Journal of Clinical Periodontology最新文献

Alshammari, A, Patel, J, Al-Hashemi, J, Cai, B, Panek, J, Huck, O, Amar, S. Kava-241 reduced periodontal destruction in a collagen antibody primed Porphyromonas gingivalis model of periodontitis. J Clin Periodontol. 2017 Nov; 44(11): 1123–1132. https://doi.org/10.1111/jcpe.12784. Epub 2017 Sep 21. PMID: 28746780; PMCID: PMC5650496.

Concerns were raised by a third party regarding the appearance of Figure 6, suggesting that the “P.Gingivalis + AB + Kava Preventive” subpanel is identical to “Kava treatment” and that the “P.Gingivalis + AB + Kava treatment” subpanel is highly similar to the “Kava preventive” panel. The authors admitted to the compilation error and were able to provide the original images. The authors confirm that all the experimental results and corresponding conclusions mentioned in the paper remain unaffected and sincerely apologize for this mistake. The corrected Figure 6 is shown as follows.

Huck, O, Mulhall, H, Rubin, G, et al. Akkermansia muciniphila reduces Porphyromonas gingivalis-induced inflammation and periodontal bone destruction. J Clin Periodontol. 2020; 47: 202–212. https://doi.org/10.1111/jcpe.13214

Concerns were raised by a third party regarding the appearance of Figure 2, suggesting that the A and D subpanels show identical images for the “H&E Control” and overlapping field of view for the “TRAP Pg”. The authors admitted to the image compilation error and were able to provide the original images. The authors confirm that all the experimental results and corresponding conclusions mentioned in the paper remain unaffected and sincerely apologize for this mistake. The corrected Figure 2 is shown as follows.

It has also been noted, that the image subpanel displayed as “Lean – PBS” in Figure 1 a was previously published by the authors elsewhere. The authors confirmed that these are indeed identical images depicting the same PBS control group, used in both studies, yet the first published image was not correctly referenced. The authors apologize for the oversight. Please find the corrected caption of Figure 1 below:

Figure 1. A. muciniphila reduced calvarial tissue destruction induced by P. gingivalis injection. (a) Macroscopic view of the tissue destruction at calvarial site 3 days following injections of PBS (control), P. gingivalis alone (Pg), A. muciniphila alone (Akk), combined P. gingivalis and A. muciniphila (Pg + Akk) in lean and obese mice. The top left “Lean – PBS” subpanel was reproduced under the terms of the Creative Commons CC BY License. [Huck et al., 2019] Copyright © 2019, The Authors (b) Quantitative evaluation of the size of the lesions in the lean mice over time. (c) Quantitative evaluation of the size of the lesion in the obese mice over time. Results were analysed by ANOVA with differences considered significant at * p ≤ .05 between groups (n = 5/group). Pg: P. gingivalis-injected group; Akk: A. muciniphila-injected group; Pg + Akk: P. gingivalis + A. muciniphila-injected concomitantly.

Aim: To apply high-frequency ultrasound (HFUS) echo intensity for characterizing peri-implant tissues at healthy and diseased sites and to investigate the possible ultrasonographic markers of health versus disease.

Materials and methods: Sixty patients presenting 60 implants diagnosed as healthy (N = 30) and peri-implantitis (N = 30) were assessed with HFUS. HFUS scans were imported into a software where first-order greyscale outcomes [i.e., mean echo intensity (EI)] and second-order greyscale outcomes were assessed. Other ultrasonographic outcomes of interest involved the vertical extension of the hypoechoic supracrestal area (HSA), soft-tissue area (STA) and buccal bone dehiscence (BBD), among others.

Results: HFUS EI mean values obtained from peri-implant soft tissue at healthy and diseased sites were 122.9 ± 19.7 and 107.9 ± 24.7 grey levels (GL); p = .02, respectively. All the diseased sites showed the appearance of an HSA that was not present in healthy implants (area under the curve = 1). The proportion of HSA/STA was 37.9% ± 14.8%. Regression analysis showed that EI of the peri-implant soft tissue was significantly different between healthy and peri-implantitis sites (odds ratio 0.97 [95% confidence interval: 0.94-0.99], p = .019).

Conclusions: HFUS EI characterization of peri-implant tissues shows a significant difference between healthy and diseased sites. HFUS EI and the presence/absence of an HSA may be valid diagnostic ultrasonographic markers to discriminate peri-implant health status.

Aim: To compare connective tissue graft (CTG) with collagen matrix (CMX) in terms of increase in buccal soft tissue profile (BSP) when applied at single implant sites.

Materials and methods: Patients with a single tooth gap in the anterior maxilla and horizontal mucosa defect were enrolled in a multi-centre randomized controlled trial. All were fully healed sites with a bucco-palatal bone dimension of at least 6 mm, and received an immediately restored single implant using a full digital workflow. Patients were randomly allocated to the control (CTG) or test group (CMX: Geistlich Fibro-Gide, Geistlich Pharma AG, Wolhusen, Switzerland) to increase buccal soft tissue thickness. Primary endpoints were increase in BSP at T1 (immediately postop), T2 (3 months), T3 (1 year) and T4 (3 years) based on superimposed digital surface models. Secondary endpoints included patient-reported, clinical and aesthetic outcomes.

Results: Thirty patients were included per group (control group: 15 males, 15 females, mean age 50.1 years; test group: 14 males, 16 females, mean age 48.2 years) and 50 could be re-examined at T4. The changes in BSP over time were significantly different between the groups (p < .001). At T4, the estimated mean increase in BSP amounted to 0.83 mm (95% confidence interval [CI]: 0.58-1.08) in the control group and 0.48 mm (95% CI: 0.22-0.73) in the test group. The estimated mean difference of 0.35 mm (95% CI: 0.06-0.65) in favour of the control group was significant (p = .021). No significant differences between the groups could be observed in terms of patients' aesthetic satisfaction (p = .563), probing depth (p = .286), plaque (p = .676), bleeding on probing (p = .732), midfacial recession (p = .667), Pink Esthetic Score (p = .366) and Mucosal Scarring Index (p = .438). However, CMX resulted in significantly more marginal bone loss (-0.43 mm; 95% CI: -0.77 to -0.09; p = .015) than CTG.

Conclusions: CTG was more effective in increasing buccal soft tissue profile and resulted in less marginal bone loss than CMX. Therefore, CTG remains the gold standard to increase soft tissue thickness at implant sites.

Clinical trial registration: This study was registered in ClinicalTrials.gov (NCT04210596).

Aim: Emerging evidence suggests association of tooth loss with impaired cognition. However, the differential effects of anterior versus posterior tooth loss, occlusal support loss and chewing ability are not considered comprehensively.

Materials and methods: We conducted cross-sectional (N = 4036) and longitudinal analyses (N = 2787) on data from Health 2000 and 2011 Surveys for associations of posterior occlusal support loss, anterior versus posterior tooth loss, and chewing ability with baseline cognition and 11-year cognitive decline. Additionally, 15-year incident dementia risk was investigated (N = 4073).

Results: After considering relevant confounders and potential reverse causality bias, posterior occlusal support loss significantly increased dementia risk across all categories indicative of posterior occlusal support loss (hazard ratios [HRs] between 1.99 and 2.89). Bilateral inadequate posterior occlusal support was associated with 11-year decline in overall cognition (odds ratio [OR] = 1.48:1.00-2.19), and unilateral inadequate posterior occlusal support with total immediate (OR = 1.62:1.14-2.30) and delayed recall decline (OR = 1.45:1.03-2.05). Moreover, posterior tooth loss was associated with dementia (HR = 2.23:1.27-3.91) and chewing ability with total immediate decline (OR = 1.80:1.04-3.13).

Conclusions: Posterior tooth and occlusal support loss significantly increases dementia risk. The impact of posterior occlusal support loss appears to be dose-dependent, and this effect is distinct from that of dentures. Dental healthcare services should be particularly attentive to the state of posterior dentition. Further studies exploring possible mechanisms are warranted.