Dental erosion is a significant topic in medical literature, both for gastroenterology and dental medicine. Dental structure loss has a psychosocial and functional significance. The pathogenesis of dental erosion in patients diagnosed with gastroesophageal reflux disease (GERD) characterized by the presence of an acidic oral environment after reflux episodes, is not well understood. The present study was designed to observe the effect of low oral pH in time on natural surfaces including enamel and dentine, but also on materials used in treating these dental destructions such as composites and ceramics. The acidic oral environment was estimated in relation to salivary pH. In the dental laboratory, 5‑mm2 and 1‑mm composite pieces of thick enamel, dentine, Emax Ceramic and Nexco Ivoclar were cut in order to be analyzed using atomic force microscopy (AFM) and to observe the surface alterations. Gastric acid was collected and mixed with saliva until a pH value of 6.0 was obtained, in which the pieces were immersed for 24, 120, 240 h. Roughness of each surface was calculated at a microstructure and nanostructure level. The results showed significant alterations in enamel and dentine exposed to a lower pH level beginning even at a short immersion time, in comparison with composites and ceramics which had no alterations. In conclusion, multidisciplinary attention should be given to detect and manage acidity of the oral cavity caused by GERD, in order to prevent dental erosion.

Background and Objectives: The aim of this study is to connect peri-implantitis to cardiovascular diseases, following the association found between periodontitis and cardiovascular conditions in recent years. Materials and Methods: PubMed, Scopus, Web of Science online databases were searched up to June 2023, with the exclusion criteria being research written in a language other than English. The MeSH search items were as follows: [“peri-implant health OR peri-implantitis OR peri-implant mucositis OR peri-implant disease”] AND [“cardiovascular diseases”]. Patient/population (P), intervention (I), comparison (C), outcome (O) framework questions were followed to identify the clinical evidence for the systematic review. Only clinical studies that used a control group to compare the relationship between cardiovascular diseases and peri-implantitis were selected. Results: A total of 118 studies were identified through electronic search of the keywords. After removing duplicates, there were 76 records to be screened. Upon exclusion of ineligible titles and abstracts, 27 studies remained for evaluation. Finally, 23 studies were excluded for not meeting the inclusion criteria, leaving 4 studies to be included in the qualitative analyses. Conclusions: This study found there is a linear association between mucosal/gingival inflammation and carotid intima–media thickness test (c-IMT) values. Peri-implant mucosal inflammation could be a contributor to the vascular disease burden of an individual; further specific clinical studies should be performed in order to demonstrate this connection.

This randomized, split-mouth, controlled clinical study assessed the additional clinical benefits of a local desiccant antimicrobial agent (HY) combined with subgingival mechanical instrumentation (SRP) vs. SRP alone in treating severe periodontitis. Patients with stages III and IV periodontitis received full-mouth periodontal examinations at baseline and after a three-month follow-up. Two randomly selected hemiarches in each periodontitis patient were treated with SRP plus HY and were included in the test group, while the other two hemiarches received only SRP and were included in the control group. In thirty patients, the analyses of the evolution of the periodontal parameters over time showed statistically significant mean differences for the probing depths and clinical attachment level values resulting from all the examined sites, as well as from the interproximal sites (p < 0.001) in both the test and control groups. The intergroup comparisons of the same four parameters showed no significant differences (p = 0.322, p = 0.36, p = 0.516, and p = 0.509, respectively). Based on these study results, no additional benefits were obtained after HY subgingival applications.

Introduction: Systemic inflammation is a key contributor to the pathophysiology of carotid plaque burden (CpB). Increasing evidence supports a link between periodontitis and systemic conditions, including endothelial dysfunction, and CpB. This study aimed to explore the relationship between periodontal status, inflammatory biomarkers, and CpB, as well as the potential impact of periodontal therapy. Methods: A pilot study was conducted on subjects presenting with both periodontitis and CpB. Of 87 initially screened participants, 10 met the inclusion criteria and completed the study. Periodontal parameters—probing pocket depth (PPD), clinical attachment loss (CAL), and bleeding on probing (BOP)—were recorded. Systemic inflammatory biomarkers, including matrix metalloproteinase-8 (MMP-8), myeloperoxidase (MPO), lipoprotein-associated phospholipase A2 (Lp-PLA2), and soluble CD40 ligand (sCD40L), were analyzed. Results: Participants demonstrated severe periodontal disease, with mean PPD of 5.5 mm (maximum 8 mm), mean CAL of 6.46 mm (maximum 12 mm), and BOP of 67%. High serum Lp-PLA2 levels were associated with increased periodontal tissue destruction and inflammatory burden, supporting its role in both periodontitis and CpB pathophysiology. MMP-8 and MPO showed positive correlations with periodontal parameters, although these did not consistently reach statistical significance. Following periodontal therapy, a significant reduction in MMP-8 and Lp-PLA2 levels was observed, while MPO and sCD40L exhibited a decreasing trend without statistical significance. Conclusion: Inflammatory biomarkers may represent important mechanistic links between periodontitis and carotid artery disease. Within the limitations of this pilot study, non-surgical periodontal therapy was associated with reductions in selected systemic inflammatory biomarkers, supporting the feasibility of investigating the periodontitis–carotid plaque axis in larger translational cohorts. Larger studies are needed to validate these findings.

Background/Objectives: Periodontitis is a multifactorial chronic inflammatory disease influenced by behavioral, metabolic, and lifestyle-related factors. This study aimed to examine the associations of selected dietary habits, body mass index (BMI), physical activity, smoking, and oral hygiene behaviors with clinical periodontal parameters in a clinical sample of adults with periodontitis from northwestern Romania. Methods: This cross-sectional study included 204 adults with clinically diagnosed periodontitis. Sociodemographic characteristics, smoking status, physical activity, toothbrushing frequency, tooth mobility, and selected dietary habits were assessed using a structured questionnaire. Periodontal status was clinically evaluated using periodontal probing depth (PPD), clinical attachment loss (CAL), and bleeding on probing (BOP), while BMI was calculated from anthropometric measurements. Descriptive and inferential statistical analyses were performed to evaluate associations between the investigated factors and periodontal parameters. Multivariable linear regression models were constructed separately for PPD, CAL, and BOP, simultaneously including age, sex, BMI, smoking status, physical activity frequency, toothbrushing frequency, tooth mobility, education level, and the assessed dietary habits. Results: In the fully adjusted multivariable analyses, fish consumption 1–3 times/week was independently associated with lower PPD, whereas sweets consumption 1–3 times/week was independently associated with higher PPD. Carbonated beverage and sweets consumption 1–3 times/week were independently associated with higher BOP. Although the multivariable model for CAL was statistically significant overall, none of the individual predictors included in the model reached statistical significance. BMI and physical activity frequency were not independently associated with PPD, CAL, or BOP after simultaneous adjustment for the other variables. Age group was significantly associated with CAL category (χ²(2) = 13.28, p = 0.001, Cramér’s V = 0.255), while educational level was significantly associated with toothbrushing frequency (χ² = 62.26, p < 0.001, Cramér’s V = 0.39). Conclusions: Selected dietary habits were independently associated with PPD and BOP after adjustment for demographic, anthropometric, lifestyle, and oral hygiene factors, whereas no individual predictor was independently associated with CAL in the fully adjusted model. BMI and physical activity were not independently associated with the periodontal parameters examined. These findings emphasize the multifactorial nature of periodontal status and suggest that specific dietary habits may be associated with different clinical dimensions of periodontal disease. However, causal relationships cannot be established due to the cross-sectional design of the study. Prospective studies using validated dietary assessment methods are needed to confirm these associations.