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Copyright of Serbian Dental Journal / Stomatološki Glasnik Srbije is the property of National Library of Serbia and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Abstract: Introduction: This article reports on the morphologic features and the frequency of ciliated epithelium in apical cysts and discusses its origin. Methods: The study material consisted of 167 human apical periodontitis lesions obtained consecutively from patients presenting for treatment during a period of 12 years in a dental practice operated by one of the authors. All of the lesions were obtained still attached to the root apices of teeth with untreated (93 lesions) or treated canals (74 lesions). The former were obtained by extraction and the latter by extraction or apical surgery. Specimens were processed for histopathologic and histobacteriologic analyses. Lesions were classified, and the type of epithelium, if present, was recorded. Results: Of the lesions analyzed, 49 (29%) were diagnosed as cysts. Of these, 26 (53%) were found in untreated teeth, and 23 (47%) related to root canal–treated teeth. Ciliated columnar epithelium was observed partially or completely lining the cyst wall in 4 cysts, and all of them occurred in untreated maxillary molars. Three of these lesions were categorized as pocket cysts, and the other was a true cyst. Conclusions: Ciliated columnar epithelium-lined cysts corresponded to approximately 2% of the apical periodontitis lesions and 8% of the cysts of endodontic origin in the population studied. This epithelium is highly likely to have a sinus origin in the majority of cases. However, the possibility of prosoplasia or upgraded differentiation into ciliated epithelium from the typical cystic lining squamous epithelium may also be considered. [Copyright &y& Elsevier]

Abstract: Irreversible pulpitis and apical periodontitis are inflammatory diseases caused by opportunistic bacteria with possible co-infection with latent herpesviruses. The objectives of this study are to identify herpesviruses, including human cytomegalovirus (HCMV), Epstein-Barr virus (EBV), herpes simplex virus (HSV-1), and Varicella zoster virus (VZV) in patients with irreversible pulpitis (n = 29) or apical periodontitis, either primary (n = 30) or previously treated (n = 23). Using primary and nested polymerase chain reaction (PCR) and reverse transcription-PCR, EBV DNA and RNA were present in endodontic pathoses in significantly higher percentages (43.9% and 25.6%, respectively) compared with healthy pulp controls (0% and 0%, respectively). HCMV DNA and RNA were found in measurable numbers in both endodontic patients (15.9% and 29.3%, respectively) and in healthy pulp controls (42.1% and 10.5%, respectively). HSV-1 DNA was found in low percentages in endodontic patients (13.4%), and only one patient showed the presence of VZV. In conclusion, EBV may be associated with irreversible pulpitis and apical periodontitis. [Copyright &y& Elsevier]

Abstract: There is continuing controversy regarding the potential for inflammatory apical cysts to heal after nonsurgical endodontic therapy. Molecular cell biology may provide answers to a series of related questions. How are the epithelial cell rests of Malassez stimulated to proliferate? How are the apical cysts formed? How does the lining epithelium of apical cysts regress after endodontic therapy? Epithelial cell rests are induced to divide and proliferate by inflammatory mediators, proinflammatory cytokines, and growth factors released from host cells during periradicular inflammation. Quiescent epithelial cell rests can behave like restricted-potential stem cells if stimulated to proliferate. Formation of apical cysts is most likely caused by the merging of proliferating epithelial strands from all directions to form a three-dimensional ball mass. After endodontic therapy, epithelial cells in epithelial strands of periapical granulomas and the lining epithelium of apical cysts may stop proliferating because of a reduction in inflammatory mediators, proinflammatory cytokines, and growth factors. Epithelial cells will also regress because of activation of apoptosis or programmed cell death through deprivation of survival factors or by receiving death signals during periapical wound healing. [Copyright &y& Elsevier]