Journal of periodontal research最新文献

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.

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.

Aim: To evaluate the 20-year outcomes of tissue-level implants placed in the posterior mandible, comparing implants surrounded by keratinized tissue (KT) or alveolar mucosa (AM).

Methods: At baseline, 128 patients (128 implants) were rehabilitated with implant-supported fixed dental prostheses in the posterior mandible and enrolled in a supportive periodontal/peri-implant care (SPC) program. Patients were categorized based on the presence (KT) or absence (AM) of keratinized mucosa. During the first 10 years of SPC, 11 AM patients underwent free gingival grafting (FGG), identifying a third group (AM + FGG). At the 20-year follow-up, peri-implant health status and soft-tissue dehiscence were assessed according to the 2018 Case Definitions. The need for additional treatment between the 10- and 20-year examinations was also recorded.

Results: Of the 98 patients evaluated at the 10-year follow-up, 64 (KT = 42; AM = 16; AM + FGG = 6; drop-out rate: 35%) attended the 20-year examination. Additional treatment was required in 11 AM patients (50%) versus 2 KT patients (5%) (p < 0.01). AM implants exhibited significantly greater marginal bone loss, bleeding on probing, and soft tissue recession compared to KT implants (p < 0.01). The application of an FGG (AM + FGG = 6) had a protective effect on peri-implant health status at 20 years. Peri-implantitis was diagnosed in 4.2% of implants surrounded by keratinized mucosa (KT or AM + FGG) versus 25% in the AM group (OR = 6.67; 95% CI: 1.09-40.9; p = 0.041).

Conclusion: Tissue level implants placed in the posterior mandible without KT showed greater marginal bone loss, bleeding on probing, soft tissue recession, and peri-implant diseases compared to implants with KT at 20 years.

The dental pulp and the periodontal tissues are crucial for maintaining oral health through supporting the structure, function, and integrity of teeth and surrounding tissues. The potential to regenerate these tissues (in case of their damage) represents a significant advancement in dental medicine. A functional regeneration could profoundly impact the quality of life for individuals with dental and periodontal diseases through offering new solutions to tissue loss and dental functional impairment, beyond what conventional dental therapies would provide. Studies on tissue engineering-based dentin-pulpal and periodontal regeneration have demonstrated promising results, using mesenchymal stromal cells (MSCs) from sources like bone marrow, adipose tissue, and cord blood. Nevertheless, MSCs derived directly from dental and periodontal tissues exhibit unique biological properties, with the potential to specifically address dental and periodontal regeneration, holding distinctive regenerative and immunomodulatory properties that may allow them to become valuable tools in clinical regenerative procedures. Their use in therapies could greatly benefit patients with oral and periodontal diseases, potentially enhancing life quality. Despite these promising findings, the distinct regenerative capacity of these cells, their mechanisms, and their potential clinical translational applications remain not fully elucidated. This review article aims to consolidate current knowledge about the biological characteristics and regenerative capabilities of dental and periodontal MSCs. By exploring the biology, isolation, and functional capacities of these cells, this work seeks to offer a deeper understanding of their potential and limitations, guiding future research and clinical strategies.

Periodontitis and noncommunicable diseases share an overall inflammatory state often sustained by concomitant oxidative stress as one of the main processes involved. A huge amount of literature supports such a main pathogenic process, which is also considered the therapeutic target. The attempt to control inflammation by acting on oxidative stress has given largely unsatisfactory results, either as preventive or as treatment approaches. To propose new ideas that will help in this field, the paper reviewed all physiological processes involved in oxidative stress in periodontitis. The discussion considers all of them, considering whether they come from endogenous sources, that is, all the intracellular physiological devices and/or processes that are involved in oxidative stress, such as mitochondria, rough endoplasmic reticulum, peroxisomes, autophagy, and aging, or from exogenous sources, that is, the external factors that affect oxidative stress, such as nutrition, physical activity, psychological status, environmental conditions, microbiome, and drugs. The most important conclusion is that all of them should be taken into consideration in future research since we need to address oxidative stress as part of a specific biological and metabolic cellular state in a multicellular organism. To understand the cellular physiology that underlies oxidative stress and consider this point in treating each of our periodontal patients according to a specific oxidative state could be called personalized/precise oxidative stress therapy (POST) and should include the following points: (1) environmental conditions, (2) individual characteristics, and (3) oxidative state of different intracellular organelles.

The central question addressed in this review revisits the historical chicken-and-egg debate: "In periodontitis, does microbial dysbiosis drive inflammation, or does inflammation shape the subgingival microbiome?" This question is reframed through the lens of inflammation resolution. Specialized pro-resolving mediators (SPMs) provide a mechanistic framework for understanding how inflammation intersects with microbial dysbiosis. Derived from omega-3 and omega-6 fatty acids, SPMs actively promote the resolution of inflammation through binding of specific cell surface receptors rather than nonspecifically suppressing it, highlighting their therapeutic potential as side-effect-free host modulators, with implications beyond periodontitis to other chronic inflammatory diseases. The evidence reviewed shows how SPMs can: (1) control inflammation by resolution rather than inhibition, (2) reverse microbial dysbiosis as a consequence of inflammation control, and (3) promote tissue regeneration through diverse biological pathways. Whether the primary dysregulation in periodontitis lies solely in resolution failure or involves additional-possibly still unidentified-mechanisms, remains unclear. All individuals harbor periodontal pathobionts, yet only a subset develop severe disease. Why do some individuals with significant biofilm accumulation maintain attachment levels, while others with reasonable plaque control become edentulous? This remains one of the most significant unanswered questions in periodontology. What is evident, however, is the need for a paradigm shift. While bacteria initiate the inflammatory process in all individuals, it is the host response that ultimately determines the progression to periodontitis.