Abstract
Dental follicle (DF) is made up of mesenchymal cells and fibers surrounding the enamel organ of a developing tooth. It has been shown that cystic and neoplastic lesions can develop from the pericoronal follicles of impacted third molars (ITMs). But themolecular transformation of DF tissues has not yetbeen uncovered and remains elusive. Accordingly, in the present study, we aimed to investigatethe differential expression of lncRNA genes in DF tissues associated with asymptomatic impacted mandibular third molars (IMTMs) that do not show pathological pericoronal radiolucency in radiographic examination. A total of 30 patients with unilateral mesioangular IMTMs were enrolled for the study. The expressions of lncRNA genes were determined in the DF and healthy gingival tissues obtained from study patients. For the determination of lncRNA expression levels, RNA was isolated from theobtained tissues, converted to cDNA samples, and analyzed by quantitative real-time PCR method. As a result, we found that thegene expression of MEG3 was increased about 10-fold in DF tissues compared to healthy gingival tissues (p < 0.0001). In addition, NORAD expression was found to be upregulated 4.2-fold (p = 0.0002) in DF tissues. Also, expression level of MALAT1 was found to be decreased 1.24-fold (p = 0.584) and TP73-AS1 increased 2.6-fold (p = 0.093) in DF tissues compared to healthy gingival tissues. Consequently, present findings suggest that differentially expressed lncRNAs in DFs might be associated with the various levels of cellular events including osteogenic differentiation, DNA damage, and the transformation into odontogenic pathology. Expression levels of MEG3 and NORAD lncRNA molecules may guide clinicians in the evaluation of asymptomatic ITM dental follicles that cannot be determined radiologically and during extraction of these teeth for prophylactic purposes.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.