Journal of periodontal research最新文献

This RCT offers a nuanced understanding of nonsurgical peri-implantitis management (air polishing with erythritol versus ultrasonic instrumentation, in combination with systemic metronidazole), integrating both clinical and patient-centered outcomes. The results showed that the ultrasonic instrumentation reduced probing depth and bleeding on probing, throughout the 12-month period.

While periodontitis is globally recognized as a significant public health problem, its common definition as a plaque-based inflammatory condition is incomplete. Disease progression, personal experience, and treatment are shaped by social, economic, and structural forces largely invisible in clinical practice and policy. A lens from medical anthropology helps us see periodontitis as more than a clinical diagnosis; it is a lived experience, deeply entangled with a person's social world. The physical reality of inflammation translates into profound emotional distress-from the shame and stigma of bleeding gums and gingival recession to the tangible fear of tooth loss. This personal suffering is often intensified by a societal focus on individual blame, which masks systemic barriers like poor insurance coverage and the simple lack of local care. Ultimately, the cultural language and assumptions surrounding oral health-what anthropologists term explanatory models and semantic networks-powerfully influence everything from a patient's decisions to the public's perception of the disease itself. We argue for a more culturally attuned approach to periodontal health-one that prioritizes prevention, centers the patient's lived experience, and confronts the systemic roots of oral health inequities. By integrating the insights of anthropology with the science of periodontics, we believe we can build a more complete model of care that leads to equitable health outcomes, creating policies and practices that acknowledge both microbial causes and patients' lived realities.

A pre-clinical rabbit study shows peri-implant tissue contains mono- and multinucleate tartrate-resistant acid phosphatase (TRAP) + cells and a plethora of punctate extracellular TRAP staining. The latter provides a putative extracellular vesicular trafficking mechanism by which these cells drive early osseointegration.

Aim: To investigate whether trained immunity occurs in gingival fibroblasts (GFs) and its relationship to the persistence of inflammation in periodontitis.

Methods: Periodontally healthy and inflammatory gingival fibroblasts (HGFs and IGFs) were cultured through continuous adherence subculture of tissue blocks. Trained immunity in HGFs was evaluated via a classic in vitro model, with relevant markers assessed via enzyme-linked immunosorbent assay, lactate content assay, glycolytic rate assay, and chromatin immunoprecipitation. A histone methyltransferase blocker and a PI3K inhibitor were added to investigate the mechanisms underlying trained immunity. The relationship between trained immunity and periodontitis was further examined via immunofluorescence staining and chromatin immunoprecipitation on IGFs.

Results: Compared with untrained cells, GFs trained with Porphyromonas gingivalis-lipopolysaccharide (P. gingivalis-LPS) exhibited a significant increase in IL-6 and TNF-α secretion, enhanced glycolytic metabolism, and enriched mono-methylation of lysine 4 on histone H3 (H3K4me1) at the enhancer regions of TNF-α and IL-6. The addition of a histone methyltransferase blocker and a PI3K inhibitor greatly reduced trained immunity. Additionally, the response of IGFs to P. gingivalis-LPS stimulation and their epigenetic modifications were similar to those observed in trained HGFs.

Conclusion: This study novelly discovered that both P. gingivalis-LPS-stimulated HGFs and IGFs in periodontitis acquired trained immunity. Following P. gingivalis-LPS stimulation, HGFs underwent metabolic and epigenetic changes via the PI3K/AKT pathway, with these epigenetic changes also observed in IGFs. This finding suggests that trained immunity in GFs may be a key mechanism underlying the recurrence and persistence of periodontitis.

Aim: To investigate the role of lipopolysaccharide (LPS) from Porphyromonas gingivalis and miR-155-5p-enriched exosomes in the formation of foam cells and the occurrence of carotid atherosclerosis (CAS).

Methods: The CAS tissue samples and plasma from the healthy control group or patients undergoing periodontitis without CAS and with CAS were collected at the Xuanwu Hospital, Capital Medical University. The expression level of miR-155-5p was evaluated by immunofluorescent analysis and qRT-PCR. Oil red O staining and lipid accumulation assays were performed to explore the effects of LPS and miR-155-5p on mouse macrophage Raw264.7 and human monocytes THP-1. The expression levels of lipid-regulated genes were detected by qRT-PCR. Dual-luciferase reporter gene assay and DET1 overexpressed or inhibited Raw264.7 cells were used to verify the target gene of exosomal miR-155-5p. ApoE^-/- mice were used to confirm the auxo-action of atherosclerosis from exosomal miR-155-5p in vivo, and LAL assay was used to detect the LPS content.

Results: miR-155-5p was higher in patients with periodontitis and CAS plasma exosomes than those in patients without CAS. The expression of miR-155-5p was significantly increased in CAS tissues compared with Normal tissues, and the expression level of miR-155-5p was associated with lipid-regulated genes in CAS tissues. MiR-155-5p-enriched exosomes accelerated lipid accumulation in macrophage-like cells and promoted the activity of lipid-accumulation genes by targeting DET1. In ApoE^-/- mice, circulating miR-155-5p-enriched exosomes captured LPS, and the LPS-laden exosomes conferred plasma access for LPS, triggering the formation of foam cells and the occurrence of CAS.

Conclusion: miR-155-5p enriched exosomes capture and escort LPS to the atherosclerotic sites, licensing the formation of foam cells and thus promoting CAS.

Aim: This systematic review and network meta-analysis aimed to answer the PICO question: In patients undergoing immediate implant placement (IIP) [P], does Computer-Assisted Implant Surgery (CAIS) [I] lead to higher accuracy [O] compared to free-hand (FH) [C] implant placement?

Methods: A systematic search of MEDLINE, Scopus, and Cochrane databases was conducted for randomized clinical trials (RCTs) published between January 2014 and September 2024, comparing accuracy of CAIS and FH for IIP. Two reviewers screened the studies and extracted data for a network meta-analysis.

Results: Of 2064 records screened, 7 RCTs (338 implants and 291 patients) met the inclusion criteria. These RCTs evaluated FH and dynamic, full static, and partial static CAIS for single or partial implant placement. No RCTs analyzing robotic-assisted implant surgery (RAIS) were found. In 71.4% of the studies, IIP was performed in the anterior maxilla using a flapless approach. Accuracy was assessed by angular, cervical, and apical deviations between planned and real implant positions. All CAIS methods demonstrated significantly higher accuracy than FH (p < 0.05), but no significant differences were observed between CAIS approaches.

Conclusions: CAIS significantly improves IIP accuracy, enhancing 3D implant positioning and prosthetic outcomes. All CAIS techniques revealed comparable accuracy, allowing clinicians to select the most suitable approach for each patient.

Trial registration: PROSPERO identification number: CRD42024554241.

Aims: This study aims to investigate the role of Plexin-B2 in tension-induced osteogenesis of periodontal ligament stem cells (PDLSCs) and its biomechanical mechanism.

Methods: In vitro, cyclic tension simulated orthodontic forces to assess Plexin-B2 expression in PDLSCs. We then knocked out Plexin-B2 using lentivirus to explore its role in tension-induced osteogenesis. In vivo, we used nickel-titanium springs to establish orthodontic tooth movement (OTM) models in mice. Local periodontal Plexin-B2 expression was knocked down using adeno-associated viruses (AAVs) to study its influence on new bone formation under mechanical tension in OTM models. Molecular mechanisms were elucidated by manipulating Plexin-B2 and RhoA expression, assessing related proteins, and observing F-actin and Yes-associated protein (YAP) through immunofluorescence.

Results: Plexin-B2 expression in PDLSCs increased under cyclic tension. Decrease of Plexin-B2 reduced the expression of osteogenic protein in PDLSCs and negatively affected new bone formation during OTM. RhoA expression and phosphorylation of ROCK2/LIMK2/Cofilin decreased in Plexin-B2 knockout PDLSCs but were reversed by RhoA overexpression. The level of F-actin decreased in Plexin-B2 knockout PDLSCs but increased after RhoA rescue. Nuclear YAP was reduced in Plexin-B2 knockout PDLSCs but increased after RhoA overexpression.

Conclusions: Plexin-B2 is involved in tension-induced osteogenesis. Mechanistically, the RhoA signaling pathway, the F-actin arrangement, and the nuclear translocation of YAP are involved in the mechanotransduction of Plexin-B2.

This cross-sectional histological/immunohistochemical study is the first to investigate the expression of the TAM pathway receptor tyrosine kinases (AXL, MERTK, and TYRO3) in healthy human masticatory mucosa, demonstrating a ubiquitous and tissue compartment-specific expression profile for each receptor.