Journal of periodontal research最新文献

Epigenetic modifications regulate gene activity in response to environmental and intrinsic factors, offering potential as reversible biomarkers and therapeutic targets. Their role in periodontitis, however, remains insufficiently defined. This review critically evaluates current evidence on epigenetic mechanisms in periodontitis, emphasizing methodological challenges such as cell-type heterogeneity, small sample sizes, and the detection of meaningful tissue-specific changes. Chronic inflammation and environmental exposures, notably tobacco smoke, induce stable, gene-specific DNA methylation changes in gingival tissues. Key epigenetic alterations have been identified in several genes such as CYP1B1, AHRR, ROBO2, and PTP4A3, which are implicated in detoxification, epithelial repair, and immune responses. These modifications are often cell-type-specific. Despite their biological relevance, most studies are limited by small cohorts and mixed-cell population analyses, complicating interpretation. DNA CpG methylation is the primary focus, given its chemical stability and established analytical platforms, while histone and RNA modifications remain understudied due to technical challenges. Epigenetic regulation appears to contribute to the pathogenesis of periodontitis, particularly in response to persistent environmental and inflammatory stimuli. However, clinical translation is constrained by methodological limitations. Future research must incorporate larger sample sizes, address cellular heterogeneity, and investigate the reversibility of epigenetic marks following periodontal therapy or elimination of harmful exposures. Advancing tissue-specific epigenetic profiling may enhance early detection, risk stratification, and personalized prevention strategies. Rigorous study designs and standardized methodologies will be essential to realizing the clinical potential of epigenetic research in periodontal disease.

The present findings demonstrate that low-level laser therapy reduces postoperative pain levels associated with the palatal donor site in free gingival graft surgeries, as well as accelerating the clinical healing of the surgical wound. Low-level laser therapy is associated with improved postoperative morbidity of the donor area in free gingival graft.

Aim: Multiple oral pathologies requiring antiseptic mouthrinses for prevention or treatment. However, nonselective elimination of the microbes may also harm beneficial commensal, healthy bacteria. Promicrobial strategies, such as probiotics, aim to rebalance the oral microbiome rather than eradicate it; however, we hypothesised that their incorporation might be challenged due to the microbiome's inherent resistance to outsiders. In this study, their combined effect on an in vitro oral biofilm model was assessed. Instead of comparing mouthrinses to probiotics, could they be combined to obtain the best of both worlds?

Methods: The compatibility of two commonly used Limosilactobacillus reuteri strains with 13 commercially available mouthrinses was tested by evaluating probiotic survival in the mouthrinses and their combined effect on a multispecies in vitro biofilm model.

Results: Differences in compatibility were observed. Several mouthrinses showed moderate compatibility and improved the probiotics incorporation into biofilms. One mouthrinse (O7 Active Oxygen) demonstrated the most favourable compatibility, enabling abundant probiotic incorporation and beneficial biofilm composition changes.

Conclusion: The combination of mouthrinses and probiotics has the potential to improve the treatment of oral pathologies and promote a healthier oral microbiome, although compatibility varies.

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.