Nlrp3 inflammasome drives regulatory T cell depletion to accelerate periapical bone erosion.

Aim: Apical periodontitis is an inflammatory disorder triggered by an immune response to bacterial infection, leading to the periapical tissue damage and alveolar resorption. However, the underlying mechanisms driving this process remain elusive, due to the complex and interconnected immune microenvironment within the local lesion site. In this study, the influence of Nlrp3 inflammasome-mediated immune response on the apical periodontitis was investigated.

Tertiary Lymphoid Structures Are Related to Inflammatory Progression and Bone Loss in Human Apical Periodontitis.

Introduction: Bone loss is strongly associated with the immunologic milieu in apical periodontitis (AP). Tertiary lymphoid structures (TLSs) are organized lymphoid cell aggregates that form in nonlymphoid tissues under persistent inflammatory circumstances. To date, there has been no relevant report of TLSs in periapical lesions.

Occlusal trauma inhibits osteoblast differentiation and bone formation through IKK-NF-κB signaling.

Background: Occlusal trauma is an important factor promoting bone loss caused by periodontal diseases. Although there are reports of traumatic force promoting bone resorption in periodontal diseases, no studies examining the inhibition of bone formation by traumatic force and the underlying mechanism have been reported. The aim of this study was to investigate the mechanism whereby traumatic force inhibits bone formation.

The effect of NLRP inflammasome on the regulation of AGEs-induced inflammatory response in human periodontal ligament cells.

Background And Objective: Diabetes influences the frequency and development of periodontitis. Inflammation of human periodontal ligament cells (HPDLCs) participates in this pathologic process. Hence, this study aims to explore whether advanced glycation end products (AGEs), by-products of diabetes, could exaggerate inflammation induced by muramyl dipeptide (MDP) in HPDLCs, and whether nucleotide-binding oligomerization domain-like receptors (NLRs) signaling pathway was involved.

EDTA Enhances Stromal Cell-derived Factor 1α-induced Migration of Dental Pulp Cells by Up-regulating Chemokine Receptor 4 Expression.

Introduction: In regenerative endodontics, irrigation is an important step to ensure the success of treatment. EDTA as a common irrigant has been recommended in the American Associations of Endodontists guidelines. It has been suggested that EDTA-treated dentin slices could increase the attachment, differentiation, and migration of dental pulp stem cells.

Jumonji domain-containing protein 3 regulates the early inflammatory response epigenetically in human periodontal ligament cells.

Objective: To investigate the role of the histone 3 lysine 27 trimethylation (H3K27me3) demethylase Jumonji domain-containing protein 3 (Jmjd3) in the epigenetic regulation of the inflammatory response in human periodontal ligament cells (HPDLs).

Design: HPDLs were stimulated with lipopolysaccharide from E. coli.

Dickkopf-1 may regulate bone coupling by attenuating wnt/β-catenin signaling in chronic apical periodontitis.

Objective: Alveolar bone loss is a common outcome of chronic apical periodontitis. In this study, we investigated the involvement of the Dickkopf-1-Wnt/β-catenin signaling pathway in the attenuation of osteogenic differentiation induced by Escherichia coli lipopolysaccharide, and we evaluated the use of Dickkopf-1 inhibitor and Dickkopf-1 recombinant protein to reverse bone loss in different phases of osteogenic differentiation.

Methods: MC3T3-E1 cells grown in osteogenic medium were treated with Escherichia coli lipopolysaccharide for 24h during osteogenic induction on days 0, 1, 7, 14 and 21.

MicroRNA-335-5p Plays Dual Roles in Periapical Lesions by Complex Regulation Pathways.

Introduction: MicroRNA-335-5p has been reported to regulate osteogenic and chondrogenic differentiations of mesenchymal stem cells. The aim of this study was to explore the function and regulation mechanism of miR-335-5p in apical periodontitis (AP).

Methods: Total RNAs were extracted from human periodontal ligament fibroblasts (HPDLFs), 10 AP tissues, and 6 healthy periodontal ligament tissues using lysis buffer.

Self-repaired Process of a Traumatized Maxillary Central Incisor with Pulp Infarct after Horizontal Root Fracture Monitored by Laser Doppler Flowmetry Combined with Tissue Oxygen Monitor.

Achieving a precise diagnosis of the pulp status of traumatized teeth is difficult. The time to interfere through endodontic treatment for these teeth is greatly dependent on the doctor's experience. A 24-year-old male patient suffered a traumatic injury to tooth #9 that resulted in an apical root horizontal fracture 3 days before he came to the hospital.

Expression Profiles of Inflammation-associated microRNAs in Periapical Lesions and Human Periodontal Ligament Fibroblasts Inflammation.

Introduction: microRNAs (miRNAs) have been identified to be closely related to inflammatory diseases. The aim of our study was to identify expression profiles of miRNAs associated with inflammation in apical periodontitis (AP) lesions and human periodontal ligament fibroblasts (HPDLFs) inflammation.

Methods: Total RNAs were extracted from 10 AP lesions, 6 control tissues, and HPDLFs using lysis buffer.

Compressive mechanical stress may activate IKK-NF-κB through proinflammatory cytokines in MC3T3-E1 cells.

Objective: To determine whether IKK-NF-κB is activated either directly by compressive mechanical stress or by proinflammatory cytokines produced by MC3T3-E1 cells under compressive stress loading.

Results: MC3T3-E1 cells subjected to cyclic uniaxial compressive stress showed increased expression of proinflammatory cytokines and activation of the IKK-NF-κB signaling pathway with nuclear translocation of p65. Following treatment with antibodies to neutralize the action of the proinflammatory cytokines, IL-1β and IL-6, the activation of IKK-NF-κB signaling was notably inhibited in MC3T3-E1 cells subjected to force loading.