Journal of periodontal research最新文献

Implant dentistry has historically centered on osseointegration, yet it is now evident that soft-tissue integration is equally critical for long-term success. The stability of bone-anchored dental implants hinges on the establishment and maintenance of a stable attachment that mirrors, at least functionally, the supracrestal attachment around teeth. This review synthesizes current understanding of how the soft tissue-implant interface forms and how it is maintained over time. This interface comprises (i) a rapidly developing peri-implant epithelium and (ii) a connective-tissue component that gradually rebuilds its collagen architecture after implant placement. Although current knowledge is surprisingly limited, evidence indicates that neither the epithelium nor the connective tissues form a true attachment to the implant surface or prosthetic components. Soft-tissue dimensions, the role of keratinization of the peri-implant epithelium, the characteristic presence of inflammation within peri-implant connective tissue, and the biological and clinical determinants shaping the formation and maintenance of this interface are discussed, highlighting major knowledge gaps for future research. Finally, we examine the contribution of soft-tissue phenotype to peri-implant diseases and soft-tissue dehiscence. A better understanding of the principles governing the development and homeostasis of soft tissue-implant interfaces may inform strategies to improve the barrier function of peri-implant soft tissues around all bone-anchored implants, ultimately guiding future translational research to enhance implant longevity.

Aim: The peri-implant soft tissue phenotype, including keratinized tissue width (KTW) and mucosal thickness (MT), plays a pivotal role in maintaining peri-implant health and stability. Various soft tissue augmentation (STA) procedures have been developed to enhance these components, employing different grafting techniques and materials. The aim of the present systematic review is to compare the effectiveness of different techniques as well as different surgical timing in order to establish their relative efficacy.

Methods: A systematic review and Bayesian network meta-analysis (NMA) was conducted following PRISMA-NMA guidelines. Randomized controlled trials (RCTs) evaluating STA around dental implants were included, focusing on KTW and MT gain as primary outcomes. Pairwise and indirect comparisons were performed using a hierarchical Bayesian model with Markov chain Monte Carlo simulations. Treatment effects were expressed as mean differences (MD) with 95% credible intervals. Additionally, subgroup analyses explored apically positioned flap (APF)-based and bilaminar techniques separately, while meta-regression assessed the influence of surgical timing.

Results: A total of 48 RCTs were included in the qualitative analysis, and 46 in the NMA. For KTW gain, APF + free gingival graft (FGG) was the most effective treatment [range of MD: 0.22-4.11 mm], whereas APF alone showed limited efficacy compared to no intervention. Bilaminar techniques did not result in significant KTW gain. For MT gain, bilaminar techniques showed the best results, with connective tissue graft (CTG) displaying the best performance [range of MD: 0.02 to 0.94 mm], followed by xenogeneic collagen matrix and buccally displaced flap. Timing did not significantly influence MT gain, while "delayed time points" might positively influence KTW. Longitudinal analysis showed variability in stability across treatments, with APF + FGG and CTG maintaining higher performance over time.

Conclusion: APF + FGG is the most reliable approach for increasing KTW, while CTG remains the gold standard for MT enhancement. The choice of technique and graft material appears more critical than surgical timing. Long-term stability of tissue dimensions and standardization of reporting across future trials are essential to refine clinical decision-making in STA procedures.

Aim: To (i) evaluate the association between posterior masticatory unit (PMU) loss and all-cause mortality, (ii) quantify mediation through dietary intake, nutritional biomarkers, and body mass index (BMI), and (iii) assess whether prosthetic rehabilitation modifies this relationship.

Methods: Data from 17 109 adults participating in NHANES 1999-2004 and 2011-2014, with mortality follow-up through 2019, were analyzed. PMUs were classified as ≥ 5 from natural teeth (reference), < 5 without posterior prosthetic rehabilitation, < 5 despite the presence of posterior prosthetic restorations, ≥ 5 achieved through removable or tooth-supported fixed prostheses, and ≥ 5 achieved through implant-supported prostheses. Weighted Cox regression estimated adjusted hazard ratios (aHRs) for all-cause mortality. Causal mediation models quantified indirect effects through diet quality, nutritional markers, and BMI. Hypothetical interventions rehabilitating lost PMUs were emulated using longitudinal modified treatment policies with targeted maximum likelihood estimation.

Results: Compared with participants with ≥ 5 PMUs from natural teeth, mortality risk was higher among those with < 5 PMUs without posterior prosthetic rehabilitation (aHR 1.60; 95% CI 1.22-2.09), < 5 PMUs despite the presence of posterior prosthetic restorations (aHR 1.29; 95% CI 1.08-1.55), and ≥ 5 PMUs achieved through removable or tooth-supported fixed prostheses (aHR 1.27; 95% CI 1.10-1.48). No excess mortality risk was observed for ≥ 5 implant-supported PMUs (aHR 1.00; 95% CI 0.77-1.30). Diet quality indices (Alternative Healthy Eating Index, Dietary Approaches to Stop Hypertension, Dietary Inflammatory Index) mediated 6%-11% of the association, while fruit and fiber intake alone mediated 5%-9%; protein intake, nutritional biomarkers, and BMI contributed smaller proportions. Under causal assumptions, emulated scenarios restoring ≥ 5 PMUs with implant-supported prostheses or maintaining ≥ 5 natural PMUs were associated with 4%-5% higher estimated survival among individuals with < 5 PMUs without posterior prosthetic rehabilitation.

Conclusion: Loss of natural PMUs is associated with increased all-cause mortality, only partially mediated by diet quality. This excess risk appears attenuated by posterior prosthetic rehabilitation and is no longer evident when ≥ 5 PMUs are restored with implant-supported prostheses. When posterior teeth are lost, implant-supported rehabilitation may be considered as an option potentially associated with improved survival.

Hyaluronic (HA)-based materials show composition- and concentration-dependent responses. Proper formulation and dosage selection are key for clinical application.

Aim: Understanding macrophage polarization in periodontitis is critical for elucidating the underlying disease mechanisms. This exploratory study aimed to characterize phenotypic features of monocyte-derived macrophages (MDMs) from treated periodontitis patients.

Methods: Peripheral blood mononuclear cells were isolated from 30 individuals classified into three groups: periodontal healthy (H) and patients with treated stage III, grade B (PIII-B) or grade C (PIII-C) periodontitis. Monocytes were differentiated into macrophages and cultured under non-polarizing (M0), M1-polarizing (LPS + IFN-γ), or M2-polarizing (IL-4 + IL-13) conditions. MDM polarization was evaluated by immunophenotyping and cytokine secretion profiling.

Results: Under M0 conditions, the percentage of M1 MDMs decreased in the H group but remained stable in both periodontitis groups, particularly in PIII-C, which exhibited a higher M1/M2 ratio. Following M1 stimulation, no significant differences in M1/M2 ratios were observed among groups. However, H MDMs increased VEGF and IL-10 secretion compared with those from PIII-B. Under M2 stimulation, PIII-C MDMs exhibited a higher proportion of M1 cells and increased IL-6 secretion, while PIII-B MDMs demonstrated an elevated M1/M2 ratio and lower IL-10 response, suggesting a shift toward a more pro-inflammatory profile.

Conclusion: In this exploratory study, MDMs from individuals with successfully treated stage III, grade B or C periodontitis exhibited a tendency toward a M1-like phenotype across different polarization conditions, indicating the possible persistence of a pro-inflammatory immune trait that requires confirmation in longitudinal and mechanistic studies.

Population-based epidemiology and clinical research are complementary and mutually reinforcing: Epidemiology quantifies disease incidence/prevalence and elucidates environmental and social determinants in populations, whereas clinical research evaluates biomarkers, therapeutics, and prognostic outcomes in patients; their convergence underpins translational science, comparative effectiveness, real-world evidence, and precision dentistry.

Irisin is an extracellular peptide stimulated by exercise and could act as both a biomarker and mediate the positive impact of exercise. This scoping review synthesizes human evidence on irisin variations in non-communicable diseases, showing an increase of irisin in saliva and gingival tissues in periodontitis, potentially reflecting reparative or immunomodulatory activity.

Cohort studies are vulnerable to confounding and time-related biases. Recent advances emphasize the importance of emulating a hypothetical target trial to minimize several of these biases. The target trial framework is a critical tool for designing cohort studies. It requires explicit specification of protocol components: eligibility criteria, treatment strategies, outcomes, timing of follow-up (time zero), and the causal contrast to be estimated. Critical to this framework is defining "time zero" when treatment assignment takes place and follow-up begins, which prevents prevalent user and immortal time bias and ensures proper temporal sequencing of confounders, exposure, and outcome. By guiding design, data collection, and analysis, the target trial framework helps align observational studies with the principles of randomized trials, improving the validity and interpretability of their findings. While it cannot eliminate unmeasured confounding, this approach promotes transparent, bias-conscious cohort design, minimizes time-related bias, and supports more robust causal inference with observational data.

Drawing on a large, nationally representative population of older American adults (n = 3610), the study shows that individuals with more than eight missing teeth have a 6%-10% higher likelihood of cardiovascular disease compared with those with fewer tooth losses. Poorer diet quality emerged as a key pathway linking tooth loss and cardiovascular outcomes.

Aim: This pilot randomized controlled trial evaluated the efficacy of demineralized dentin graft (DDG) combined with injectable platelet-rich fibrin (I-PRF) and metronidazole (MTZ) versus DDG with I-PRF and DDG alone in alveolar ridge preservation (ARP) of chronically infected extraction sockets.

Methods: Patients with non-restorable teeth and chronic periapical infection in the maxillary anterior and premolar regions were randomly assigned to three groups (n = 18/group): DDG alone, DDG + I-PRF, and DDG + I-PRF/MTZ. After extraction, graft materials were placed into sockets. Cone-beam CT scans at baseline and 6 months assessed vertical and horizontal ridge dimensions. Virtual implant planning evaluated the need for further augmentation. Pain was recorded daily for 7 days using a visual analogue scale (VAS). Bone biopsies at 6 months were harvested during implant placement for histomorphometric analysis.

Results: Fifty-four patients were analyzed. No significant differences were found in vertical and horizontal ridge dimensional changes (p > 0.05). Minimal additional augmentation was needed. The DDG + I-PRF/MTZ group showed significantly the highest mineralized bone percentage (55.02% ± 3.65%), followed by DDG + I-PRF (41.14% ± 7.00%) and DDG alone (30.21% ± 3.72%) (p < 0.05). Soft tissue proportion histologically was significantly lowest in the DDG + I-PRF/MTZ group (p < 0.05).

Conclusion: All protocols were effective for ARP. Addition of I-PRF with MTZ enhanced bone mineralization.

Trial registration: www.

Clinicaltrials: gov: NCT06374784.