Journal of periodontal research最新文献

Aim: To assess ultrasonographic tissue elasticity at teeth and implant sites and its variation after peri-implant soft tissue augmentation with a connective tissue graft (CTG).

Methods: Twenty-eight patients, each contributing with one clinically healthy dental implant exhibiting a soft tissue dehiscence (PSTD), were included. Implant sites were augmented with CTG and monitored over 12 months. Ultrasonographic strain elastography, expressed as strain ratios (SR₁, SR₂, and SR₃, respectively) was assessed at baseline, 6-, and 12-month, and compared with the corresponding contralateral homologous natural tooth. SR₁ assessed the strain/elasticity of the midfacial coronal portion of the soft tissue in comparison to the natural tooth crown/implant-supported crown, SR₂ evaluated the strain of the midfacial coronal soft tissue in relation to the one of the alveolar mucosa, while SR₃ depicted the strain of the midfacial soft tissue in relation to the interproximal soft tissue on the transverse ultrasound scan.

Results: SR₁ in natural dentition and at implant sites was 0.20 ± 0.08 and 0.30 ± 0.14, respectively (p = .002), indicating that the coronal portion of the soft tissue around teeth is generally more elastic than its counterpart around dental implants. Soft tissue augmentation with CTG promoted an increased stiffness of the midfacial coronal portion of the soft tissue over 12 months (p < .001 for SR₁, SR₂, and SR₃). Strain ratios at the 12-month time points were significantly higher than the values observed at 6 months (p < .001). Regression analysis demonstrated that strain elastography ratios in natural dentition were significantly associated with keratinized gingiva width, and gingival thickness. At implant sites, SR₁ was significantly associated with keratinized mucosa width and mucosal thickness (p < .001 for both correlations), SR₂ was significantly associated with keratinized mucosa width (p = .013), and SR3 was significantly associated with the surgical technique performed in combination with CTG (p = .022).

Conclusion: Ultrasound strain elastography captures and quantifies tissue elasticity and its changes after soft tissue augmentation. A different baseline tissue elasticity was observed between teeth and dental implants in the most coronal aspect of the soft tissue. The main factors affecting tissue elasticity-related outcomes were the keratinized tissue width, and mucosal thickness.

The bidirectional associations between periodontitis and inflammatory bowel disease (IBD) with temporal directionality remain inconclusive. This study aims to evaluate the bidirectional associations between periodontitis and IBD through a systematic review and meta-analysis. Five databases (PubMed, Embase, Web of Science, Scopus and Cochrane Library) were systematically searched from inception to 27 February 2024. Two independent reviewers performed a review of the retrieved studies. Longitudinal studies, including cohort and nested case-control studies, were considered eligible for the study design. The pooled risk ratio (RR) and hazard ratio (HR) derived from the meta-analysis were used to assess whether periodontitis (or IBD) was a risk factor for IBD (or periodontitis). Trial sequential analysis (TSA) was performed to evaluate the reliability of the results. Four studies (n = 10 270 912) on the risk of IBD in patients with periodontitis and two (n = 33 420) on the risk of periodontitis in patients with IBD were included. The result suggested that periodontitis did not increase the risk of IBD (pooled RR = 1.04, 95% confidence interval [CI]: 0.99-1.09; p = .164; I-squared statistic [I²] = 27%). For subtypes of IBD, periodontitis was associated with the occurrence of ulcerative colitis (UC) (pooled RR = 1.12, 95% CI: 1.04-1.21; p = .003; I² = 38%), but not with Crohn's disease (CD) (pooled RR = 0.98, 95% CI: 0.92-1.04; p = .475; I² = 0%). Specifically, the risk of UC was higher among men (pooled HR = 1.11, 95% CI: 1.01-1.22; p = .025; I² = 0%) and smokers (pooled HR = 1.23, 95% CI: 1.07-1.42; p = .004; I² = 0%) with periodontitis than their counterparts without periodontitis. Patients with IBD may have a higher risk of developing periodontitis (pooled HR = 1.37, 95% CI: 1.26-1.49; p < .001; I² = 18%); however, whether IBD subtypes increased the occurrence of periodontitis remained uncertain. The TSA results confirmed the reliability of the primary findings. Based on limited longitudinal evidence, patients with periodontitis do not exhibit an increased risk of developing IBD overall, but they are at increased risk of UC (not CD). On the contrary, patients with IBD have a higher risk of developing periodontitis over time. More high-quality longitudinal studies are needed to determine the effect of specific subtypes of IBD on periodontitis.

Aims: To test whether titanium surface roughness disparity might be used to specifically guide the behavior of gingiva fibroblasts and keratinocytes, thereby improving the quality of soft tissue (ST) integration around abutments.

Methods: Titanium discs resembling the roughness of enamel (M) or cementum (MA) were created with normal or increased hydrophilicity and used as substrates for human fibroblasts and keratinocytes. Adhesion and proliferation assays were performed to assess cell-type specific responses upon encountering the different surfaces. Additionally, immunofluorescence and qPCR analyses were performed to study more in depth the behavior of fibroblasts and keratinocytes on MA and M surfaces, respectively.

Results: While enamel-like M surfaces supported adhesion, growth and a normal differentiation potential of keratinocytes, cementum-emulating MA surfaces specifically impaired the growth of keratinocytes. Vice versa, MA surfaces sustained regular adhesion and proliferation of fibroblasts. Yet, a more intimate adhesion between fibroblasts and titanium was achieved by an increased hydrophilicity of MA surfaces, which was associated with an increased expression of elastin.

Conclusion: The optimal titanium implant abutment might be achieved by a bimodal roughness design, mimicking the roughness of enamel (M) and cementum with increased hydrophilicity (hMA), respectively. These surfaces can selectively elicit cell responses favoring proper ST barrier by impairing epithelial downgrowth and promoting firm adhesion of fibroblasts.

Aims: This study sought to explore the impact of Fusobacterium nucleatum on hepatic steatosis in apolipoprotein E (ApoE) knockout (KO) mice induced by a high-fat diet (HFD) and elucidate the underlying mechanism.

Methods: ApoE KO mice, on a HFD, received F. nucleatum oral inoculation every other day. After 24 weeks, body weight, liver weight, and liver index were assessed. Serum biochemistry and pro-inflammatory factors in serum and liver were analyzed. The histopathology of right maxilla and live were performed. Oil red O, immunohistochemistry, and immunofluorescence staining for the liver were conducted. Myeloperoxidase (MPO) activity, apoptosis, lipid reactive oxygen species (ROS), ROS, lipid peroxides, and hepatic lipids were also evaluated. Liver inflammation, fibrosis, de novo lipogenesis (DNL)-related molecule, and Nrf2/Keap1-related signaling molecule gene/protein expression were determined by real-time PCR (RT-PCR) and/or Western blot (WB) analysis.

Results: HFD-fed ApoE KO mice infected by F. nucleatum demonstrated significant changes, including increased body and liver weight, elevated proinflammatory factors and lipids in serum and liver, as well as neutrophil infiltration, fibrosis, apoptosis, oxidative stress, and lipid peroxidation in the liver. Additionally, F. nucleatum stimulates hepatic lipid accumulation and activates de novo lipogenesis (DNL), while simultaneously suppressing the Nrf2/Keap1 antioxidant pathway.

Conclusion: In conclusion, our study reveals that oral inoculation of F. nucleatum might promote hepatic steatosis by inhibiting Nrf2/Keap1 pathway.

This systematic review aims to investigate the microbial basis underlying the association between oral microbiota and colorectal cancer. A comprehensive search was conducted across four databases, encompassing potentially relevant studies published up to April 2024 related to the PECO question: "Is there a differentiation in oral microbial composition between adult patients diagnosed with colorectal cancer compared to healthy patients?". The Newcastle-Ottawa Scale was used to evaluate the quality of the studies included. The level of evidence was assessed through the GRADE (Grading of Recommendations, Assessment, Development and Evaluation) tool. Sixteen studies fulfilled the eligibility criteria. Based on low to moderate evidence profile, high levels of certain subspecies within Firmicutes (such as Streptococcus anginosus, Peptostreptococcus stomatis, S. koreensis, and S. gallolyticus), Prevotella intermedia, Fusobacterium nucleatum, and Neisseria oralis were found to be associated with colorectal cancer. Conversely, certain bacteria (e.g., Lachnospiraceae, F. periodonticum, and P. melaninogenica) could exert a symbiotic protective effect against colorectal cancer. Based on existing evidence, it appears that variations in oral microbiota composition exist among individuals with and without colorectal cancer. However, further research is necessary to determine the mechanisms of oral dysbiosis in colorectal carcinogenesis.