Background: Psychological stress is increasingly recognized as a potential modifier of periodontal disease through both behavioral and biological mechanisms. Cortisol, a key stress hormone, exerts complex immunomodulatory effects and may influence periodontal inflammation and tissue breakdown. This study aimed to compare salivary levels of cortisol, interleukin-1β, and interleukin-6 in patients with varying periodontitis severity and examine their associations with clinical periodontal parameters. Methods: A total of 67 patients diagnosed with periodontitis were classified according to the 2017 World Workshop Classification into Stage I/II vs. Stage III/IV and Grade B vs. Grade C. Unstimulated saliva samples were collected and analyzed for cortisol using electrochemiluminescence immunoassay, and for IL-1β and IL-6 using ELISA. Statistical analyses included Mann-Whitney U test, Spearman’s correlations, and multivariate regression. Results: Median salivary cortisol levels were significantly higher in Stage III/IV (11.90 nmol/L) than in Stage I/II (7.64 nmol/L; p = 0.014) and in Grade C (10.60 nmol/L) vs. Grade B (7.70 nmol/L; p = 0.019). In multivariate analysis, cortisol independently predicted both Stage III/IV (OR = 1.23, p = 0.007) and Grade C (OR = 1.24, p = 0.026) periodontitis. ROC analysis showed that salivary cortisol had moderate diagnostic performance for Stage III/IV periodontitis (AUC = 0.68, cut-off 11.57 nmol/L) and Grade C (AUC = 0.67, cut-off 9.76 nmol/L). Cortisol showed significant positive correlations with clinical markers of disease severity and with IL-1β (r = 0.399, p = 0.001) and IL-6 (r = 0.424, p < 0.001). Conclusions: Salivary cortisol is a promising non-invasive biomarker reflecting both stress-related physiological burden and clinical severity in periodontitis. Cortisol measurement may represent a valuable addition to multifactorial assessments and risk stratification in periodontitis, pending further validation in longitudinal studies.

Salivary cortisol is widely used to investigate stress–periodontitis interactions, but its measurement is affected by methodological limitations. Cortisone, the predominant salivary glucocorticoid, may offer analytical advantages, yet its role in periodontitis remains unexplored. This study evaluated salivary cortisone in relation to periodontal disease severity and compared its performance with cortisol. Sixty-seven periodontitis patients were classified as Stage I/II (n = 32) or Stage III/IV (n = 35). A comprehensive periodontal examination was performed, including FMPS, FMBS, PPD, CAL, BoP, and the BL/Age ratio. Unstimulated morning saliva samples were analyzed for cortisone and cortisol using liquid chromatography–tandem mass spectrometry, and for IL-1β and IL-6 using ELISA. Both cortisone and cortisol levels were significantly higher in Stage III/IV periodontitis (p = 0.014). Cortisone correlated strongly with cortisol (ρ = 0.523, p < 0.001) and was positively associated with IL-6 (ρ = 0.322, p = 0.008) and multiple clinical indicators of periodontal disease severity. ROC analysis showed comparable discriminatory performance for cortisone and cortisol (AUC = 0.675), with cortisone demonstrating higher specificity (94%) for Stage III/IV periodontitis. Our findings suggest that salivary cortisone performs similarly to cortisol and warrants further investigation as an alternative salivary glucocorticoid marker in periodontal research.

The sympathetic nervous system (SNS) is crucial for stress response regulation and immune modulation. Prolonged SNS activation, often induced by stress exposure, disrupts immune homeostasis and intensifies inflammatory processes, contributing to periodontal disease progression. This study investigates the relationship between SNS activity and periodontitis severity, utilizing salivary biomarkers chromogranin A (CgA) and alpha-amylase (sAA) alongside pro-inflammatory cytokines interleukin-1β (IL-1β) and interleukin-6 (IL-6). Saliva samples from 67 patients, categorized by periodontitis severity (Stages I/II and III/IV), were analyzed using enzyme-linked immunosorbent assay (ELISA). The results revealed significantly higher median levels of CgA (9.45 vs. 3.93 pmol/mL) and IL-1β (257.81 vs. 220.11 pg/mL) in patients with Stage III/IV periodontitis compared with those with Stage I/II, indicating heightened SNS activity and inflammatory response. Correlations between these biomarkers and clinical periodontal parameters, such as probing depth and clinical attachment loss, further support these findings. Despite elevated sAA levels in severe cases, statistical significance was not achieved. IL-6 levels also showed no significant variation across disease stages, although trends aligned with increased severity. This study highlights the interplay between SNA activation and periodontal inflammation, as evidenced by elevated salivary levels of CgA and IL-1β in patients with advanced periodontitis. By integrating neuroendocrine and inflammatory biomarkers into the diagnostic process, clinicians may be able to better identify patients at increased risk for periodontal breakdown and to consider adjunctive interventions such as stress management, thereby supporting more personalized approaches to periodontitis treatment.

Purpose: To compare the effectiveness between the coronally advanced flap alone and in combination with a platelet-rich fibrin membrane for the treatment of gingival recessions Miller class I and II. Materials and methods: 30 gingival recessions Miller Class I /II were surgically treated randomly divided into 2 groups: 15 recessions in the test group (CAF + PRF) and 15 recessions in the control group (CAF). Before the surgical intervention and on the 6th month postoperatively, the following clinical parameters were evaluated: depth (RD) and width (RW) of gingival recession, probing pocket depth (PPD), clinical attachment level (CAL), amount of keratinized gingiva (KTH) and gingival thickness (GT). In the 6th month, the achieved mean root coverage in percentage (MRC, %) was evaluated. Results: A similar success of both techniques was demonstrated in terms of achieved MRC % - 88.44 % ± 16.99 % in the CAF + PRF group vs. 84.44% ± 20.38% in the CAF group (p = 0.56), as well as in the improvement of the following parameters: RD, RW, PPD, CAL and KTH. The additional use of PRF membrane to CAF resulted in a statistically significant increase in gingival thickness when the results were assessed 6 months after the surgical treatment of the recessions in the CAF + PRF group compared to CAF - a mean increase of 0.32 mm vs. 0.06 mm (p < 0.01). Conclusions: Combining CAF with PRF membrane is a more effective approach to increase soft tissue thickness and achieve stable root coverage to maintain periodontal health in patients with sufficient keratinized gingiva in gingival recessions Miller class I and II.

Objectives : Periodontitis is a chronic inflammatory disease whose severity is strongly influenced by environmental factors, particularly smoking. Smoking is a well-established risk factor for both the onset and progression of periodontitis, contributing to impaired immune responses, delayed healing, and enhanced tissue destruction. In this pilot study, we explored differences in immune-related gene expression between smokers and non-smokers with severe periodontitis. Methods : Gene expression analysis was performed on RNA isolated from saliva samples of six smokers and four non-smokers with severe periodontitis using a targeted NanoString panel comprising 249 immune-related genes. Results : Comparative analysis revealed a distinct expression pattern in smokers, with significantly higher expression of several pro-inflammatory genes, including IL1A , CCL3 , CCL4 , and IL8 . These genes are involved in leukocyte recruitment, chemotaxis, and inflammatory signaling. Conclusion : Although limited by the small sample size, these findings suggest an association between smoking and an enhanced inflammatory gene expression profile in patients with severe periodontitis. The results should be interpreted as exploratory, providing preliminary molecular insights into the way tobacco exposure modulates immune responses in periodontal disease.

Background: Biological sex influences immune function and inflammatory regulation, but its molecular role in periodontal disease remains insufficiently understood. This pilot study investigated sex-dependent differences in immune gene expression in patients with severe periodontitis. Methods: Ten systemically healthy, non-smoking adults (five men and five women) with stage III/IV periodontitis were examined. Total RNA was extracted from saliva and analyzed using the nCounter ^® Human Inflammation Panel (NanoString, Bruker Spatial Biology, USA). Results: Among 249 immune-related genes analyzed, two showed notable preliminary trends of sex-associated differences: AREG was upregulated in males (log ₂ FC = −0.67, d = −1.73, p = 0.03), and NOD2 was elevated in females (log ₂ FC = 1.00, d = 1.36, p = 0.03), although these did not remain statistically significant after FDR correction. Conclusion: These exploratory results suggest hypothesis-generating trends regarding sex-dependent differences in epithelial repair and innate immunity, highlighting AREG and NOD2 as candidate transcripts for further investigation. These initial findings may serve as a foundation for future, larger-scale multicenter studies with sex-stratified designs integrating transcriptomic, hormonal, and epigenetic analyses to clarify how biological sex influences molecular pathways involved in periodontal inflammation.