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BackgroundPeriodontitis is the most common chronic inflammatory disease caused by complex interaction between the microbial biofilm and host immune responses. In the present study, high-throughput RNA sequencing was utilized to systemically and precisely identify gene expression profiles and alternative splicing.MethodsThe pooled RNAs of 10 gingival tissues from both healthy and periodontitis patients were analyzed by deep sequencing followed by computational annotation and quantification of mRNA structures.ResultsThe differential expression analysis designated 400 up-regulated genes in periodontitis tissues especially in the pathways of defense/immunity protein, receptor, protease, and signaling molecules. The top 10 most up-regulated genes were CSF3, MAFA, CR2, GLDC, SAA1, LBP, MME, MMP3, MME-AS1, and SAA4. The 62 down-regulated genes in periodontitis were mainly cytoskeletal and structural proteins. The top 10 most down-regulated genes were SERPINA12, MT4, H19, KRT2, DSC1, PSORS1C2, KRT27, LCE3C, AQ5, and LCE6A. The differential alternative splicing analysis revealed unique transcription variants in periodontitis tissues. The EDB exon was predominantly included in FN1, while exon 2 was mostly skipped in BCL2A1.ConclusionsThese findings using RNA sequencing provide novel insights into the pathogenesis mechanism of periodontitis in terms of gene expression and alternative splicing.Electronic supplementary materialThe online version of this article (doi:10.1186/s40246-016-0084-0) contains supplementary material, which is available to authorized users.

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PurposeThe aim of this study was to evaluate the influence of the crown-to-implant (C/I) ratio on the change in marginal bone level around the implant and to determine the site-related factors influencing the relationship between the C/I ratio and periimplant marginal bone loss.MethodsA total of 259 implants from 175 patients were evaluated at a mean follow-up of five years. Implants were divided into two groups according to their C/I ratios: ≤1, and >1. Site-related factors having an influence on the relationship between C/I ratio and periimplant marginal bone loss were analyzed according to the implant location, implant diameter, implant manufacturer, prosthesis type, and guided bone regeneration (GBR) procedure.ResultsIt was found that 1) implants with a C/I ratio below 1 exhibited greater periimplant marginal bone loss than implants with a C/I ratio more than 1, 2) site-related factors had an effect on periimplant marginal bone loss, except for the implant system used, 3) the C/I ratio was the factor having more dominant influence on periimplant marginal bone loss, compared with implant diameter, prosthesis type, implant location, and GBR procedure, 4) implants with a C/I ratio below 1 showed greater periimplant marginal bone loss than implants with a C/I ratio greater than 1 in the maxilla, but not in the mandible, 5) and periimplant marginal bone loss was more affected by the implant system than the C/I ratio.ConclusionsWithin the limitations of this study, implants with a higher C/I ratio exhibited less marginal bone loss than implants with a lower C/I ratio in the posterior regions. The C/I ratio was a more dominant factor affecting periimplant marginal bone loss in the maxilla than the mandible. Meanwhile, the implant system was a more dominant factor influencing periimplant marginal bone loss than the C/I ratio.

Furan (C4H4O) is a volatile compound formed mostly during the thermal processing of foods. The toxicity of furan has been well documented previously, and it was classified as “possible human carcinogen (Group 2B)” by the International Agency for Research on Cancer. Various pathways have been reported for the formation of furan, that is, thermal degradation and/or thermal rearrangement of carbohydrates in the presence of amino acids, thermal degradation of certain amino acids, including aspartic acid, threonine, α-alanine, serine, and cysteine, oxidation of ascorbic acid at higher temperatures, and oxidation of polyunsaturated fatty acids and carotenoids. Owing to the complexity of the formation mechanism, a vast number of studies have been published on monitoring furan in commercial food products and on the potential strategies for reducing furan. Thus, we present a comprehensive review on the current status of commercial food monitoring databases and the possible furan reduction methods. Additionally, we review analytical methods for furan detection and the toxicity of furan.