Journal of periodontal research最新文献

Soft tissue augmentation around teeth and dental implants is a central aspect of periodontal and peri-implant plastic surgery. Autogenous soft tissue grafts are generally regarded as the gold standard for increasing keratinized mucosa, mucosal thickness, and soft tissue height, supported by extensive long-term evidence. However, limitations such as restricted tissue availability, increased surgical time, and donor-site morbidity have encouraged the development of soft tissue graft substitutes, including xenogeneic and allogeneic matrices, and collagen derivatives, among other biomaterials. Over the past two decades, these alternatives have shown promising results, particularly in sites with favorable anatomical conditions, including optimal bone support, tall and wide papillae, and adequate hard and soft tissue phenotype; although their predictability remains variable across the literature and is often lower than that of autogenous grafts in complex defects and esthetically demanding areas. Nevertheless, the growing emphasis on patient-reported outcomes has led several authors to explore the use of graft substitutes in different clinical scenarios, sometimes in combination with smaller autogenous grafts. This manuscript aims to summarize the current state-of-the-art on soft tissue graft substitutes for managing deficiencies at both teeth and implant sites. A comprehensive literature review is provided, together with clinical decision trees designed to guide clinicians in selecting autogenous grafts versus substitutes across different scenarios. These tools highlight the main factors influencing treatment selection, including baseline keratinized mucosa, buccal bone conditions, site anatomy, esthetic requirements, and patient preference. By integrating current evidence with practical algorithms, this review seeks to support clinicians in making informed, patient-centered decisions regarding soft tissue augmentation at teeth and implants.

Aims: To investigate how Porphyromonas gingivalis induces endothelial dysfunction, focusing on the regulatory role of Sirtuin 3 (Sirt3) in mitochondrial function.

Methods: Differentially expressed Sirtuin family genes in P. gingivalis-infected human aortic endothelial cells (HAECs) were identified through RNA sequencing and validated by quantitative real-time PCR and Western blot. Mitochondrial and endothelial functions were assessed in P. gingivalis-infected HAECs with or without Sirt3-specific agonist Honokiol. Cyclophilin D (CypD) K167 point mutation plasmids were constructed, and Co-immunoprecipitation was performed to investigate the Sirt3-CypD interaction. The vasorelaxation of aortas from mice orally administrated with P. gingivalis was also evaluated.

Results: Porphyromonas gingivalis infection in HAECs resulted in mitochondrial and endothelial dysfunction. Mechanistic studies revealed that Sirt3-mediated deacetylation of CypD at K167 was pivotal in alleviating P. gingivalis-induced mitochondrial and endothelial dysfunction. Oral inoculation of P. gingivalis in mice significantly impaired endothelial-dependent vasodilation, disrupted aortic endothelial integrity, increased endothelial cell apoptosis, and elevated mitochondrial reactive oxygen species production. Notably, Sirt3 activation reversed mitochondrial and endothelial dysfunction induced by P. gingivalis both in vivo and in vitro.

Conclusion: The present study demonstrated that P. gingivalis induced mitochondrial and endothelial dysfunction, which was mediated through Sirt3-dependent CypD deacetylation.

Aim: The study aimed to elucidate a putative association between severe periodontitis and the incidence of recurrent cardiovascular events in patients with cardiovascular disease (CVD) within 10 years after their initial hospitalisation.

Methods: A cohort of 1002 stationary patients with angiographically proven CVD was included. They were examined regarding prevalence of severe periodontitis (≥ 30% of the teeth with proximal attachment loss of ≥ 5 mm), probing depth, clinical attachment loss, bleeding on probing, number of missing teeth and oral care habits. Recurrent events were summarised as combined end point (myocardial infarction, stroke/transitory ischemic attack, cardiovascular death and death caused by stroke). Survival analyses were carried out after a 10-year follow-up period. Hazard ratios (HRs) were adjusted for known cardiac risk factors using Cox regression.

Results: The follow-up was completed by 792 patients. The overall incidence of the combined end point was 42.8%. Severe periodontitis was associated with recurrent cardiovascular events (adjusted hazard ratio [HR] = 1.26, 95% confidence interval [CI] 1.0-1.58 and Standard error [SE] 0.11), whereas both, tooth brushing more than once a day (adjusted HR = 0.74, 95% CI 0.57-0.97, SE 0.13) and performing interdental hygiene (adjusted HR = 0.71, 95% CI 0.52-0.99, SE 0.16) decreased this risk.

Conclusions: Severe periodontitis is a putative risk factor for recurrent cardiovascular events.

Trial registration: ClinicalTrials.gov identifier: NCT01045070.

Aims: Elevated levels of Herpes Simplex Virus 1 (HSV-1) have been reported in periodontitis, however, the tropism and relationship with periodontal inflammation are poorly characterized. This study investigated how inflammation affects viral tropism toward human periodontal ligament stem cells (hPDLSCs).

Methods: HSV-1 gB and gD transcripts in healthy and diseased human gingiva were measured by RT-qPCR and confirmed in HSV-1-infected murine gingiva. HSV-1 infection in hPDLSCs was analyzed by imaging and flow cytometry. hPDLSCs were individually treated with IL-6, TNF-α, GMCSF, IL-10, or PgLPS, and HSV-1 replication was assessed by infecting with the 17 GFP strain. Lineage markers in virally infected hPDLSCs during osteogenic differentiation were measured by RT-qPCR and immunofluorescence in vitro and validated in vivo. Mice subjected to ligature-induced periodontitis (LIP) and infected with HSV-1 were examined for gingival histology, inflammatory cytokines, and alveolar bone loss.

Results: Inflamed human gingiva showed higher expression of viral transcripts compared to healthy controls. In mouse oral HSV-1 infection, gB and gD expression increased over time, with higher levels in mice with ligature-induced periodontitis. Virus infected hPDLSCs challenged with inflammatory mediators or PgLPS showed higher GFP, while IL-10 treatment attenuated GFP levels. Importantly, HSV-1 17 GFP infection affected osteoblast lineage commitment by promoting the expression of key transcription factors in vitro and in vivo. Compared to the LIP alone group, higher levels of inflammatory markers and bone loss were evident in HSV-1 infected with LIP.

Conclusion: hPDLSCs are trophic to HSV-1 in vitro and in vivo, with periodontal inflammation playing a significant role in viral tropism.

Aims: Diabetes induces disorders in macrophage immunometabolism, leading to increased destruction of periodontal tissue. Identifying key factors to restore metabolic alterations and promote resolution of inflammation remains an unmet objective.

Methods: In the present study, the effect of macrophage efferocytosis on inflammatory regression and tissue repair was assessed using a diabetic periodontitis (DPD) model. The mitochondrial function of macrophages cultured under different conditions was assessed in vitro, and macrophage efferocytosis function and polarization phenotypes were examined. Osteogenic differentiation and migration capacity were examined using periodontal ligament stem cells (PDLSCs) co-cultured with macrophages to assess the effect on tissue repair.

Results: We demonstrated that the high-glucose inflammatory microenvironment exacerbated the pro-inflammatory metabolic profile of macrophages and disrupted mitochondrial dynamics. Rats with DPD exhibited heightened periodontal tissue damage during the ligation period, characterized by increased neutrophil infiltration and apoptotic cells. Following ligature removal, the transition to the repair phase was inhibited. Impaired efferocytosis in macrophages led to reduced expression of anti-inflammatory cytokines. Inhibiting excessive mitochondrial division mitigated macrophage damage, ultimately improving the osteogenic differentiation and migration of PDLSCs.

Conclusions: This research suggested the critical role of mitochondria in the resolution of inflammation in diabetic periodontitis through regulating macrophage efferocytosis and interaction with PDLSCs.

Aim: The correlation between periodontitis and colorectal cancer (CRC) has drawn widespread attention. However, how periodontitis affects CRC progression remains unclear.

Methods: C57BL/6 mice were used to establish experimental periodontitis and CRC model. Histological alterations of periodontium and colon were observed by hematoxylin and eosin staining. Micro-computed tomography (micro-CT) was applied to evaluate alveolar bone loss (ABL). Tumor growth was detected by immunofluorescence. Gut bacteria were analyzed using 16S rRNA sequencing. Gas chromatography-mass spectrometry (GC-MS) was performed to observe the alterations of gut microbial metabolites. The detection of associated pathways was carried out using quantitative real-time PCR (qRT-PCR).

Results: Experimental periodontitis significantly induced increases in tumor number in mice with CRC. Double immunofluorescence for Ki67 and β-catenin, as well as Cyclin D1 and β-catenin, indicated that experimental periodontitis observably promoted tumor growth. 16S rRNA sequencing and untargeted metabolomics analysis displayed that experimental periodontitis altered gut microbial community and metabolite profiles in CRC mice. Notably, we found that experimental periodontitis dramatically increased the level of three oncometabolites (serotonin, adenosine, and spermine) in mice with CRC.

Conclusion: Alterations of gut microbial community and metabolites might be relevant in experimental periodontitis deteriorating CRC.

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.

Aim: This prospective cohort study aimed to evaluate the incidence and risk/protective factors of peri-implantitis over time.

Methods: A university-representative cohort was evaluated at baseline and after a mean follow-up time of 3.9 years. The main outcome was the incidence of peri-implantitis, defined as bone loss > 1 mm between the two examinations in implants showing bleeding on probing. Putative risk/protective factors assessed at baseline were tested through multilevel (mixed-effects) logistic regression analyses.

Results: A total of 73 patients with 322 implants were included. During the follow-up period, 14 implants (4.3%) were lost in 9 patients (12.3%). Incidence of peri-implantitis was observed in 22.2% of patients and 9.4% of implants. In the final multilevel multiple logistic regression model, the following factors were associated with occurrence of peri-implantitis: periodontitis severity (stage IV periodontitis: OR = 41.29; 95% CI: 4.10-415.54), periodontal bone loss/age ratio (> 1: OR = 8.87; 95% CI: 1.47-53.73), smoking (current smokers: OR = 7.84; 95% CI: 1.83-33.50), sleep duration (> 7 h: OR = 19.97; 95% CI: 1.69-236.39), implant location (incisor: OR = 60.60; 95% CI: 4.04-908.33), restoration type (full-arch fixed restorations: OR = 89.84; 95% CI: 3.66-2202.97), and restoration margin location (juxta-marginal: OR = 14.17; 95% CI: 1.20-166.76). Keratinized tissue width assessed at baseline was not associated with incidence of peri-implantitis.

Conclusion: Approximately one in five patients and one in 10 implants experienced incident peri-implantitis over a nearly four-year period. Periodontitis (Stage IV and Grade C), lifestyles (smoking and sleep duration), implant location, and prosthetic factors (restoration type and margin location) emerged as risk factors for peri-implantitis.