Current concepts in the pathogenesis of periodontitis: from symbiosis to dysbiosis.

The primary etiological agent for the initiation and progression of periodontal disease is the dental plaque biofilm which is an organized aggregation of microorganisms residing within a complex intercellular matrix. The non-specific plaque hypothesis was the first attempt to explain the role of the dental biofilm in the pathogenesis of periodontal diseases. However, the introduction of sophisticated diagnostic and laboratory assays has led to the realisation that the development of periodontitis requires more than a mere increase in the biomass of dental plaque. Indeed, multispecies biofilms exhibit complex interactions between the bacteria and the host. In addition, not all resident microorganisms within the biofilm are pathogenic, since beneficial bacteria exist that serve to maintain a symbiotic relationship between the plaque microbiome and the host's immune-inflammatory response, preventing the emergence of pathogenic microorganisms and the development of dysbiosis. This review aims to highlight the development and structure of the dental plaque biofilm and to explore current literature on the transition from a healthy (symbiotic) to a diseased (dysbiotic) biofilm in periodontitis and the associated immune-inflammatory responses that drive periodontal tissue destruction and form mechanistic pathways that impact other systemic non-communicable diseases.

Evaluation of technology-based learning by dental students during the pandemic outbreak of coronavirus disease 2019.

INTRODUCTION: Although technology-based learning (TB learning) has been accepted as an efficient educational tool in the field of dentistry, the evaluation of TB learning in non-prepared situations such as pandemics has not been fully investigated. This study aimed to evaluate different aspects of TB learning amongst undergraduate dental students during the pandemic outbreak of COVID-19. MATERIALS AND METHODS: Dental students in selected Iraqi universities (University of Baghdad, University of Sulaimani and Dijlah University College) were invited to join the study. A questionnaire was created using a Google platform and answered by students. Satisfaction and attitude towards TB learning plus total evaluation scores for lecturers were examined. RESULTS: A total of 832 out of 1800 dental students participated in the study. The majority of participants have basic (40.7%) and intermediate (47.5%) computer skills, and more than half of them lack any experience in TB learning. The overall satisfaction and positive attitude towards TB learning were less than 50%. Students at final grade, with advanced computer skills and TB learning experience, showed higher satisfaction (OR: 3.031, 2.876, 3.644, respectively) and a more positive attitude (OR: 3.172, 3.035, 3.477, respectively) towards TB learning than those at earlier grades. Total evaluation scores for lecturers were higher amongst females (11.5 ± 5.8) than males (9.9 ± 7.2) as well as amongst participants at final grade (14.0 ± 6.2), with advanced computer skills (13.8 ± 6.1) and TB learning experience (16.2 ± 6.0). CONCLUSIONS: Dental students demonstrated low-moderate satisfaction and positive attitude towards TB learning and the quality of material presented to them. Integrating TB learning into the dental education curriculum is an essential step in enhancing the acceptance of TB learning in the future.

Identification of key determinants in Porphyromonas gingivalis host-cell invasion assays.

The periodontal pathogen Porphyromonas gingivalis can invade host cells, a virulence trait which may contribute to the persistence of infection at subgingival sites. Whilst the antibiotic protection assay has been commonly employed to investigate and quantify P. gingivalis invasion, data obtained have varied widely and a thorough investigation of the factors influencing this is lacking. We investigated the role of a number of bacterial and host-cell factors and report that the growth phase of P. gingivalis, source (laboratory strain vs. clinical strain), host-cell identity (cell line vs. primary), host-cell lysis method, and host-cell passage number had no significant effect on bacterial invasion. However, incubation time, host-cell seeding density, method of quantification (viable count vs. DNA), and whether host cells were plated or in suspension, were shown to influence invasion. Also, cells isolated by rapid adhesion to fibronectin exhibited higher levels of P. gingivalis invasion, possibly as a result of increased levels of active α5ß1 integrin. Interestingly, this may represent a population of cells with stem cell-like properties. This study provides important new information by identifying the most important factors that influence P. gingivalis invasion assays and may help to explain variations in the levels previously reported.

The Periodontal Pathogen Porphyromonas gingivalis Preferentially Interacts with Oral Epithelial Cells in S Phase of the Cell Cycle.

Porphyromonas gingivalis, a key periodontal pathogen, is capable of invading a variety of cells, including oral keratinocytes, by exploiting host cell receptors, including alpha-5 beta-1 (α5ß1) integrin. Previous studies have shown that P. gingivalis accelerates the cell cycle and prevents apoptosis of host cells, but it is not known whether the cell cycle phases influence bacterium-cell interactions. The cell cycle distribution of oral keratinocytes was characterized by flow cytometry and BrdU (5-bromo-2-deoxyuridine) staining following synchronization of cultures by serum starvation. The effect of cell cycle phases on P. gingivalis invasion was measured by using antibiotic protection assays and flow cytometry, and these results were correlated with gene and surface expression levels of α5 integrin and urokinase plasminogen activator receptor (uPAR). There was a positive correlation (R = 0.98) between the number of cells in S phase and P. gingivalis invasion, the organism was more highly associated with cells in S phase than with cells in G2 and G1 phases, and S-phase cells contained 10 times more bacteria than did cells that were not in S phase. Our findings also show that α5 integrin, but not uPAR, was positively correlated with cells in S phase, which is consistent with previous reports indicating that P. gingivalis invasion of cells is mediated by α5 integrin. This study shows for the first time that P. gingivalis preferentially associates with and invades cells in the S phase of the cell cycle. The mechanism of targeting stable dividing cells may have implications for the treatment of periodontal diseases and may partly explain the persistence of this organism at subgingival sites.