Peri-implantitis, a common biological complication of dental implants, is characterized by soft-tissue inflammation and progressive bone loss. Oxidative stress is increasingly implicated in its pathogenesis, yet the diagnostic potential of salivary redox biomarkers remains unclear. This study’s objective was to assess the association between salivary malondialdehyde (MDA) and total antioxidant capacity (TAC) and peri-implant disease via a pre-registered, quantitative meta-analysis of previously published studies using predefined statistical criteria. Following a priori PROSPERO registration, we systematically searched PubMed, Scopus, and Web of Science (2004–September 2025), extracted data in duplicate, and pooled effects using random-effects models; certainty of evidence was appraised with GRADE (Grading of Recommendations Assessment, Development and Evaluation) and risk of bias with ROBINS-I (Risk Of Bias In Non-randomized Studies of Interventions)/QUADAS-2 (Quality Assessment of Diagnostic Accuracy Studies-2). Twelve studies were included qualitatively: seven (n = 726) contributed to MDA and five (n = 485) to TAC meta-analyses. Peri-implant disease was associated with elevated MDA (SMD = 1.64, 95% CI 1.39–1.88) and reduced TAC (SMD = −1.88, 95% CI −2.17 to −1.58); statistical heterogeneity was not detected, and results were robust to sensitivity and exploratory assay-based subgroup analyses. Salivary MDA and TAC show consistent, large, standardized differences in peri-implant disease; however, observational designs, assay variability, and the absence of validated diagnostic thresholds warrant cautious interpretation and prospective validation before clinical adoption.

Background: Type 1 diabetes (T1D) is a chronic autoimmune disorder characterized by the destruction of pancreatic β-cells, leading to absolute insulin deficiency. Despite advancements in insulin therapy and glucose monitoring, achieving optimal glycemic control remains a challenge. Emerging technologies and novel therapeutic strategies are transforming the landscape of T1D management, offering new opportunities for improved outcomes. Methods: This review synthesizes recent advancements in T1D treatment, focusing on innovations in continuous glucose monitoring (CGM), automated insulin delivery systems, smart insulin formulations, telemedicine, and artificial intelligence (AI). Additionally, we explore biomedical approaches such as stem cell therapy, gene editing, immunotherapy, gut microbiota modulation, nanomedicine-based interventions, and trace element-based therapies. Results: Advances in digital health, including CGM integration with hybrid closed-loop insulin pumps and AI-driven predictive analytics, have significantly improved real-time glucose management. AI and telemedicine have enhanced personalized diabetes care and patient engagement. Furthermore, regenerative medicine strategies, including β-cell replacement, CRISPR-based gene editing, and immunomodulatory therapies, hold potential for disease modification. Probiotics and microbiome-targeted therapies have demonstrated promising effects in maintaining metabolic homeostasis, while nanomedicine-based trace elements provide additional strategies to regulate insulin sensitivity and oxidative stress. Conclusions: The future of T1D management is shifting toward precision medicine and integrated technological solutions. While these advancements present promising therapeutic avenues, challenges such as long-term efficacy, safety, accessibility, and clinical validation must be addressed. A multidisciplinary approach, combining biomedical research, artificial intelligence, and nanotechnology, will be essential to translate these innovations into clinical practice, ultimately improving the quality of life for individuals with T1D.

Background/Objectives: This study aims to compare the effects of conventional surgical techniques and laser-assisted methods on salivary oxidative stress biomarkers following third molar extraction, in order to evaluate the potential benefits of laser surgery in reducing oxidative stress and promoting faster recovery. Methods: A total of 154 patients, aged 16–30, undergoing third molar extractions were included in the study. Patients were divided into two groups: conventional surgery (n = 75) and laser-assisted surgery (n = 79). Saliva samples were collected at baseline, and 24, 48, 72, and 168 h postoperatively. The levels of total antioxidant capacity (TAC), malondialdehyde (MDA), and 8-hydroxy-2′-deoxyguanosine (8-OHdG) were measured as indicators of oxidative stress. Results: Initial biomarker levels were similar across all participants. Postoperative oxidative stress increased in both groups, with significantly higher levels in the conventional surgery group at 48 and 72 h. Salivary biomarkers of oxidative stress were significantly lower in the laser group at 48 and 72 h post-surgery (p < 0.05), indicating a faster recovery. By 168 h, biomarker levels in the laser group had nearly returned to baseline, whereas levels in the conventional group remained slightly elevated. Conclusions: Laser-assisted surgery significantly reduces oxidative stress and promotes faster recovery when compared with conventional methods, as evidenced by the more rapid normalization of salivary biomarkers. These findings suggest that laser techniques may offer superior clinical outcomes in third molar extractions.

Background: Angiogenesis, the formation of new blood vessels from pre-existing ones, plays a pivotal role in wound healing, particularly in surgical contexts. Methods and results: However, this process can be significantly impaired in patients with childhood obesity, resulting in delayed healing and additional complications. The biological process of wound healing is complex, involving angiogenesis, cell proliferation, inflammation, and tissue remodeling. This review aims to explore recent advancements in research on angiogenesis in surgical wounds in patients with childhood obesity, with a focus on growth factors, inflammation, microcirculation, and innovative therapeutic strategies. Conclusions: It highlights therapeutic approaches such as the administration of growth factors and the application of biomaterials to enhance angiogenesis.

Background: Periodontitis affects approximately 7–11% of the global adult population in its severe forms and has been epidemiologically associated with cardiovascular, cardiometabolic, and neurodegenerative diseases. Low-grade chronic inflammation represents the unifying mechanism; however, an integrative framework connecting the oral cavity, the gut, and the brain into a single mechanistic continuum is lacking. Objective: This narrative review, conducted with structured (but non-systematic) elements and PRISMA-2020 style reporting used solely as a transparency tool, synthesizes current evidence on the oral–gut–brain axis. A comprehensive literature search was conducted in PubMed/MEDLINE, Scopus, Web of Science, and Google Scholar (2000–March 2026), yielding 159 included studies after structured screening and eligibility assessment. The review focuses on: the molecular mechanisms by which periodontal dysbiosis may disrupt intestinal homeostasis and contribute to neuroinflammation; the role of salivary and intestinal biomarkers as monitoring tools for the entire axis; and emerging pharmacological opportunities targeting this tripartite pathway. Results: Periodontal pathogens, particularly Porphyromonas gingivalis (P. gingivalis) and Fusobacterium nucleatum, have been detected ectopically in the gut and are associated with reduced tight junction protein expression and altered Firmicutes/Bacteroidetes ratios in preclinical and observational studies. These perturbations have been associated with increased blood–brain barrier (BBB) permeability, microglial activation, and amyloid-beta (Aβ) accumulation, although causal directionality in humans remains to be established. Salivary biomarkers (MMP-8, IL-1β, IL-6, BDNF) and intestinal biomarkers (short-chain fatty acids, calprotectin) reflect systemic inflammatory burden and offer potential for non-invasive screening. Conclusions: The oral–gut–brain axis provides a plausible unifying framework for understanding comorbidity among periodontal, cardiometabolic, and neurodegenerative diseases; however, current evidence is predominantly associative, and mechanistic extrapolation from preclinical models requires validation in longitudinal human studies. Salivary biomarkers may serve as candidate first-line tools for systemic risk assessment, and pharmacological interventions targeting this axis represent promising investigational directions warranting further clinical evaluation.

Dental amalgam remains widely used in restorative dentistry due to its durability and cost-effectiveness, yet concerns persist regarding potential biological effects related to mercury release. This narrative review critically synthesizes current evidence on oral mucosal alterations and salivary biomarker changes reported in association with amalgam restorations. Experimental research supports biological plausibility for oxidative and inflammatory responses to mercury exposure; however, most human evidence derives from observational studies demonstrating heterogeneous associations rather than consistent causal relationships. Reported variations in salivary biomarkers, including interleukin-8 and ceruloplasmin, are generally modest and influenced by confounding factors such as periodontal status, smoking, and systemic inflammation. Histopathological findings adjacent to amalgam restorations include epithelial and inflammatory changes, though many are nonspecific and comparable to other chronic irritative conditions. Overall, current clinical and epidemiological data do not indicate uniform or clinically significant adverse effects in the general population attributable solely to dental amalgam. Regulatory phase-down initiatives primarily reflect environmental and precautionary policies. Available evidence supports a balanced and evidence-based interpretation of amalgam-related biological findings in contemporary dental practice.