Although a strong relationship between periodontal disease (PD) and atherosclerosis was shown in adults, little data are published in younger PD patients. Therefore, this study aimed to investigate and correlate clinical parameters of PD, pro- and immunoregulatory cytokines in gingival crevicular fluid (GCF) and serum, biochemical and hematological parameters associated with atherosclerosis risk, and carotid intima-media thickness (IMT) in our younger study participants (n = 78) (mean age 35.92 ± 3.36 years) who were divided into two equal groups: subjects with and without PD. PD patients had higher values of IMT, hs-CRP, triglycerides, total cholesterol, and LDL; most proinflammatory and Th1/Th17-associated cytokines in GCF; and IL-8, IL-12, IL-18, and IL-17A in serum compared to subjects without PD. These cytokines in GCF positively correlated with most clinical periodontal parameters. Clinical periodontal parameters, TNF-α and IL-8 in GCF and IL-17A, hs-CRP, and LDL in serum, had more significant predictive roles in developing subclinical atherosclerosis (IMT ≥ 0.75 mm) in comparison with other cytokines, fibrinogen, and other lipid status parameters. Hs-CRP correlated better with the proinflammatory cytokines than the parameters of lipid status. Except for serum IL-17A, there was no significant association of clinical and immunological PD parameters with lipid status. Overall, these results suggest that dyslipidemia and PD status seem to be independent risk factors for subclinical atherosclerosis in our younger PD population.

Background and Objectives: Diabetes mellitus (DM) is associated with impaired wound healing and increased oxidative stress, posing a significant challenge in dental wound healing. Low-level laser therapy (LLLT) has emerged as a potential regenerative treatment to enhance tissue repair. This study aims to investigate the effects of LLLT on oral mucosal wound healing and oxidative stress markers in rats with DM. Materials and Methods: Male Wistar rats (n = 108) were divided into six equal groups (healthy and diabetic, with or without mucosal ulcers, with or without LLLT). DM was induced with alloxan, and standardized mucosal ulcers were created. Every other day for 10 days, LLLT (6 J/cm²) was applied, and tissue samples were collected after 3, 7, and 10 days. Wound healing was assessed by planimetry, while systemic biochemical analyses included total oxidative status (TOS), total antioxidant capacity (TAC), superoxide dismutase (SOD) activity, and oxidative stress index (OSI). Results: LLLT significantly accelerated oral ulcer closure and showed between-group differences in redox markers. In healthy rats, LLLT increased wound closure on day 7 (p = 0.018). In diabetic rats, LLLT improved closure on day 3 (p = 0.035) and on day 7 (p = 0.001). Across groups, oxidative markers differed significantly (e.g., TOS on day 10 overall, p = 0.011; OSI on day 10 overall, p = 0.047; SOD p < 0.001 at all time points). In diabetic rats, on day 10, median TOS was lower with LLLT (p = 0.004). Conclusions: LLLT enhances oral wound healing and restores redox balance in diabetic rats, which supports the potential usage of LLLT as an adjunctive therapy for managing oral lesions in diabetic patients.

Background: Abdominal obesity in young adults may reflect a biologically active metabolic phenotype, even before full metabolic syndrome develops. However, how endocrine, adipokine, insulin-resistance, and fibrinolysis-related biomarkers vary across early metabolic phenotypes remains incompletely understood. This study examined whether selected circulating biomarkers differ among normal-weight controls, young adults with abdominal obesity, and those with metabolic syndrome. Methods: This cross-sectional secondary biomarker analysis included 175 young adults aged 19–21 years who were classified according to International Diabetes Federation criteria as controls (n = 106), abdominal obesity (n = 37), or metabolic syndrome (n = 32). Fasting insulin, HOMA-IR, cortisol, 25-hydroxyvitamin D, leptin, adiponectin, the adiponectin/leptin ratio (A/L ratio), ghrelin, and plasminogen activator inhibitor-1 (PAI-1) were analyzed. Between-group differences were assessed using nonparametric tests, ordered trends were evaluated across the phenotype gradient, sensitivity analyses were adjusted for sex, smoking status, and physical activity, and penalized logistic regression was used to explore biomarker associations with abdominal obesity and metabolic syndrome. Results: Insulin, HOMA-IR, cortisol, leptin, and PAI-1 showed positive ordered phenotype-related patterns, whereas ghrelin, adiponectin, and the A/L ratio showed negative ordered patterns. Vitamin D concentrations were lower in the abdominal obesity and metabolic syndrome groups than in controls. The strongest between-group effects were observed for PAI-1, cortisol, ghrelin, adiponectin, and the A/L ratio. Overall group effects remained significant after adjustment and false discovery rate correction. In mutually adjusted penalized models, the A/L ratio remained associated with abdominal obesity, whereas PAI-1 remained associated with metabolic syndrome. Conclusion: Young adults with abdominal obesity showed measurable endocrine, adipokine, insulin-resistance, and fibrinolysis-related alterations, including those who did not meet criteria for metabolic syndrome. The A/L ratio and PAI-1 may provide complementary information, with the A/L ratio more closely associated with abdominal obesity and PAI-1 more closely associated with metabolic syndrome in exploratory models. These findings support further evaluation of phenotype-based biomarker profiling for characterizing early cardiometabolic dysregulation in young adults and should be confirmed in larger, sex-balanced cohorts.