Background: Periodontal dysbiosis contributes to liver injury through systemic inflammation, oral–gut microbial translocation, and endotoxemia. Lipopolysaccharides (LPSs) and virulence factors derived from periodontal pathogens, particularly Porphyromonas gingivalis (P. gingivalis) activate Toll-like receptor (TLR) signaling, trigger NF-κB-mediated cytokine release (e.g., TNF-α, IL-1β, IL-6), and promote oxidative stress and Kupffer cell activation within the liver. The present systematic review summarized clinical evidence supporting these mechanistic links between periodontal pathogens and hepatic outcomes, highlighting the role of microbial crosstalk in liver pathophysiology. Methods: A PRISMA-compliant systematic review was conducted by searching PubMed, Scopus, and the Cochrane library, as well as gray literature. Eligible study designs were observational studies and trials evaluating P. gingivalis and other periodontal pathogens (Aggregatibacter actinomycetemcomitans, Prevotella intermedia, and Tannerella forsythia) for liver phenotypes (Non-Alcoholic Fatty Liver Disease [NAFLD]/Metabolic Dysfunction-Associated Steatotic Liver Disease [MASLD], fibrosis/cirrhosis, acute alcoholic hepatitis [AAH], and Hepatocellular carcinoma [HCC]). Risk of bias was assessed using the Newcastle–Ottawa Scale adapted for cross-sectional studies (NOS-CS) for observational designs and the RoB 2 scale for single randomized controlled trials (RCTs). Due to the heterogeneity of exposures/outcomes, results were summarized narratively. Results: In total, twenty studies (2012–2025; ~34,000 participants) met the inclusion criteria. Population-level evidence was conflicting (no clear association between anti-P. gingivalis serology and NAFLD), while clinical cohorts more frequently linked periodontal exposure, particularly to P. gingivalis, to more advanced liver phenotypes, including fibrosis. Microbiome studies suggested stage-related changes in oral communities rather than the effect of a single pathogen, and direct translocation into ascitic fluid was not observed in decompensated cirrhosis. Signals from interventional and behavioral research (periodontal therapy; toothbrushing frequency) indicate a potential modifiability of liver indices. The overall methodological quality was moderate with substantial heterogeneity, precluding meta-analysis. Conclusions: Current evidence supports a biologically plausible oral–liver axis in which periodontal inflammation, often involving P. gingivalis, is associated with liver damage. Causality has not yet been proven; however, periodontal evaluation and treatment may represent a low-risk option in periodontitis-associated NAFLD. Well-designed, multicenter prospective studies and randomized trials with standardized periodontal and liver measurements are needed.

Background: Instrument separation is a frequent issue in root canals, often complicated by intriguing anatomical variations that make treatment more challenging. These variations in canal structure can lead to various iatrogenic complications, such as missed canals, instrument separation, gouging, perforation, and overextension of obturation materials. One such complication is instrument breakage, which can disrupt the cleaning and shaping processes and potentially cause pain or discomfort. Materials and Methods: The present systematic review was conducted following PRISMA guidelines and the Cochrane Handbook for Systematic Reviews of Interventions. The present systematic review aimed to identify all clinical trials focused on the removal of separated instruments from endodontic canals using an endodontic surgical approach. Results: A total of 21 studies were included, reporting 22 cases involving surgical approaches for separated instrument removal. Conclusions: The analysis of available evidence, although prim Information added.arily based on clinical cases and case series, emphasizes that surgical approaches for removing separated endodontic instruments are a viable therapeutic option when non-surgical treatments are ineffective or not feasible. Techniques such as apicoectomy, intentional replantation, surgical removal, and the technique provide innovative, customized solutions for addressing complications related to separated instruments, showing favorable clinical and radiographic success rates in follow-up assessments.

Background: Cold atmospheric plasma (CAP) has emerged as a promising experimental anticancer strategy, yet its influence on oral squamous cell carcinoma (OSCC) migration and viability remains moderately understood. The aim of this workpaper was to examine how CAP exposure influences wound closure, WST-1 metabolic signal, and key proteins involved in epithelial adhesion and cell-cycle regulation in OSCC models. Methods: HSC-3 and CAL27 head and neck squamous cell carcinoma (HNSCC) cells were exposed to CAP generated via Piezoelectric Direct Discharge (PDD) technology for 20 s under standardized conditions. Wound closure was assessed by wound-healing assay under proliferation-restricted conditions (50 μM Ara-C), while relative cellular metabolic activity was measured using WST-1. E-cadherin, N-cadherin, and Cyclin A were evaluated by Western blot. Publicly available baseline transcriptomic data were additionally analyzed to characterize migration- and cytoskeleton-related expression patterns in the two HNSCC models. These transcriptomic data were independent of CAP treatment. Results: A 20 s CAP exposure significantly delayed wound closure in both HNSCC cell lines under proliferation-restricted conditions and reduced the WST-1 signal. Cyclin A levels also decreased, supporting an effect on cell growth and cell-cycle regulation, although the available data do not establish cell-cycle arrest. E-cadherin increased after CAP treatment, whereas N-cadherin remained low without a statistically significant change. Baseline transcriptomic mapping further showed differences between HSC-3 and CAL27 in genes related to actin-cytoskeleton organization, focal adhesion, and migration. These data were used to contextualize the experimental phenotype and were not interpreted as CAP-induced transcriptional changes. Conclusions: In these in vitro OSCC models, CAP exposure was associated with slower wound closure, lower WST-1 signal, increased E-cadherin, and reduced Cyclin A expression. These findings suggest further investigation of CAP as a potential modulator of OSCC cellular metabolic activity, adhesion-related markers, and cell-cycle-associated proteins.