We are committed to writing this narrative review given that carbon-based nanomaterials are revolutionizing dental medicine. Since the groundbreaking discovery of carbon nanotubes in 1991, their dental applications have skyrocketed. The numbers speak for themselves: in 2024, the global carbon nanotubes market hit USD 1.3 billion and is set to double to USD 2.6 billion by 2029. Over the past few decades, various forms of carbon nanomaterials have been integrated into dental practices, elevating the quality and effectiveness of dental treatments. They represent a transformative advancement in dentistry, offering numerous benefits such as augmented mechanical properties, antimicrobial activity, and potential for regenerative applications. Both carbon nanotubes (CNTs) and carbon dots (CDs) are derived from carbon and integral to nanotechnology, showcasing the versatility of carbon nanostructures and delivering cutting-edge solutions across diverse domains, such as electronics, materials science, and biomedicine. CNTs are ambitiously examined for their capability to reinforce dental materials, develop biosensors for detecting oral diseases, and even deliver therapeutic agents directly to affected tissues. This review synthesizes their current applications, underscores their interdisciplinary value in bridging nanotechnology and dentistry, identifies key barriers to clinical adoption, and discusses hybrid strategies warranting further research to advance implementation.

Smoking and diabetes mellitus have been recognized as significant modifying factors of the evolution of periodontitis, being considered at the moment as descriptive factors in the periodontitis grading system. The purpose of this study was to assess the consequence of smoking, type 2 diabetes, and the combination of these two factors on clinical periodontal parameters, on the levels of gingival crevicular fluid (GCF), and also on ratios of pro-inflammatory and anti-inflammatory cytokines by using a commercially available kit-based multiplex fluorescent immunoassay. The study was carried out on 124 volunteers (control (C) group = 29, diabetes mellitus (DM) group = 32, smoking (S) group = 31, and S + DM group = 32). Total mean bleeding on probing was significantly lower in the S and S + DM groups, compared to that of the other groups (p < 0.05). Total amounts of TGF-β, MIP-1α, IL-6, IL-2, and IL-17 were significantly increased in the periodontally healthy sites of diabetes patients (p < 0.05), compared to those of the controls. Systemically healthy smoking patients had higher values of GM-CSF, TGF-β, IL-4, TNF-α, IL-5, and IL-7, while diabetic smoking patients showed higher values of IL-4, TGF-β, and MIP-1α. In smoking and systemically healthy patients, IL-23, IL-7, and IL-12 showed increased concentrations, while concentrations of TGF-β, MIP-1α, IL-2, IL-7, IL-12, IL-17, IL-21, and IL-23 were higher in smoking DM patients. In conclusion, in our study, diabetes mellitus induced a general pro-inflammatory state, while smoking mainly stimulated immunosuppression in the periodontal tissues of periodontitis subjects.

Different methods and products have been investigated as measures of adjunctive therapy to scaling and root planing (SRP). Probiotic use has gained interest for this particular application, especially Lactobacillus spp. This split-mouth interventional prospective study aimed to evaluate the clinical effects of L. reuteri DSM 17938 with local application in periodontal pockets of severe periodontitis patients. The study was conducted on 40 subjects with stage 3–4 periodontitis who, based on a split-mouth model, followed SRP and SRP + L. reuteri solution in five weekly sessions. Probing depth (PD), clinical attachment loss (CAL), and bleeding on probing (BOP) were assessed at baseline and at three months after probiotic treatment completion. Both SRP and SRP + L. reuteri generated significant improvements of all three clinical parameters, but the changes were significantly better for SRP + L. reuteri treated sites. Therefore, we can conclude that adjunctive therapy with L. reuteri DSM 17938 could represent an interesting treatment option, particularly for severe periodontitis cases.

Periodontitis and type 2 diabetes mellitus (T2DM) are linked through systemic inflammation and endothelial dysfunction, yet it remains uncertain whether periodontal inflammatory burden independently reflects early, multi-organ microvascular vulnerability beyond glycemic exposure. This study aimed to assess the independent association between periodontal inflammatory burden, measured by PISA, and retinal microvascular impairment on OCT-A, and to examine relationships with renal trajectories, small-fiber neuropathy, and inflammatory/endothelial biomarkers. This cross-sectional observational study included 285 never-smoking adults with T2DM. The primary outcome was a pre-specified OCT-A microvascular impairment composite. Secondary outcomes included eGFR slope and log(UACR) slope, corneal nerve fiber length (CNFL), and a multi-organ microvascular burden score. Biomarkers comprised hsCRP, IL-6, sICAM-1, sVCAM-1, sE-selectin, PAI-1, angiopoietin-2 (Ang-2), and vWF:Ag. Multivariable linear regression estimated associations per 1 SD higher PISA, adjusting for age, sex, diabetes duration, HbA1c, CGM time in range, CGM coefficient of variation, systolic blood pressure, LDL cholesterol, BMI, and medication classes (SGLT2 inhibitors, GLP-1 receptor agonists, ACEi/ARB, statins). False discovery rate (FDR) control (q = 0.10) was applied for secondary endpoints. Higher PISA was independently associated with worse OCT-A microvascular impairment (adjusted β = 0.138, 95% CI 0.061–0.216; p = 0.0005). Although statistically significant, the effect sizes were modest in magnitude, and their translation into clinically meaningful differences in microvascular outcomes warrants investigation in prospective settings. Higher PISA was also associated with greater multi-organ microvascular burden (β = 0.101, 95% CI 0.040–0.163; p = 0.0014; FDR q = 0.005) and lower CNFL (β = −0.224, 95% CI −0.397 to −0.052; p = 0.0113; FDR q = 0.023). PISA was associated with higher levels of inflammatory and endothelial activation/injury biomarkers (all FDR q < 0.10). In this cross-sectional study, periodontal inflammatory burden was independently associated with quantitative retinal microvascular impairment, lower corneal nerve fiber length, and a consistent pattern of endothelial activation biomarker elevations in never-smoking adults with T2DM. The clinical significance of the observed effect sizes requires further evaluation, and longitudinal studies are needed to establish temporality.

Background: Computer-guided static implant surgery (CGSIS) is widely adopted to enhance the precision of dental implant placement. However, significant heterogeneity in reported accuracy values complicates evidence-based clinical decision-making. This variance is likely attributable to a fundamental lack of standardization in the methodologies used to assess dimensional accuracy. Objective: This scoping review aimed to systematically map, synthesize, and analyze the clinical methodologies used to quantify the dimensional accuracy of CGSIS. Methods: The review was conducted in accordance with the PRISMA-ScR guidelines. A systematic search of PubMed/MEDLINE, Scopus, and Embase was performed from inception to October 2025. Clinical studies quantitatively comparing planned versus achieved implant positions in human patients were included. Data were charted on study design, guide support type, data acquisition methods, reference systems for superimposition, measurement software, and accuracy metrics. Results: The analysis of 21 included studies revealed extensive methodological heterogeneity. Key findings included the predominant use of two distinct reference systems: post-operative CBCT (n = 12) and intraoral scanning with scan bodies (n = 6). A variety of proprietary and third-party software packages (e.g., coDiagnostiX, Geomagic, Mimics) were employed for superimposition, utilizing different alignment algorithms. Critically, this heterogeneity in measurement approach directly manifests in widely varying reported values for core accuracy metrics. In addition, the definitions and reporting of core accuracy metrics—specifically global coronal deviation (range of reported means: 0.55–1.70 mm), global apical deviation (0.76–2.50 mm), and angular deviation (2.11–7.14°)—were inconsistent. For example, these metrics were also reported using different statistical summaries (e.g., means with standard deviations or medians with interquartile ranges). Conclusions: The comparability and synthesis of evidence on CGSIS accuracy are significantly limited by non-standardized measurement approaches. The reported ranges of deviation values are a direct consequence of this methodological heterogeneity, not a comparison of implant system performance. Our findings highlight an urgent need for a consensus-based minimum reporting standard for future clinical research in this field to ensure reliable and translatable evidence.

Background/Objectives: Periodontitis can elevate systemic inflammation and negatively impact glucose regulation. This cross-sectional study investigated relationships between periodontal inflammatory burden, measured by periodontal inflamed surface area (PISA), and insulin resistance and systemic inflammation in never-smokers attending a periodontal clinic with unknown diabetes status. Methods: A total of 154 adults underwent full-mouth periodontal assessments to determine PISA. Fasting blood samples were taken for glucose, insulin, and hs-CRP, and HOMA-IR was calculated. An inflammation composite was created from z-scored log(hs-CRP), IL-6, and TNF-α. Primary analysis involved regressing log(HOMA-IR) and log(hs-CRP) on PISA, scaled by interquartile range (IQR) increases, with sequential adjustments. Mediation analysis, adjusted for age, sex, and waist circumference, used bootstrap testing to evaluate inflammation as a mediator. Results: HOMA-IR and hs-CRP increased across PISA tertiles (HOMA-IR: 2.01 to 3.17; hs-CRP: 0.73 to 2.48 mg/L; both p < 0.001). In the prespecified primary adjusted model (age, sex, waist circumference, education, physical activity, family history of diabetes, and medication use), each IQR increase in log(PISA) was associated with 85.2% higher hs-CRP (95% CI 53.1% to 124.1%; p < 0.001) and 15.7% higher HOMA-IR (95% CI −0.8% to 34.9%; p = 0.064). Estimates were similar with additional adjustment for BMI and SBP, whereas adding plaque (% sites) attenuated associations (hs-CRP: +15.2%; p = 0.234; HOMA-IR: +1.0%; p = 0.925). Mediation analysis (adjusted for age/sex/waist circumference) was consistent with an indirect pathway via the inflammation composite (a × b = 0.212; 95% CI 0.094 to 0.337), while the direct effect was not supported (c′ = −0.047; 95% CI −0.207 to 0.125). Conclusions: Higher periodontal inflammatory burden was strongly associated with systemic inflammation and showed weaker, model-dependent associations with insulin resistance; the findings were consistent with an inflammation-linked pathway in exploratory, partially adjusted mediation analyses; given the cross-sectional design, causal inference is not possible.