Epidemiological studies have consistently established a positive association between periodontal disease (PD) and cardiovascular disease (CVD). However, large-scale investigations exploring the impact of changes in PD status on CVD risk are scarce. This study aimed to investigate the association between the dynamics in PD and the risk of incident CVD in a nationally representative population.
Utilising data from the Korean National Health Insurance Service, a cohort of 1,242,570 participants who underwent oral health exams in 2003 and a follow-up exam in 2005–2006 was analysed. Participants were categorized into groups based on changes in PD status: absent, improvement, onset and persistent. Cox proportional hazard models were employed to assess the multivariate-adjusted hazard ratios (HRs) for composite CVD outcomes, including death, myocardial infarction and stroke.
Over a mean follow-up of 14.4 years, 79,810 (6.4%) cases of composite CVD occurred, including 14,296 (1.2%) myocardial infarctions, 3247 (0.3%) hemorrhagic strokes and 8900 (0.7%) ischemic strokes. Individuals with persistent PD showed the highest risk of CVD (HR: 1.04, 95% CI: 1.03–1.06, p < 0.001). In the pairwise comparisons, the PD improvement group exhibited a lower composite CVD risk than the PD persistent group (HR: 0.97, 95% CI: 0.96–0.99, p = 0.010); similarly, the PD onset group showed a lower risk than the PD persistent group (HR: 0.94, 95% CI: 0.93–0.96, p < 0.001). This pattern was consistent in the risk of death, with both the PD improvement and PD onset groups showing a lower risk of death than the PD persistent group.
This study suggests the dynamic nature of PD as a potential modifiable risk factor for CVD. Individuals with chronically persistent PD showed an elevated incidence risk of CVD, emphasizing the importance of managing PD in preventive strategies.
To discover new salivary biomarkers to diagnose periodontitis and evaluate the impact of age and smoking on predictive capacity.
Saliva samples were collected from 44 healthy periodontal individuals and 41 with periodontitis. Samples were analysed by sequential window acquisition of all theoretical mass spectra (SWATH-MS), and proteins were identified by employing the UniProt database. The diagnostic capacity of the molecules was determined with generalized additive models. The models obtained were single-protein unadjusted and adjusted for age and smoking status, besides two-protein combinations.
Eight single salivary proteins had a bias-corrected accuracy (bc-ACC) of 78.8%–86.8% (bc-sensitivity/bc-specificity of 62.5%–86.9%/60.9%–98.1%) to diagnose periodontitis. Predictive capacity increased more by adjusting for age (bc-ACC: 94.1%–98.2%; bc-sensitivity/bc-specificity: 90.2%–98.6%/93.6%–97.2%) than smoking (bc-ACC: 83.9%–90.4%; bc-sensitivity/bc-specificity: 73.6%–89.9%/76.2%–96.4%). These proteins were keratin, type II cytoskeletal 1, protein S100-A8, β-2-microglobulin, neutrophil defensin 1, lysozyme C, ubiquitin-60S ribosomal protein L40, isoform 2 of tropomyosin α-3 chain and resistin. Two dual combinations showed bc-sensitivity/bc-specificity of > 90%: β-2-microglobulin with profilin-1, and lysozyme C with zymogen granule protein 16 homologue B.
New salivary biomarkers show good or excellent ability to diagnose periodontitis. Age has a more significant influence on the accuracy of the single biomarkers than smoking, with results comparable to two-protein combinations.
Porphyromonas gingivalis , a consensus periodontal pathogen, is thought to be involved in Alzheimer's disease (AD) progression, and P. gingivalis -derived outer membrane vesicles (PgOMVs) are a key toxic factor in inducing AD pathology. This study aimed to clarify the regulatory mechanism underlying the PgOMV-induced AD-like phenotype.
We intraperitoneally injected PgOMVs into the periphery of wild-type and CatB knockout mice for 4 or 8 weeks to assess the effect of CatB on PgOMV-induced AD pathology. Mice were evaluated for cognitive change, tau phosphorylation, microglial activation, neuroinflammation and synapse loss. Microglial and primary neuron culture were prepared to verify the in vivo results.
CatB deficiency significantly alleviated PgOMV-induced cognitive dysfunction, microglia-mediated neuroinflammation, tau hyperphosphorylation and synapse loss. Subsequent transcriptomic analysis, immunofluorescence and immunoblotting suggested that CatB modulates microglia-mediated neuroinflammation through stress-activated protein kinases (SAPK)/Jun amino-terminal kinases (JNK) signals after administration of PgOMVs, which in turn regulates neuronal tau phosphorylation and synapse loss in a SAPK/JNK-dependent manner.
Our study unveils a previously unknown role of CatB in regulating PgOMV-induced AD pathology.
To determine bone regeneration following sinus floor elevation (SFE) at sites with or without prior sinus membrane perforation.
The sinus membranes in the maxillary sinuses of 12 rabbits were intentionally perforated (≥ 5 mm) on one side, followed by application of a collagen matrix. SFE was performed on both sinuses after 8 weeks of healing, presenting two groups: SFE with a previous large sinus membrane perforation (group SFE_Perf), and in an intact sinus (group SFE). The animals were euthanized at 2 and 4 weeks after SFE. Micro-computed tomographic and histomorphometric analyses were performed.
The amount of newly formed bone within the augmented area did not differ significantly between the two groups at 2 weeks and 4 weeks (4.7 ± 1.0 mm2 vs. 5.3 ± 1.4 mm2 and 9.2 ± 1.7 mm2 vs. 10.8 ± 2.2 mm2, respectively, mean ± SD; p > 0.05). However, the amount of newly formed bone near the middle of the sinus membranes was significantly greater in group SFE than in group SFE_Perf (p < 0.05). There was no significant difference in the augmented volume. Fewer subepithelial glands and denser collagen fibres within the sinus membranes were observed in group SFE_Perf than in group SFE.
A large perforation of the sinus membrane followed by an 8-week healing period did not jeopardize new bone formation following SFE.
This narrative review aims to synthesize current knowledge on integrating single-cell genomics technologies with animal models of periodontitis and peri-implantitis.
Single-cell RNA sequencing (scRNAseq) reveals cellular heterogeneity and specific cell roles in periodontitis and peri-implantitis, overcoming the limitations of bulk RNA sequencing. Under controlled conditions and genetic manipulation, animal models facilitate studying disease progression, gene functions and systemic disease links, aiding targeted therapy development. Knockout models have started to elucidate the impact of genetic mutations on periodontal disease and host responses. scRNAseq in animal models has been used to examine connections between periodontitis and systemic diseases, revealing altered immune environments and cellular interactions. Emerging studies are now applying these methods to animal models of peri-implantitis. Integrating these datasets into single-cell and spatially resolved atlases will enable future meta-analyses, providing deeper insights into disease mechanisms considering factors such as sex, strain, and age.
Integrating scRNAseq with animal models advances the understanding of periodontitis and peri-implantitis pathogenesis and precision therapies. The combined use of single-cell and spatial genomics and scRNAseq will further enhance data insights significantly for drug discovery and preclinical testing, making these technologies pivotal in validating animal models and translating findings into clinical practice.
Aim: The objective of this cross-sectional survey was to assess the attitude among general practitioners (GPs) and periodontal specialists (PSs) in Norway towards developing and implementing guideline-based periodontal referral practise.
Material and methods: A multiple-choice questionnaire was distributed online to a sample of professionally active GPs and PSs. The survey included questions on demographics, practise profile, proficiency and insight among oral healthcare providers, periodontal referral patterns, and attitude on establishing guideline-based referral practise. Logistic regression analyses were employed to estimate associations between dependent and selected independent variables. Inverse probability weights (IPW) were applied to adjust for non-response in the logistic regression models.
Results: Analyses were based on answers from 353 GPs and 49 PSs. The majority of GPs (77.9%) considered periodontal referral guidelines as a useful tool if they were available, and 59.2% of PSs expressed a positive attitude for implementing guideline-based referral practise to prevent premature or delayed referrals. In total, 93.9% of PSs reported that patients with periodontitis were being referred from GPs too late either frequently or sometimes. Females tended to be more interested in utilising referral guidelines than males (odds ratio, OR = 2.89, p < 0.001). Older GPs and those with increasing years of practising, were less interested in using referral guidelines than younger and more inexperienced GPs (both p < 0.05).
Conclusions: The findings document a positive attitude and significant need for developing and implementing periodontal referral guidelines among GPs and PSs, ensuring timely identification and referral of patients with periodontitis.
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