Search

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. Objectives: The aim of this review was to answer the following question using the PICO format: In the adult human permanent dentition (P), what is the efficacy of diagnostic imaging of the periapical tissues (I) using histopathology as a reference standard (C) in the diagnosis of apical periodontitis, in terms of diagnostic accuracy (O). Methods: MEDLINE, EMBASE, Scopus and Cochrane Library were searched for English articles published through October 2021. At least two independent reviewers evaluated the study design, imaging modality used, histopathological assessment, outcome measures, results and conclusions for each article. The risk of bias was assessed using the Quality Assessment Tool for Diagnostic Accuracy Studies‐2. Results: The initial search strategy identified 544 articles. Seven articles were included for analysis in the final review, all of which involved tissue samples obtained from cadavers. No clinical studies were identified that met the eligibility criteria. A consistently low sensitivity score and negative predictive value were reported for periapical radiography, especially in comparison to CBCT, which scored highly. Both modalities achieved high scores for specificity and positive predictive value. Diagnostic accuracy of CBCT was lower for root‐filled teeth in comparison to non‐root‐filled teeth. Discussion: Assessment of the periapical tissues using periapical radiographs was shown to have a low to moderate agreement with the histopathological assessment. CBCT was reported to be more accurate than PR and demonstrated a good agreement with histopathology, especially for non‐root‐filled teeth. Conclusions: This review identified a need for greater standardization in methodology and reporting, and as the findings are based on cadaver studies, their clinical relevance must be interpreted with caution. Registration: PROSPERO (CRD42021272147). [ABSTRACT FROM AUTHOR]

Abstract 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. We use primary human gingival epithelial cells (HGEC) and an in vitro grown biofilm, comprising nine frequently studied and representative subgingival plaque bacteria. Results We describe the growth of a mature 'subgingival' in vitro biofilm, its composition during development, its ability to adapt to aerobic conditions and how we expose in vitro a HGEC monolayer to this biofilm. Challenging the host derived HGEC with the biofilm invoked apoptosis in the epithelial cells, triggered release of pro-inflammatory cytokines and in parallel induced rapid degradation of the cytokines by biofilm-generated enzymes. Conclusion We developed an experimental in vitro model to study processes taking place in the gingival crevice during the initiation of inflammation. The new model takes into account that the microbial challenge derives from a biofilm community and not from planktonically cultured bacterial strains. It will facilitate easily the introduction of additional host cells such as neutrophils for future biofilm:host cell challenge studies. Our methodology may generate particular interest, as it should be widely applicable to other biofilm-related chronic inflammatory diseases.

Abstract 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. Live bacteria strongly upregulated intrinsic and extrinsic apoptotic pathways. Pro-apoptotic molecules such as caspase-3, -8, -9, Bid and Bax were upregulated after 24 hours. The anti-apoptotic Bcl-2 was also upregulated, but this was not sufficient to ensure cell survival. The main P. gingivalis proteases arginine and lysine gingipains are necessary and sufficient to induce host cell apoptosis. Thus, live P. gingivalis can invoke gingival epithelial cell apoptosis in a time and dose dependent manner with significant apoptosis occurring between 12 and 24 hours of challenge via a gingipain-dependent mechanism. Conclusion The present study provides evidence that live, but not heat-killed, P. gingivalis can induce apoptosis after 24 hours of challenge in primary human gingival epithelial cells. Either arginine or lysine gingipains are necessary and sufficient factors in P. gingivalis elicited apoptosis.

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. This article will review the history, composition, research findings, and clinical applications of this versatile endodontic material. [ABSTRACT FROM AUTHOR]

El artículo trata el rol de los polimorfismos genéticos en la periodontitis. Afirma que la genética puede determinar la gravedad y grado de la periodontitis y que se está aplicando tecnología genética en el diagnóstico y tratamiento de esta enfermedad. Sugiere que la periodontitis puede explicarse en base a varias polimorfismos de alto riesgo que tienen perfiles de alta susceptibilidad.