Objective: To identify gingival crevicular fluid (GCF)-derived inflammatory markers of periodontitis progression and periodontal treatment impact.
Methods: Periodontally healthy (H; n = 112) and periodontitis (P; n = 302) patients were monitored bi-monthly for 1 year without therapy. Periodontitis patients were re-examined 6 months after non-surgical periodontal therapy (NSPT). Levels of 64 biomarkers were measured in the GCF samples collected at each visit from progressing (n = 12 sites in H; n = 76 in P) and stable (n = 100 in H, n = 225 in P) sites. Clinical parameters and log-transformed analyte levels were averaged within clinical groups at each time point and analysed using linear mixed models.
Results: During monitoring, progressing sites had significantly higher levels of IL-1β, MMP-8, IL-12p40, EGF and VEGF. MMP-9 and Periostin were significantly more elevated in stable sites. Distinct cytokine profiles were observed based on baseline PD. Treatment led to significant reductions in Eotaxin, Flt-3L, GDF-15, GM-CSF, IL-1β, IL-17, MIP-1d, RANTES and sCD40L, and increases in IP-10 and MMP-9.
Conclusion: Distinct cytokine signatures observed in stable and progressing sites were maintained over time in the absence of treatment and significantly affected by NSPT.
Aim: To assess the impact of active (APT) and supportive periodontal therapy (SPT) on the change in probing depth (PD) and annual tooth loss in partially and fully compliant and drop-out patients.
Material and methods: Data of 280 periodontally treated partially and fully compliant (regular supportive visits, SPT duration 5.5 ± 4.5 years) and 55 drop-out patients (SPT and drop-out duration 8.3 ± 3.8 years, only drop-out duration 5.3 ± 3.7 years) were recorded. PD data and the number of teeth present at the start of APT (T1) and at the start of SPT (T2) were taken from the patient files and evaluated at the time of the final examination (T3).
Results: Annual tooth loss during SPT was significantly higher (p < 0.001) in drop-out patients than in partially and fully compliant patients (0.31 ± 0.50 vs. 0.19 ± 0.55, respectively). In partially and fully compliant and drop-out patients, the mean PD (all available site data) decreased significantly between T1 (3.61 ± 0.82 vs. 3.70 ± 0.73 mm) and T2 (2.68 ± 0.40 vs. 2.76 ± 0.42 mm), while the values increased again slightly up to T3 (2.74 ± 0.41 vs. 2.99 ± 0.75 mm).
Conclusions: In partially and fully compliant patients, SPT had a positive impact on PD stability and medium-term tooth preservation. In contrary to expectations, drop-out patients, PD did not return to baseline values, although PD stability was not achieved.
Aim: To investigate the hypothesis supporting the link between periodontitis and dopaminergic neuron degeneration.
Materials and methods: Adult male Wistar rats were used to induce dopaminergic neuronal injury with 6-hydroxydopamine (6-OHDA) neurotoxin and experimental periodontitis via ligature placement. Motor function assessments were conducted before and after periodontitis induction in controls and 6-OHDA-injury-induced rats. Tissue samples from the striatum, jaw and blood were collected for molecular analyses, encompassing immunohistochemistry of tyrosine hydroxylase, microglia and astrocyte, as well as micro-computed tomography, to assess alveolar bone loss and for the analysis of striatal oxidative stress and plasma inflammatory markers.
Results: The results indicated motor impairment in 6-OHDA-injury-induced rats exacerbated by periodontitis, worsening dopaminergic striatal degeneration. Periodontitis alone or in combination with 6-OHDA-induced lesion was able to increase striatal microglia, while astrocytes were increased by the combination only. Periodontitis increased striatal reactive oxygen species levels and plasma tumour necrosis factor-alpha levels in rats with 6-OHDA-induced lesions and decreased the anti-inflammatory interleukin-10.
Conclusions: This study provides original insights into the association between periodontitis and a neurodegenerative condition. The increased inflammatory pathway associated with both 6-OHDA-induced dopaminergic neuron lesion and periodontal inflammatory processes corroborates that the periodontitis-induced systemic inflammation may aggravate neuroinflammation in Parkinson's-like disease, potentially hastening disease progression.
To assess the impact of the timing of soft-tissue augmentation (STA) on mean buccal bone changes following immediate implant placement (IPP) in the anterior maxilla.
Patients with a failing tooth and intact buccal bone wall in the anterior maxilla (15–25) were enrolled in this randomized controlled trial. Following single IIP and socket grafting, they were randomly allocated to the control group (immediate STA performed during the same surgical procedure) or the test group (delayed STA performed 3 months later). Implants were placed with a surgical guide and immediately restored with an implant-supported provisional crown. Changes in bone dimensions were assessed using superimposed CBCT images taken prior to surgery and at 1-year follow-up. Clinical outcomes were registered at 1-year follow-up.
Twenty patients were randomized to each group (control: 16 females, 4 males, mean age 57.6; test: 9 females, 11 males, mean age 54.2). Ten patients in the control group and 13 patients in the test group had a thick bone wall phenotype. Estimated marginal mean horizontal buccal bone loss at 1 mm below the implant shoulder was −0.553 and −0.898 mm for the control and test group, respectively. The estimated mean difference of 0.344 mm in favour of the control group was not significant (95% CI: −0.415 to 1.104; p = 0.363). Also at all other horizontal and vertical levels, no significant differences could be observed between the groups. The combination of socket grafting and STA enabled counteraction of any buccal soft-tissue loss (≥ 0 mm) at 1 mm below the implant shoulder in 82% of the patients in the control group and in 75% of the patients in the test group (p = 1.000). The clinical outcome was favourable in both groups, yet implants in the control group demonstrated slightly less marginal bone loss (median difference 0.20 mm; 95% CI: 0.00–0.44; p = 0.028).
In patients with an intact and mainly thick buccal bone wall in the anterior maxilla, the timing of STA following IIP had no significant impact on mean buccal bone loss.
ClinicalTrials.gov identifier: NCT05537545
To examine the independent and joint associations of oral microbiome diversity and diet quality with risks of all-cause and cause-specific mortality.
We included 7,055 eligible adults from the U.S. National Health and Nutrition Examination Survey (NHANES). Oral microbiome diversity was measured with α-diversity, including the Simpson Index, observed amplicon sequence variants (ASVs), Faith's phylogenetic diversity, and Shannon–Weiner index. Dietary quality was assessed using the Healthy Eating Index-2015 (HEI-2015). Cox proportional hazard models were used to assess the corresponding associations.
During a mean follow-up of 9.0 years, we documented 382 all-cause deaths. We observed independent associations of oral microbiome diversity indices and dietary quality with all-cause mortality (hazard ratio [HR] = 0.63; 95% confidence interval [CI]: 0.49–0.82 for observed ASVs; HR = 0.68, 95% CI: 0.52–0.89 for HEI-2015). Jointly, participants with the highest tertiles of both oral microbiome diversity (in Simpson index) and HEI-2015 had the lowest hazard of mortality (HR = 0.37, 95% CI: 0.23–0.60). In addition, higher oral microbiome diversity was associated with lower risks of deaths from cardiometabolic disease and cancer.
Higher oral microbiome α-diversity and diet quality were independently associated with lower risk of mortality.
Periodontal diseases are chronic inflammatory conditions that require early screening for effective long-term management. Oral neutrophil counts (ONCs) correlate with periodontal inflammation. This study investigates a point-of-care test using a neutrophil enzyme activity (NEA) colorimetric strip for measuring periodontal inflammation.
This prospective study had two phases. Phase 1 validated the relationship between ONCs and periodontal inflammation with 90 participants. Phase 2 examined the test's applicability in a real-world setting through a multicentre clinical trial with 375 participants at four sites. ONCs were quantified in oral rinses using laboratory-based methods, and the NEA strip was used for ONC stratification. Clinical measures included bleeding on probing (BoP), probing depth (PD) and clinical attachment loss (CAL).
ONCs were significantly elevated in patients with Grade B periodontitis and deep periodontal pockets (PD ≥ 5 mm, CAL ≥ 5 mm). The NEA strip accurately classified patients into high or low ONC categories, showing 80% sensitivity, 82.5% specificity and an AUC of 0.89. It also assessed the effectiveness of periodontal therapy in reducing ONC and inflammation. The test was user-friendly, with no reported discomfort among patients.
The NEA strip is a user-friendly and rapid screening tool for detecting high ONCs associated with periodontal inflammation and for evaluating the effectiveness of periodontal therapy.
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