Alexandra Cornelia Teodorescu

Periodontitis, the sixth most prevalent oral disease globally, is a chronic and multifactorial inflammatory condition defined by the progressive and irreversible destruction of tooth-supporting structures, such as the periodontal ligament, cementum, and alveolar bone. In the absence of periodontal treatment, this destructive process leads to increased tooth mobility and even tooth loss. Consequently, this will impair masticatory and esthetic functions and overall quality of life. Clinical guidelines, including those from the European Federation of Periodontology, underline the importance of thorough disruption of supragingival and subgingival biofilm as a fundamental component of periodontal therapy at all stages. In the last two decades, air-polishing devices have emerged as valuable adjuncts and even alternatives to conventional hand and ultrasonic instrumentation for managing supragingival and subgingival biofilm. These devices operate by delivering a controlled, pressurized mixture of water, compressed air, and abrasive powder particles onto tooth surfaces, thereby disrupting dental biofilm. The development of low-abrasivity powders like glycine, erythritol, and trehalose has extended the use of air-polishing technology in subgingival spaces. This has resulted in more effective biofilm removal in periodontal pockets while minimizing the potential damage to root surfaces and soft tissues. Clinical studies indicate that air polishing is a safe, comfortable, and time-efficient tool that complements scaling and root planing during active nonsurgical periodontal therapy. Additionally, air polishing can be used as a supportive periodontal therapy approach, serving as a standalone method for managing residual pockets. This could provide clinical outcomes comparable to conventional instrumentation, increase patient comfort, and reduce treatment duration.

Background/Objectives: Individuals with autism spectrum disorder (ASD) represent a special population whose characteristics may adversely affect both their own and their families’ quality of life. These characteristics include poor oral health, sensory hypersensitivity, restrictive and repetitive behaviours, communication difficulties, medication-related adverse effects, and associated comorbidities. This scoping review aimed to evaluate the oral health-related quality of life (OHRQoL) of children and adolescents with ASD, as perceived by their parents/caregivers, and to identify the factors associated with these outcomes. Methods: Literature searches were conducted in the MEDLINE/PubMed, Scopus, Web of Science, Embase, and Google Scholar databases. Studies published between 2016 and May 2026 were considered for inclusion. Results: Of the 799 records identified, 23 studies met the eligibility criteria. Among these, 15 used the Parental-Caregiver Perceptions Questionnaire (P-CPQ), an instrument specifically developed for children with cognitive impairments. Most studies reported statistically significant associations between poorer OHRQoL and dental caries experience, lower household income, older age, male sex, and lower parental oral health literacy. Conversely, preventive interventions and comprehensive dental rehabilitation performed under general anaesthesia were associated with improvements in the quality of life of both children and their families. Parents of children with ASD also reported a greater emotional burden, primarily related to responsibility for toothbrushing, dental attendance, the child’s general health status, and the family’s financial situation. Conclusions: The majority of the included studies indicate that, according to parental reports, children and adolescents with ASD experience poor OHRQoL, particularly in the domains of emotional well-being, social well-being, functional limitations, and oral symptoms. These findings highlight the need for targeted preventive strategies and multidisciplinary interventions aimed at improving both oral health and overall quality of life in this vulnerable population.

Background/Objectives: This prospective observational cohort study aimed to evaluate the influence of heated tobacco (HT) and electronic cigarettes (ECs) on bone remodeling markers such as receptor activator of nuclear factor kappa-B ligand (RANKL) and osteoprotegerin (OPG), and periodontal status, at baseline and at 3 months after initial periodontal therapy. Methods: The sample comprised 236 participants (130 women, 106 men; mean age 38.96 ± 7.69 years), distributed across non-smokers (n = 72), heated tobacco/HT product users (n = 83), and electronic cigarette/EC users (n = 81). For each patient, the periodontal charting included periodontal probing depth (PPD), bleeding on probing (BOP), and clinical attachment loss (CAL). Unstimulated saliva samples were analyzed for RANKL and OPG levels. All patients underwent nonsurgical periodontal therapy (scaling and root planing). Between-group comparisons were performed using the Kruskal–Wallis test followed by Bonferroni-adjusted pairwise comparisons, while within-group changes over time were assessed using the Wilcoxon signed-rank test. To complement the primary nonparametric analyses, two-way mixed-design ANOVA and ANCOVA models adjusted for baseline values and periodontitis stage were performed as sensitivity analyses. Statistical significance was set at p < 0.05. Results: At baseline, both product user groups exhibited significantly higher PPD (p = 0.005) and CAL (p = 0.001) compared with non-smokers, with no differences between HT and EC users. Salivary RANKL levels were significantly higher in HT and EC users than in non-smokers, and OPG levels did not differ significantly. Following non-surgical periodontal therapy, all parameters improved significantly across groups (p < 0.001). At the 3-month follow-up, both product user groups maintained higher PPD (p = 0.008), CAL (p = 0.001), and salivary RANKL levels, compared with non-smoking individuals (p < 0.001). The RANKL/OPG ratio remained significantly different only for EC users compared with non-smokers (p < 0.001). Conclusions: HT and EC use were associated with differences in periodontal parameters and higher RANKL levels, while differences in the RANKL/OPG ratio were observed in EC users compared with non-smokers. Non-surgical periodontal therapy improved clinical parameters and reduced the RANKL/OPG ratio, highlighting the importance of biofilm control.

Background/Objectives: Cigarette smoking is a major risk factor for periodontitis, but the salivary host-response profile associated with smoking-related periodontal inflammation remains incompletely characterized. This study compared salivary NETosis-related and oxidative-inflammatory biomarkers among current smokers, former smokers, and never-smokers with periodontitis. Methods: This cross-sectional study included 159 systemically healthy adults with periodontitis (53 per group: current smokers, former smokers, never-smokers). Individuals with systemic diseases or concomitant medications that could interfere were excluded. Unstimulated whole saliva was analyzed for NETosis-related biomarkers (MPO-DNA complexes, citrullinated histone H3, neutrophil elastase, cell-free DNA) and oxidative-inflammatory markers (MMP-8, IL-1β, IL-6, TNF-α, 8-OHdG, total antioxidant capacity). Results: Salivary MPO-DNA complexes differed significantly among groups (current smokers 33.52 ± 9.96, former smokers 26.90 ± 8.38, never-smokers 19.20 ± 7.50 ng/mL; p < 0.001, η² = 0.317). The composite NETosis score (η² = 0.702) and oxidative-inflammatory score (η² = 0.718) showed the same graded pattern. Biochemical verification confirmed clear group separation (salivary cotinine: current smokers 312.3 ± 77.0, former smokers 9.7 ± 5.1, never-smokers 3.2 ± 1.4 ng/mL). Smoking exposure was positively correlated with biomarker levels and the severity of periodontal disease. Smoking status remained independently associated with MPO-DNA complexes and the NETosis score after covariate adjustment. Conclusions: Current smoking was associated with an enhanced salivary NETosis-related and oxidative-inflammatory phenotype. Former smokers displayed an intermediate profile. Salivary MPO-DNA complexes and composite biomarker scores warrant further investigation as candidate non-invasive indicators of smoking-associated periodontal inflammatory burden, pending diagnostic performance analyses and prospective validation.

Background/Objectives: Matrix metalloproteinases (MMP-8 and MMP-9) are key mediators of periodontal tissue degradation and have been proposed as salivary biomarkers of disease activity. However, their comparative responsiveness to non-surgical periodontal therapy remains insufficiently clarified. This study aimed to assess short-term changes in salivary MMP-8 and MMP-9 following full-mouth disinfection (FMD), to evaluate their association with clinical periodontal parameters, and to explore potential differences according to depressive comorbidity. Methods: Eighty patients were included and divided into two groups: 40 patients without depressive disorder (PAR group) and 40 patients with depressive disorder (DEP group). Clinical periodontal parameters (probing depth and clinical attachment loss) and salivary levels of MMP-8 and MMP-9 were assessed at baseline and 12 weeks following FMD. Salivary MMP-8 and MMP-9 levels were determined using the enzyme-linked immunosorbent assay (ELISA). Results: Significant reductions in probing depth and clinical attachment loss were observed following therapy (p < 0.01). Salivary MMP-9 levels decreased significantly in both groups (PAR: 2.4 to 1.1 ng/mL, p = 0.002; DEP: 2.6 to 1.5 ng/mL, p = 0.004), whereas MMP-8 did not show statistically significant changes (p > 0.05). Moderate positive correlations were identified between MMP-9 and clinical parameters (r = 0.46–0.51), while MMP-8 showed no significant associations. No significant differences in treatment response or biomarker dynamics were observed between groups. Conclusions: The findings indicate a differential salivary biomarker response to periodontal therapy, with MMP-9 showing greater responsiveness than MMP-8 under the conditions of this study. These results suggest a potential role for salivary MMP-9 in reflecting short-term periodontal changes; however, further longitudinal and controlled studies are required to establish its clinical applicability. Depressive comorbidity did not appear to influence short-term outcomes, although this finding should be interpreted cautiously due to the lack of a standardized severity assessment.

Background/Objectives: Periodontitis and low BMD often occur after menopause, but the role of nutritional status in the oral–skeletal link is unclear. This study examined whether nutritional biomarkers relate to periodontitis severity and modify the relationship between low BMD and periodontal destruction in postmenopausal women. Methods: This cross-sectional study included 120 postmenopausal women who underwent comprehensive periodontal measurements at six sites per tooth and were classified according to the 2017 World Workshop staging and grading framework. Areal BMD was measured using dual-energy X-ray absorptiometry (DXA). Objective biomarkers included serum 25(OH)D, plasma vitamin C, RBC omega-3 index, and serum ferritin. Mechanistic measures were serum CTX, P1NP, and urinary 8-OHdG/creatinine. The main periodontal outcome was the mean CAL. Results: Low BMD was associated with greater periodontal destruction (mean CAL 2.06 vs. 1.45 mm; adjusted β = 0.664 mm, 95% CI 0.465–0.863; p < 0.001). Higher 25(OH)D and omega-3 index were independently associated with lower mean CAL (β = −0.024 mm per 1 ng/mL and β = −0.107 mm per 1%, respectively), with false discovery rate control applied across nutritional biomarkers. Across the cohort, serum 25(OH)D showed a weak inverse correlation with CTX (r = −0.14; p = 0.141), and exploratory mediation analyses suggested only small indirect effects via CTX and 8-OHdG. Conclusions: In women after menopause, lower BMD is associated with greater periodontal tissue loss. Objective nutritional biomarkers, especially 25(OH)D and omega-3 levels, correlate with biologically plausible pathways involved in periodontal destruction and remodeling. This supports the idea that nutrition could be a key factor linking oral health and skeletal health.

Background/Objectives: Air-polishing has become, in recent years, a very popular additional tool to subgingival debridement for treating periodontal disease. Vitamin D₃ plays a crucial role in bone metabolism and calcium-phosphate homeostasis. The aim of our retrospective study was to determine the additional effect of subgingival air-polishing with two types of powders (glycine and erythritol) on patients with different stages of periodontitis and low serum levels of Vitamin D₃. Methods: We collected and analysed the data of 62 patients (demographics, vitamin D₃ levels, plaque index, periodontal probing depth, bleeding on probing, clinical attachment loss, periodontitis stage and type of air-polishing powder) used during periodontal therapy. Results: We did not observe a significant correlation between periodontal status and vitamin D₃ levels/status (mean Vitamin D₃ levels: Stage I—20.19 ± 4.413 ng/mL; Stage II—19.482 ± 3.814 ng/mL; Stage III—17.681 ± 5.869 ng/mL; Stage IV—17.578 ± 5.94 ng/mL; and p = 0.539), nor did we find any significant differences in clinical outcomes when using glycine or erythritol in addition to scaling and root planning (SRP) at 3 months after treatment (all p > 0.05). Conclusions: The discrete association between lower levels of vitamin D₃ and more advanced stages of periodontitis could suggest a possible influence of vitamin D₃ insufficiency on periodontal disease progression. Although safe, easy to use and comfortable for patients, glycine and erythritol showed no differences in periodontal clinical parameters when compared as an addition to SRP.

The aim of this study was to assess whether baseline the neutrophil-to-lymphocyte ratio (NLR), the platelet-to-lymphocyte ratio (PLR), the systemic immune-inflammation index (SII), and C-reactive protein (CRP) could predict postoperative outcomes in systemically healthy patients receiving dental implants. A retrospective analysis of 116 systemically healthy adults receiving dental implants was conducted. To minimise confounding, individuals over 50 years old, smokers, and those with systemic diseases, stage III/IV periodontitis, or current medication use were excluded. Periodontal status was classified as clinically healthy or stable. Baseline CRP and complete blood count-derived indices (NLR, PLR, SII) were recorded preoperatively. The primary outcome was osseointegration (proper versus impaired). Implant success was 95.7% (n = 111), with early implant failure occurring in 4.3% (n = 5). Females exhibited higher PLR values than males (p = 0.041), and SII was higher in periodontally stable patients compared to clinically healthy ones (p = 0.036). In systemically healthy patients, routine preoperative screening based on NLR, PLR, and CRP did not improve prediction of early implant failure, whereas SII demonstrated good, statistically significant discrimination (p = 0.015). These findings emphasise the need for further research to clarify the predictive value of blood inflammatory biomarkers.

RANKL (receptor activator of nuclear factor kappa-βligand) and OPG (osteoprotegerin) are two proteins involved in bone remodelling. During the active phase of periodontal disease, an imbalance between the ratios of the two elements can be noticed. While the expression of RANKL is elevated compared with that of OPG, the RANKL is available to bond with RANK (receptor activator of nuclear factor kappa-β). This study was conducted on 41 patients: 19 with generalized aggressive periodontitis, 18 with severe chronic periodontitis, and 4 periodontal healthy subjects. For each patient included, we determined the salivary levels of RANKL and OPG with the help of two Human ELISA kits. The results show that the patients affected by periodontitis, either aggressive or chronic, have significant higher values of RANKL and RANKL/OPG ratio. This values correlate with the local inflammation status.