Transcriptomic phases of periodontitis lesions using the nonhuman primate model
Abstract We used a nonhuman primate model of ligature-induced periodontitis to identify patterns of gingival transcriptomic after changes demarcating phases of periodontitis lesions (initiation, progression, resolution). A total of 18 adult Macaca mulatta (12–22 years) had ligatures placed (premolar...
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2021-04-01
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doaj-48c76a8884504a86b2dcc36917ce6dcb2021-05-02T11:32:28ZengNature Publishing GroupScientific Reports2045-23222021-04-0111111810.1038/s41598-021-88803-6Transcriptomic phases of periodontitis lesions using the nonhuman primate modelJeffrey L. Ebersole0Radhakrishnan Nagarajan1Sreenatha Kirakodu2Octavio A. Gonzalez3Department of Biomedical Sciences, School of Dental Medicine, B221, University of Nevada Las VegasCenter for Oral and Systemic Disease, Marshfield Research FoundationCenter for Oral Health Research College of Dentistry, University of KentuckyCenter for Oral Health Research College of Dentistry, University of KentuckyAbstract We used a nonhuman primate model of ligature-induced periodontitis to identify patterns of gingival transcriptomic after changes demarcating phases of periodontitis lesions (initiation, progression, resolution). A total of 18 adult Macaca mulatta (12–22 years) had ligatures placed (premolar, 1st molar teeth) in all 4 quadrants. Gingival tissue samples were obtained (baseline, 2 weeks, 1 and 3 months during periodontitis and at 5 months resolution). Gene expression was analyzed by microarray [Rhesus Gene 1.0 ST Array (Affymetrix)]. Compared to baseline, a large array of genes were significantly altered at initiation (n = 6049), early progression (n = 4893), and late progression (n = 5078) of disease, with the preponderance being up-regulated. Additionally, 1918 genes were altered in expression with disease resolution, skewed towards down-regulation. Assessment of the genes demonstrated specific profiles of epithelial, bone/connective tissue, apoptosis/autophagy, metabolism, regulatory, immune, and inflammatory responses that were related to health, stages of disease, and tissues with resolved lesions. Unique transcriptomic profiles occured during the kinetics of the periodontitis lesion exacerbation and remission. We delineated phase specific gene expression profiles of the disease lesion. Detection of these gene products in gingival crevicular fluid samples from human disease may contribute to a better understanding of the biological dynamics of the disease to improve patient management.https://doi.org/10.1038/s41598-021-88803-6 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Jeffrey L. Ebersole Radhakrishnan Nagarajan Sreenatha Kirakodu Octavio A. Gonzalez |
spellingShingle |
Jeffrey L. Ebersole Radhakrishnan Nagarajan Sreenatha Kirakodu Octavio A. Gonzalez Transcriptomic phases of periodontitis lesions using the nonhuman primate model Scientific Reports |
author_facet |
Jeffrey L. Ebersole Radhakrishnan Nagarajan Sreenatha Kirakodu Octavio A. Gonzalez |
author_sort |
Jeffrey L. Ebersole |
title |
Transcriptomic phases of periodontitis lesions using the nonhuman primate model |
title_short |
Transcriptomic phases of periodontitis lesions using the nonhuman primate model |
title_full |
Transcriptomic phases of periodontitis lesions using the nonhuman primate model |
title_fullStr |
Transcriptomic phases of periodontitis lesions using the nonhuman primate model |
title_full_unstemmed |
Transcriptomic phases of periodontitis lesions using the nonhuman primate model |
title_sort |
transcriptomic phases of periodontitis lesions using the nonhuman primate model |
publisher |
Nature Publishing Group |
series |
Scientific Reports |
issn |
2045-2322 |
publishDate |
2021-04-01 |
description |
Abstract We used a nonhuman primate model of ligature-induced periodontitis to identify patterns of gingival transcriptomic after changes demarcating phases of periodontitis lesions (initiation, progression, resolution). A total of 18 adult Macaca mulatta (12–22 years) had ligatures placed (premolar, 1st molar teeth) in all 4 quadrants. Gingival tissue samples were obtained (baseline, 2 weeks, 1 and 3 months during periodontitis and at 5 months resolution). Gene expression was analyzed by microarray [Rhesus Gene 1.0 ST Array (Affymetrix)]. Compared to baseline, a large array of genes were significantly altered at initiation (n = 6049), early progression (n = 4893), and late progression (n = 5078) of disease, with the preponderance being up-regulated. Additionally, 1918 genes were altered in expression with disease resolution, skewed towards down-regulation. Assessment of the genes demonstrated specific profiles of epithelial, bone/connective tissue, apoptosis/autophagy, metabolism, regulatory, immune, and inflammatory responses that were related to health, stages of disease, and tissues with resolved lesions. Unique transcriptomic profiles occured during the kinetics of the periodontitis lesion exacerbation and remission. We delineated phase specific gene expression profiles of the disease lesion. Detection of these gene products in gingival crevicular fluid samples from human disease may contribute to a better understanding of the biological dynamics of the disease to improve patient management. |
url |
https://doi.org/10.1038/s41598-021-88803-6 |
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