also significantly prevented osteolysis. The osteolytic inflammatory response, fueled by ultrasonic scaling of Ti implants, results from an inflammatory positive feedback loop and osteoclastogenic stimulation. Our findings suggest that blocking IL1β, IL6, and/or TNFα systemically or locally around titanium implants is a promising therapeutic approach for the clinical management of peri-implant bone loss.

Peri-implant inflammations represent serious diseases after dental implant treatment, which affect both the surrounding hard and soft tissue. Due to prevalence rates up to 56%, peri-implantitis can lead to the loss of the implant without multilateral prevention and therapy concepts. Specific continuous check-ups with evaluation and elimination of risk factors (e.g. smoking, systemic diseases and periodontitis) are effective precautions. In addition to aspects of osseointegration, type and structure of the implant surface are of importance. For the treatment of peri-implant disease various conservative and surgical approaches are available. Mucositis and moderate forms of peri-implantitis can obviously be treated effectively using conservative methods. These include the utilization of different manual ablations, laser-supported systems as well as photodynamic therapy, which may be extended by local or systemic antibiotics. It is possible to regain osseointegration. In cases with advanced peri-implantitis surgical therapies are more effective than conservative approaches. Depending on the configuration of the defects, resective surgery can be carried out for elimination of peri-implant lesions, whereas regenerative therapies may be applicable for defect filling. The cumulative interceptive supportive therapy (CIST) protocol serves as guidance for the treatment of the peri-implantitis. The aim of this review is to provide an overview about current data and to give advices regarding diagnosis, prevention and treatment of peri-implant disease for practitioners.

Peri-implant infection is one of the biggest threats to the success of dental implant. Existing coatings on titanium surfaces exhibit rapid decrease in antibacterial efficacy, which is difficult to promisingly prevent peri-implant infection. Herein, we report an N-halamine polymeric coating on titanium surface that simultaneously has long-lasting renewable antibacterial efficacy with good stability and biocompatibility. Our coating is powerfully biocidal against both main pathogenic bacteria of peri-implant infection and complex bacteria from peri-implantitis patients. More importantly, its antibacterial efficacy can persist for a long term (e.g., 12~16 weeks) in vitro, in animal model, and even in human oral cavity, which generally covers the whole formation process of osseointegrated interface. Furthermore, after consumption, it can regain its antibacterial ability by facile rechlorination, highlighting a valuable concept of renewable antibacterial coating in dental implant. These findings indicate an appealing application prospect for prevention and treatment of peri-implant infection. Infection is a major problem for dental implants with current antibacterial coatings losing efficacy quickly. Here, the authors report on the N-halamine polymeric coating of titanium implants to create a long-lasting renewable antibacterial layer and demonstrate application in vivo.

Peri-implantitis is an inflammatory condition affecting the hard and soft tissues surrounding osseointegrated implants, characterized by progressive alveolar bone destruction. The long non-coding RNA Negative Regulator of Interferon Response (lncRNA ) is widely recognized as a biomarker for certain autoimmune diseases and participates in their pathogenesis. However, our previous studies revealed significant upregulation of in peri-implantitis, suggesting its potential role in peri-implantitis. In peri-implantitis lesions, there is often a substantial infiltration of M1 macrophages. Thus, this study investigated the regulatory role and underlying mechanisms of in macrophage polarization during peri-implantitis. Transcriptome sequencing analysis revealed radical S-adenosyl methionine domain containing 2 ( ) as an -interacting mRNA in macrophages. Using siRNA gene knockdown technology, we suppressed and expression in M1 macrophages derived from THP-1 cells. Subsequently, we employed RT-qPCR, Western blot, flow cytometry, and immunofluorescence staining to assess the levels of inflammatory cytokines and M1 macrophage-associated markers, aiming to elucidate the involvement of / /NF-κB axis in macrophage polarization. Supernatants from -knockdown macrophages were collected to prepare the culture medium for bone marrow mesenchymal stem cells (BMSCs). The expression of osteogenic-related factors in BMSCs was evaluated through RT-qPCR, Western blot, Alkaline phosphatase (ALP) activity, and alizarin red S (ARS) staining. Furthermore, a rat peri-implantitis model was established, and the degree of peri-implant tissue inflammation and bone loss was assessed using micro-CT scanning and immunohistochemistry after treatment with various macrophage supernatants. knockdown reduced expression and suppressed activation of the NF-κB pathway, consequently decreasing inflammatory cytokines and M1 macrophage-associated cytokine expression in THP-1 macrophages. Functionally, knockdown in macrophages promoted osteogenic differentiation of BMSCs. In vivo experiments showed that supernatants derived from -knockdown macrophages resulted in reduced inflammatory infiltration, diminished bone resorption, and increased expression of osteogenesis-related factors. This study demonstrates that functions as a pro-inflammatory modulator in peri-implantitis by activating M1 macrophages through the /NF-κB axis, providing novel insights into peri-implantitis pathogenesis that may inform future preventive and therapeutic strategies.

Background: Retrograde peri-implantitis (RPI) is a pathological entity with an unclear etiology (e.g., overheating during implant insertion, residual infection of the tooth replaced by the implant or the endodontic lesion of neighboring teeth) and an extremely low prevalence and has been scarcely investigated. Therefore, the aim of this cross-sectional survey was to evaluate the knowledge and attitude of Italian implantologists regarding RPI. Methods: An anonymous questionnaire was sent via email to implantologists randomly selected, including a section about demographic information and questions related to RPI origin, radiographic representation, symptoms and treatment options. All questions were multiple answer and close-ended. Binomial logistic regression was performed to investigate the relationship between correct answers and the following independent variables: age, years of experience and number of dental implants placed per year. Results: In total, 475 implantologists completed the questionnaire, with a response rate of 46.3%. Based on the results of the study, incorrect answers were associated with less experienced participants (<80 implants/year) for all questions evaluated, with the exception of treatment strategies. Furthermore, 26.7% of the survey takers did not recognize radiographic representation of RPI and 35.5% picked “implant removal” when asked about treatment modality. Conclusions: The majority of participants were able to recognize symptoms and indicated the probable causes of RPI; however, around 30% of them showed very limited knowledge of available management strategies.

Peri-implantitis (PI) is a chronic inflammatory disease that ultimately leads to the dysfunction and loss of implants with established osseointegration. Ferroptosis has been implicated in the progression of PI, but its precise mechanisms remain unclear. This study explores the molecular mechanisms of ferroptosis in the pathology of PI through bioinformatics, offering new insights into its diagnosis and treatment. The microarray datasets for PI (GSE33774 and GSE106090) were retrieved from the GEO database. The differentially expressed genes (DEGs) and ferroptosis-related genes (FRGs) were intersected to obtain PI-Ferr-DEGs. Using three machine learning algorithms, the Least Absolute Shrinkage and Selection Operator (LASSO), Support Vector Machine-Recursive Feature Elimination (SVM-RFE), and Boruta, we successfully identified the most crucial biomarkers. Additionally, these key biomarkers were validated using a verification dataset (GSE223924). Gene set enrichment analysis (GSEA) was also utilized to analyze the associated gene enrichment pathways. Moreover, immune cell infiltration analysis compared the differential immune cell profiles between PI and control samples. Also, we targeted biomarkers for drug prediction and conducted molecular docking analysis on drugs with potential development value. A total of 13 PI-Ferr-DEGs were recognized. Machine learning and validation confirmed toll-like receptor-4 (TLR4) and FMS-like tyrosine kinase 3 (FLT3) as ferroptosis biomarkers in PI. In addition, GSEA was significantly enriched by the biomarkers in the cytokine–cytokine receptor interaction and chemokine signaling pathway. Immune infiltration analysis revealed that the levels of B cells, M1 macrophages, and natural killer cells differed significantly in PI. Ibudilast and fedratinib were predicted as potential drugs for PI that target TLR4 and FLT3, respectively. Finally, the occurrence of ferroptosis and the expression of the identified key markers in gingival fibroblasts under inflammatory conditions were validated by RT-qPCR and immunofluorescence analysis. This study identified TLR4 and FLT3 as ferroptosis and immune cell infiltration signatures in PI, unraveling potential novel targets to treat PI.

ObjectivesTo compare clinical, radiographic, biological and technical long-term outcomes of two types of dental implants over a period of 10 years.Materials and methodsNinety-eight implants were placed in 64 patients, randomly allocated to one of two manufacturers (AST and STM). All implants were loaded with fixed restorations. Outcome measures were assessed at implant insertion (Ti), at baseline examination (TL), at 1, 3, 5, 8 and 10 (T10) years. Data analysis included survival, bone level changes, complications and clinical measures.ResultsRe-examination was performed in 43 patients (23 AST and 20 STM) at 10 years. The implant level analysis was based on 37 (AST) and 32 (STM) implants. Survival rates of 100% were obtained for both groups. The median changes of the marginal bone levels between baseline and T10 (the primary endpoint) amounted to a loss of 0.07 mm for group AST and a gain of 0.37 mm for group STM (intergroup p = 0.008).Technical complications occurred in 27.0% of the implants in group AST and in 15.6% in group STM.The prevalence of peri-implant mucositis was 29.7% (AST) and 50.1% (STM). The prevalence of peri-implantitis amounted to 0% (AST) and 6.3% (STM).ConclusionsIrrespective of the implant system used, the survival rates after 10 years were high. Minimal bone level changes were observed, statistically significant but clinically negligible in favor of STM. Technical complications were more frequently encountered in group AST, while group STM had a higher prevalence of peri-implant mucositis.

The oral microbiome comprises over 700 distinct species, forming complex biofilms essential for maintaining oral and systemic health. When the microbial homeostasis in the periodontium is disrupted, pathogens within the biofilm can cause periodontitis and peri-implantitis, inducing host immune responses. Understanding the role of microbial communities and the immune mechanisms in oral health and disease is crucial for developing improved preventive, diagnostic and therapeutic strategies. However, many questions remain about how changes in bacterial populations contribute to the development and progression of these conditions. An electronic and manual literature search was conducted using PubMed, Excerpta Medica, Frontiers Reports and the Wiley Online Library databases for relevant articles. Data from these publications were extracted and the overall findings were summarized in a narrative manner. The variations in microbial communities and immune responses of periodontitis and peri-implantitis are explored. Dysbiosis of the subgingival microbiome—characterized by an increase in pathogenic bacteria such as Porphyromonas gingivalis , Tannerella forsythia , and Aggregatibacter actinomycetemcomitans —plays a pivotal role in the initiation and progression of periodontitis. As for peri-implantitis, alterations include a higher abundance of opportunistic pathogens and reduced microbial diversity around implants. Moreover, oral dysbiosis potentially influencing systemic health through immune-mediated pathways. Regional immunity of periodontium involving neutrophils, T helper cells-17, and immune-related cytokines is crucial for maintaining periodontal homeostasis and responding to microbial imbalances. Additionally, the impact of non-mechanical treatments—such as probiotics and laser therapy—on the oral microbiome is discussed, demonstrating their potential in managing microbial dysbiosis. These findings underscore that bacterial dysbiosis is a central factor in the development of periodontitis and peri-implantitis. Maintaining microbial balance is essential for preventing these diseases, and interventions targeting the microbiome could enhance treatment outcomes. Strategies focusing on controlling pathogenic bacteria, modulating immune responses, and promoting tissue regeneration are key to restoring periodontal stability. Further research is needed to clarify the mechanisms underlying the transition from peri-implant mucositis to peri-implantitis and to optimize prevention and treatment approaches, considering the complex interactions between the microbiome and host immunity.

The oral microbiota change dramatically with each part of the oral cavity, even within the same mouth. Nevertheless, the microbiota associated with peri-implantitis and periodontitis have been considered the same. To improve our knowledge of the different communities of complex oral microbiota, we compared the microbial features between peri-implantitis and periodontitis in 20 patients with both diseases. Although the clinical symptoms of peri-implantitis were similar to those of periodontitis, the core microbiota of the diseases differed. Correlation analysis revealed the specific microbial co-occurrence patterns and found some of the species were associated with the clinical parameters in a disease-specific manner. The proportion of Prevotella nigrescens was significantly higher in peri-implantitis than in periodontitis, while the proportions of Peptostreptococcaceae sp. and Desulfomicrobium orale were significantly higher in periodontitis than in peri-implantitis. The severity of the peri-implantitis was also species-associated, including with an uncultured Treponema sp. that correlated to 4 clinical parameters. These results indicate that peri-implantitis and periodontitis are both polymicrobial infections with different causative pathogens. Our study provides a framework for the ecologically different bacterial communities between peri-implantitis and periodontitis and it will be useful for further studies to understand the complex microbiota and pathogenic mechanisms of oral polymicrobial diseases.

The endemic of peri-implantitis affects over 25% of dental implants. Current treatment depends on empirical patient and site-based stratifications and lacks a consistent risk grading system. We investigated a unique cohort of peri-implantitis patients undergoing regenerative therapy with comprehensive clinical, immune, and microbial profiling. We utilized a robust outlier-resistant machine learning algorithm for immune deconvolution. Unsupervised clustering identified risk groups with distinct immune profiles, microbial colonization dynamics, and regenerative outcomes. Low-risk patients exhibited elevated M1/M2-like macrophage ratios and lower B-cell infiltration. The low-risk immune profile was characterized by enhanced complement signaling and higher levels of Th1 and Th17 cytokines. and were significantly enriched in high-risk individuals. Although surgery reduced microbial burden at the peri-implant interface in all groups, only low-risk individuals exhibited suppression of keystone pathogen re-colonization. Peri-implant immune microenvironment shapes microbial composition and the course of regeneration. Immune signatures show untapped potential in improving the risk-grading for peri-implantitis.