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Long non‐coding RNA and mRNA expression profiles in peri‐implantitis vs periodontitis
Author(s) -
Liu Yudong,
Liu Qifan,
Li Zhipeng,
Acharya Aneesha,
Chen Danying,
Chen Zetao,
Mattheos Nikos,
Chen Zhuofan,
Huang Baoxin
Publication year - 2020
Publication title -
journal of periodontal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.31
H-Index - 83
eISSN - 1600-0765
pISSN - 0022-3484
DOI - 10.1111/jre.12718
Subject(s) - peri implantitis , periodontitis , rankl , chronic periodontitis , long non coding rna , microarray , gene expression , osteoclast , biology , cancer research , gene , medicine , dentistry , rna , implant , genetics , activator (genetics) , surgery , in vitro
Background and Objective Peri‐implantitis is a biofilm‐mediated infectious disease that results in progressive loss of implant‐supporting bone. As compared to its analogue periodontitis, peri‐implantitis is generally known to be more aggressive, with comparatively rapid progression and less predictable treatment outcomes, especially when advanced. An understanding of molecular mechanisms underpinning the similarities and differences between peri‐implantitis and periodontitis is essential to develop novel management strategies. This study aimed to compare long non‐coding RNAs (lncRNAs) and messenger RNA (mRNA) expression profiles between peri‐implantitis and periodontitis. Methods Inflamed soft tissue from peri‐implantitis and periodontitis lesions, and healthy gingival tissue controls were analyzed by microarray. Cluster graphs, gene ontology (GO) analysis, and pathway analysis were performed. Quantitative real‐time PCR was employed to verify microarray results. The expression levels of RANKL and OPG in the three tissue types were also evaluated, using qRT‐PCR. Coding non‐coding (CNC) network analyses were performed. Results Microarray analyses revealed 1079 lncRNAs and 1003 mRNAs as differentially expressed in peri‐implantitis when compared to periodontitis. The cyclooxygenase‐2 pathway was the most up‐regulated biological process in peri‐implantitis as compared to periodontitis, whereas hemidesmosome assembly was the most down‐regulated pathway. Osteoclast differentiation was relatively up‐regulated, and RANKL / OPG ratio was higher in peri‐implantitis than in periodontitis. Conclusions The study demonstrated that peri‐implantitis and periodontitis exhibit significantly different lncRNA and mRNA expression profiles, suggesting that osteoclast differentiation‐related pathways are comparatively more active in peri‐implantitis. These data highlight potential molecular targets for periodontitis and peri‐implantitis therapy development.