Efficacy of imaging techniques for the diagnosis of apical periodontitis: A systematic review.

Background: Apical periodontitis (AP) is a chronic inflammatory response of microbial aetiology. Pathological changes associated with AP may not be visible on radiographic images and may linger without causing any symptoms. Clinicians rely mostly on clinical examination and imaging techniques to establish a diagnosis.

The Influence of Cone Beam Computed Tomography-Derived 3D-Printed Models on Endodontic Microsurgical Treatment Planning and Confidence of the Operator.

Introduction: Currently, there are no studies evaluating the impact of 3-dimensional (3D) printed models on endodontic surgical treatment planning. The aims of this study were: 1) to determine if 3D models could influence treatment planning; and 2) to assess the effect of 3D supported planning on operator confidence.

Materials: Endodontic practitioners (n = 25) were asked to analyze a preselected cone beam computed tomography (CBCT) scan of an endodontic surgical case and answer a questionnaire that elucidated their surgical approach.

Non-coding RNAs in endodontic disease.

The immunocompetence and regeneration potential of the dental pulp and its surrounding apical tissues have been investigated extensively in the field of endodontics. While research on the role of non-coding RNAs in these tissues is still in its infancy, it is envisioned that improved understanding of the regulatory function of ncRNAs in pulpal and periapical immune response will help prevent or treat endodontic disease. Of particular importance is the role of these RNAs in regenerating the dentin-pulp complex.

Identification and validation of novel biomarkers and therapeutics for pulpitis using connectivity mapping.

Aim: To create an irreversible pulpitis gene signature from microarray data of healthy and inflamed dental pulps, followed by a bioinformatics approach using connectivity mapping to identify therapeutic compounds that could potentially treat pulpitis.

Methodology: The Gene Expression Omnibus (GEO) database, an international public repository of genomics data sets, was searched for human microarray datasets assessing pulpitis. An irreversible pulpitis gene expression signature was generated by differential expression analysis.

Predicting the response of the dental pulp to SARS-CoV2 infection: a transcriptome-wide effect cross-analysis.

Pulpitis, inflammation of the dental pulp, is a disease that often necessitates emergency dental care. While pulpitis is considered to be a microbial disease primarily caused by bacteria, viruses have also been implicated in its pathogenesis. Here, we determined the expression of the SARS-CoV2 receptor, angiotensin converting enzyme 2 (ACE2) and its associated cellular serine protease TPMRSS2 in the dental pulp under normal and inflamed conditions.

Detecting Dentinal Microcracks Using Different Preparation Techniques: An In Situ Study with Cadaver Mandibles.

Introduction: This study assessed the frequency of dentinal microcracks using a cadaver mandible model in teeth instrumented with TRUShape (TS; Dentsply Sirona, York, PA), WaveOne Gold (WO, Dentsply Sirona), or K-files (KF) compared with an uninstrumented control group (CG).

Methods: Fifteen human mandibles with 95 single-rooted teeth were randomly distributed into the following groups: CG (no preparation, n = 11), TS (n = 28), WO (n = 28), and KF (step-back preparation with K-Flex-o-files [Dentsply Sirona], n = 28). Teeth were prepared to apical sizes of #25/.

Biological Markers for Pulpal Inflammation: A Systematic Review.

Background And Objective: Pulpitis is mainly caused by an opportunistic infection of the pulp space with commensal oral microorganisms. Depending on the state of inflammation, different treatment regimes are currently advocated. Predictable vital pulp therapy depends on accurate determination of the pulpal status that will allow repair to occur.

Mineral trioxide aggregate (MTA): its history, composition, and clinical applications.

Mineral trioxide aggregate (MTA) has been a revolutionary material in endodontics. Since its introduction in the 1990s several studies have demonstrated its use in various clinical applications. MTA has been extensively studied and is currently used for perforation repairs, apexifications, regenerative procedures, apexogenesis, pulpotomies, and pulp capping.

Periapical microsurgery: the effect of root dentinal defects on short- and long-term outcome.

Introduction: The purpose of this prospective clinical study was to evaluate the clinical outcome of endodontic microsurgery on roots exhibiting the presence or absence of dentinal defects at 1-year and 3-year follow-up period.

Methods: One hundred fifty-five teeth were treated with periapical microsurgery using a modern microsurgical protocol in a private practice setting. The root apices were resected and inspected for dentinal defects with a surgical operating microscope and a 0.

Diabetes aggravates periodontitis by limiting repair through enhanced inflammation.

Periodontitis is the most common lytic bone disease and one of the first clinical manifestations of diabetes. Diabetes increases the risk of periodontitis. The aim of the present study was to examine mechanisms by which diabetes aggravates periodontitis.

Mammalian target of rapamycin (mTOR) regulates TLR3 induced cytokines in human oral keratinocytes.

Recent studies implicate the mammalian target of rapamycin (mTOR) pathway in the control of inflammatory responses following Toll-like receptor (TLR) stimulation in myeloid cells but its role in non-myeloid cells such as human keratinocytes is unknown. Here we show that TLR3 signaling can induce robust cytokine secretion including interleukin 1 beta (IL-1β), tumor necrosis factor alpha (TNFα), IL-12p70 and interferon beta (IFN-β), and our data reveal for the first time that inhibiting mTOR with rapamycin, suppresses these TLR3 induced responses but actually enhances bioactive IL-12p70 production in human oral keratinocytes. Rapamycin inhibited the phosphorylation of the 70-kDa ribosomal protein S6 kinase (p70S6K) and the 4E binding protein 1 (4EBP-1), and suppressed the mitogen activated protein kinase (MAPK) pathway by decreasing phosphorylation of c-Jun N-terminal kinase (JNK).

Sphingosine kinase-1 is required for toll mediated beta-defensin 2 induction in human oral keratinocytes.

Background: Host defense against invading pathogens is triggered by various receptors including toll-like receptors (TLRs). Activation of TLRs is a pivotal step in the initiation of innate, inflammatory, and antimicrobial defense mechanisms. Human beta-defensin 2 (HBD-2) is a cationic antimicrobial peptide secreted upon gram-negative bacterial perturbation in many cells.

Epithelial cell pro-inflammatory cytokine response differs across dental plaque bacterial species.

Aim: The dental plaque is comprised of numerous bacterial species, which may or may not be pathogenic. Human gingival epithelial cells (HGECs) respond to perturbation by various bacteria of the dental plaque by production of different levels of inflammatory cytokines, which is a putative reflection of their virulence. The aim of the current study was to determine responses in terms of interleukin (IL)-1beta, IL-6, IL-8 and IL-10 secretion induced by Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, Fusobacterium nucleatum and Streptococcus gordonii in order to gauge their virulence potential.

In vitro modeling of host-parasite interactions: the 'subgingival' biofilm challenge of primary human epithelial cells.

Background: Microbial biofilms are known to cause an increasing number of chronic inflammatory and infectious conditions. A classical example is chronic periodontal disease, a condition initiated by the subgingival dental plaque biofilm on gingival epithelial tissues. We describe here a new model that permits the examination of interactions between the bacterial biofilm and host cells in general.

Modulation of TLR2 protein expression by miR-105 in human oral keratinocytes.

Mammalian biological processes such as inflammation, involve regulation of hundreds of genes controlling onset and termination. MicroRNAs (miRNAs) can translationally repress target mRNAs and regulate innate immune responses. Our model system comprised primary human keratinocytes, which exhibited robust differences in inflammatory cytokine production (interleukin-6 and tumor necrosis factor-alpha) following specific Toll-like receptor 2 and 4 (TLR-2/TLR-4) agonist challenge.

Porphyromonas gingivalis induce apoptosis in human gingival epithelial cells through a gingipain-dependent mechanism.

Background: The oral pathogen Porphyromonas gingivalis has been shown to modulate apoptosis in different cell types, but its effect on epithelial cells remains unclear.

Results: We demonstrate that primary human gingival epithelial cells (HGECs) challenged with live P. gingivalis for 24 hours exhibit apoptosis, and we characterize this by M30 epitope detection, caspase-3 activity, DNA fragmentation and Annexin-V staining.

Neutrophils rescue gingival epithelial cells from bacterial-induced apoptosis.

In the pathogenesis of chronic inflammatory periodontal disease, neutrophils are recognized as a major cellular component from the histopathology of the periodontal lesion around teeth and from clinical cases where absence or dysfunction of neutrophils results in major periodontal destruction. Neutrophils are recruited in vast numbers into the gingival crevice during periodontal inflammation, attracted by microbial plaque chemoattractants and chemokines released following microbial perturbation of gingival epithelial cells. Porphyromonas gingivalis, a major periodontopathogen, triggers a vast array of cellular responses in gingival epithelial cells but also induces apoptosis.

P. gingivalis interactions with epithelial cells.

Dental plaque, a microbial biofilm that accumulates on teeth and initiates periodontal disease, is composed of hundreds of different bacterial species within an organized structure. The biofilm bacteria and their byproducts irritate the gingival epithelium and induce an "inflammatory response". The perturbation of epithelial cells by bacteria is the first stage in the initiation of inflammatory and immune processes which eventually cause destruction of the tissues surrounding and supporting the teeth, and ultimately result in tooth loss.

Interleukin-6 receptor gene polymorphisms and periodontitis in a non-smoking Japanese population.

Aim: The indispensable role of interleukin-6 receptor (IL-6R) in regulating IL-6 responses has been clearly established. We have previously reported that IL6R polymorphisms strongly influenced the serum levels of soluble IL-6R. In this study, we investigated the association between these genetic variations and periodontitis.

Imbalance between soluble tumour necrosis factor receptors type 1 and 2 in chronic periodontitis.

Background: Soluble types of tumour necrosis factor (TNF) receptors type 1 and 2 modulate the TNF-alpha-mediated inflammatory responses in chronic periodontitis (CP).

Objectives: This study investigated the levels of TNF-alpha, soluble TNF receptor type 1 and 2 in gingival crevicular fluid (GCF) and serum of healthy subjects and CP patients.

Materials And Methods: Thirty-eight sera and 73 GCF samples were collected from 16 healthy subjects and 22 CP patients.