This study identifies a transcriptomic profile of long noncoding RNAs in gingival crevicular fluid samples in pregnant women with gestational diabetes risk. NEAT1 and LINC-PINT were increased expression in gingival crevicular fluid samples in pregnancies later diagnosed with gestational diabetes mellitus.
The main goal of periodontal therapy is to arrest the destructive progression of disease and preserve natural dentition. The resolution of inflammation, the reduction of pocket depth (PD), and the stabilization or improvement of clinical attachment level (CAL) are the core objectives of treatment. These therapeutic outcomes are typically pursued through a stepwise approach beginning with risk factor control and non-surgical therapy (Step I and II) [1]. Ideally, these early interventions lead to a clinical scenario characterized by probing depths of ≤ 4 mm, a biologically favorable condition that enables long-term periodontal stability [2, 3]. However, in many patients, pockets ≥ 4 mm with bleeding on probing persist despite comprehensive non-surgical therapy [4, 5]. These sites represent an ongoing risk for disease progression and typically warrant surgical intervention to achieve a more stable periodontal environment [6].
Periodontal therapy offers three distinct histological outcomes: repair, most commonly characterized by the formation of a long junctional epithelium; regeneration, involving the restoration of periodontal ligament, cementum, and alveolar bone; and what might be termed a “reset”—the reestablishment of a physiologic situation with a short junctional epithelium and a minimal probing depth, achieved through apical positioning of the marginal periodontal tissues [7]. Each of these outcomes carries different biological and clinical implications, and the chosen surgical strategy should take into account the patient-specific risk profile, reflect the anatomy of the defect, and aim to achieve predictable long-term therapeutic outcomes.
Among available surgical modalities, flap surgery with osseous resection (ORS) remains a well-established and predictable technique, specifically aimed at eliminating periodontal pockets, reestablishing a “correct” and maintainable anatomical architecture, and preserving or increasing an adequate band of attached gingiva [8, 9]. Despite the concept—supported by controlled clinical trials—that long-term outcomes of different periodontal surgical procedures may converge, ORS continues to represent a highly effective and predictable clinical tool. Its goal is not only to eliminate pockets but also to correct soft and hard tissue deformities, thereby restoring a functional dento-alveolar relationship conducive to long-term stability. When properly indicated and meticulously executed, ORS contributes meaningfully to periodontal health and remains one of the principal surgical strategies with documented long-term success. Importantly, ORS achieves the anatomical, histological, and physiological outcome of a healthy periodontium albeit positioned at a more apical level. This deliberate architectural reset creates a new, stable marginal profile that facilitates effective plaque control and reduces the risk of disease rec
Aim: To assess the prevalence of peri-implant diseases and buccal peri-implant soft-tissue dehiscence (PISTD) and to identify the associated risk indicators.
Methods: Patients previously rehabilitated with implant-supported rehabilitations at the University of Turin Dental School were specifically recalled with a registry-based approach for this cross-sectional study. Data collection included medical and dental history, full-mouth clinical examination, and periapical radiographs. Moderate/severe peri-implantitis was diagnosed based on bone loss (direct criterion, when available) or bone level (indirect criterion) ≥ 2 mm and the presence of bleeding/suppuration. PISTD was defined as mucosal dehiscence on the buccal aspect of at least one implant site. Multilevel, multivariable logistic regression models were applied to identify factors associated with moderate/severe peri-implantitis and buccal PISTD.
Results: Of the 397 patients contacted, 146 were included (mean age 61.1 ± 14.5 years; current smokers 34.3%; stage III-IV periodontitis 65.1%) with a total of 511 dental implants (mean function time: 13.3 years [2-31]). Implant survival rate was 96.5%. Moderate/severe peri-implantitis was detected in 56.8% of patients and 34.7% of implants. Prevalence of buccal PISTD was 54.1% and 40.5%, respectively. Protective indicators for moderate/severe peri-implantitis included supportive peri-implant care > twice a year (OR = 0.16; 95% CI: 0.03-0.95), > 2 mm of keratinized tissue height (OR = 0.44; 95% CI: 0.21-0.95), and correct mesio-distal implant positioning (OR = 0.54; 95% CI: 0.32-0.94). Risk indicators included stage III-IV periodontitis (OR = 2.82; 95% CI: 1.30-6.15), function time ≥ 10 years (OR = 3.02; 95% CI: 1.55-5.89), bisphosphonate use during follow-up (OR = 5.96; 95% CI: 1.33-26.66), and presence of a cantilever (OR = 5.51; 95% CI: 1.56-19.38). For PISTD, protective indicators were mandibular location (OR = 0.45; 95% CI: 0.25-0.81), thick buccal soft-tissue phenotype (OR = 0.18; 95% CI: 0.08-0.42), and > 2 mm of keratinized tissue height (OR = 0.05; 95% CI: 0.02-0.15). Risk indicators included peri-implantitis (OR = 2.21; 95% CI: 1.25-3.91), use of intermediate abutments (OR = 4.92; 95% CI: 1.92-12.58), and proximity to adjacent implants (OR = 3.35; 95% CI: 1.50-7.48) or edentulous spaces (OR = 3.38; 95% CI: 1.51-7.54).
Conclusion: In this long-term, university-based cohort, peri-implant diseases and PISTD were highly prevalent. Multiple patient- and implant-level factors emerged as significant risk or protective indicators. Despite the widespread occurrence of peri-implant diseases, long-term implant survival remained high, challenging current diagnostic thresholds and underscoring the need for refined, progression-based definitions.
Nearly three decades have now passed since autologous platelet concentrates (APCs) were introduced into clinical practice. Harnessing the body's innate intrinsic capacity for healing, the concepts of platelet-rich plasma (PRP) and platelet-rich fibrin (PRF) emerged to concentrate growth factors and cells at supra-physiological levels. Nearly three decades ago, Professor Robert Marx demonstrated that PRP-obtained via centrifugation of whole blood with anti-coagulants-could accelerate healing across a wide range of indications in both dentistry and medicine. Subsequent research showed that eliminating anti-coagulants, leading to the development of PRF, resulted in an even more natural and faster healing process. In dentistry, APCs have been consistently shown to accelerate healing of both soft and hard tissues, either as standalone treatments or in combination with other biomaterials. PRF, in particular, has demonstrated benefits within several dental applications, spanning from root coverage, periodontal regeneration of intra-bony and furcation defects, ridge preservation, third molar extraction healing, sinus grafting, guided bone regeneration (GBR), and peri-implant soft tissue healing. Beyond dentistry, PRF has also proven effective in various medical indications-improving outcomes in the treatment of diabetic ulcers, managing joint pain and cartilage degradation in sports medicine, and enhancing outcomes in esthetic medicine. This review highlights the evolution of APCs, with a focus on their clinical applications and recent technological advancements. These include horizontal centrifugation techniques for PRF and more refined protocols for producing concentrated PRF (C-PRF). Lastly, the article introduces extended-PRF (e-PRF) membranes, created through heat-induced albumin denaturation, which prolong membrane degradation from the typical 2-3 weeks to up to 4 months. These innovative e-PRF membranes, composed of albumin gel and liquid PRF (Alb-PRF), are now being used as alternatives to collagen membranes in routine dental procedures.
In a large cohort of periodontitis patients, molar furcation involvement was highly prevalent but mostly of lower severity. Tooth-specific factors are primary drivers of risk, with maxillary molars and second molars having significantly higher odds of being affected.
Aim: This quasi-randomized clinical trial evaluated the additional benefit of soft-tissue phenotype modification via free palatal graft (FPG) as an adjunct to non-surgical therapy for peri-implant mucositis. A secondary objective was to determine whether any observed effects were mediated by improved plaque control.
Methods: Forty-three patients (55 implants) with peri-implant mucositis and keratinized tissue width (KTW) < 2 mm were enrolled. One month after oral hygiene instructions and non-surgical treatment, participants were quasi-randomly allocated to either an FPG procedure (test group, n = 22) or no additional intervention (control group, n = 21). The primary outcome was bleeding on probing (BoP) extent at 6 months (i.e., number of bleeding sites per implant). Secondary outcomes included peri-implant phenotype parameters (KTW, tissue thickness, and vestibular depth), plaque extent, and other peri-implant health measures (BoP severity, probing pocket depth [PPD], peri-implant soft-tissue dehiscence [PISTD], and treatment success). Intergroup comparisons were performed using regression analyses, and a mediation analysis assessed whether treatment effects were mediated by improved plaque control.
Results: At 6 months, FPG significantly increased KTW (mean difference [MD] = 2.36 mm; p < 0.001) and tissue thickness (MD = 0.97 mm; p < 0.001), while reducing plaque extent (MD = -1.49; p < 0.001), compared with the control group. BoP extent was significantly lower in the test group (0.75 ± 1.07) than in controls (1.83 ± 1.20) (MD = -1.06; 95% CI: -1.67 to -0.44; p = 0.001). Additionally, the test group exhibited lower BoP severity (MD = -0.50; p < 0.001) and higher treatment success (OR = 8.44; p = 0.001). No significant differences were observed in PPD and PISTD. Mediation analysis suggested that the observed benefits of FPG on peri-implant health were largely independent of improved plaque control.
Conclusion: FPG effectively modified the peri-implant soft-tissue phenotype and, as an adjunct to non-surgical therapy, provided additional benefits in managing peri-implant mucositis. The effects on peri-implant health were not attributable to improved plaque control.
The interactions between Limosilactobacillus reuteri and oral bacteria are poorly understood. This study seeks to characterize how two strains of L. reuteri coaggregate with Fusobacterium nucleatum, determining the impact on the biofilm composition and immunogenicity.
A series of in vitro experiments was conducted using L. reuteri DSM 17938 and ATCC PTA 5289, Fusobacterium nucleatum ATCC 25586, and Porphyromonas gingivalis W50. The coaggregation between individual strains of L. reuteri, F. nucleatum, and P. gingivalis was evaluated using the tube coaggregation assay and confocal microscopy. Biofilm compositions were determined by confocal microscopy and culture. The effect of coaggregation on the immunogenicity of L. reuteri-F. nucleatum aggregates were evaluated using periodontal ligament fibroblasts, oral epithelial cells, and monocytes.
Both L. reuteri DSM and PTA strains demonstrated coaggregation with F. nucleatum. This interaction reduced the amount of F. nucleatum in biofilm by 1000-fold. Additionally, the coaggregation between L. reuteri and F. nucleatum lowered its immunogenicity. Furthermore, the coaggregation of L. reuteri with F. nucleatum led to a 50% reduction in the amount of P. gingivalis present in the biofilm.
This study demonstrates novel mechanisms through which L. reuteri can exert its effects as a probiotic. The coaggregation with L. reuteri modulates the immunogenicity of F. nucleatum and impairs its ability to serve as the bridging species, altering the biofilm composition, thus limiting the extent of dysbiosis.
Aim: To assess (i) the risk indicators of peri-implantitis and peri-implant soft-tissue dehiscence (PISTD), and (ii) the accuracy of clinical parameters and peri-implant crevicular fluid (PICF) immunological markers in diagnosing peri-implantitis, within a Turkish university population.
Methods: A total of 324 implants in 112 patients were included. The outcomes for the risk indicators analysis were the presence of peri-implantitis and PISTD, with peri-implantitis also serving as the reference standard for the diagnostic accuracy analysis. Several potential risk indicators-including demographic, medical, and dental history, clinical and radiographic parameters, and dental chart data-were assessed using multilevel logistic regressions. The diagnostic performance of clinical parameters and PICF immunological markers was evaluated using logistic regressions and reporting sensitivity, specificity, positive/negative predictive values, and area under the curve (AUC) values.
Results: In the final multilevel logistic regression, the following indicators were associated with peri-implantitis: stage III-IV periodontitis (OR = 5.67), irregular maintenance (SPIC) compliance (OR = 7.71), history of implant loss (OR = 14.44), implant system, absence of keratinized mucosa (KM) (OR = 8.41), and clinical attachment loss in adjacent teeth (OR = 3.75). Risk indicators for PISTD included: mandibular location (OR = 0.22), implant system, absence of KM (OR = 5.95), and mucosal thickness < 2 mm (OR = 197.01). Peri-implant bleeding on probing (BoP) at 2 or more sites had the highest sensitivity for peri-implantitis (98.0%), while the highest specificity was observed for BoP severity (modified Bleeding Index 2-3 = 96.4%). The highest AUC was found for peri-implant probing pocket depth (PPD) ≥ 6 mm (0.88). Among PICF immunological markers, IL-2 and IL-10 exhibited the highest sensitivity (100.0%), while TNF-α had the highest specificity (92.9%). IL-8 and TNF-α had the highest AUC values (0.80).
Conclusion: In this Turkish university cohort, several risk indicators were identified for peri-implantitis and PISTD. Among clinical parameters, only PPD ≥ 6 mm demonstrated strong diagnostic accuracy for peri-implantitis. Several PICF immunological markers, particularly IL-8 and TNF-α, showed promising diagnostic potential.
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