DNA methylation levels of SOCS1 and LINE-1 in oral epithelial cells from aggressive periodontitis patients.
OBJECTIVE
DNA methylation has been shown to be critical in the regulation of inflammatory genes. Infections are able to trigger susceptibility to disease and it can be considered as potential epimutagenic factors in reshaping the epigenome. Therefore, what would be the DNA methylation status in cells present in an infected and inflamed oral environment? The aim was to verify the DNA methylation pattern in oral epithelium cells from aggressive periodontitis (AgP) patients in a specific gene involved in the inflammation control, as suppressor of cytokine signalling (SOCS)1 and in a broader way through long interspersed nuclear element (LINE)-1.


METHODS
Genomic DNA from oral cells of 30 generalized AgP patients and 30 healthy patients were purified and modified by sodium bisulfite. DNA methylation patterns were analyzed using combined bisulfite restriction analysis (COBRA) for SOCS1 and LINE-1.


RESULTS
An overall scenario of demethylation was seen for both groups, whereas the healthy group presented a higher percentage of demethylation (p<0.001), also presenting the majority of total demethylated samples (83.3% versus 70.8% in the AgP group). Total LINE-1 methylation or at each specific loci presented significant differences amongst groups.


CONCLUSIONS
Epithelial cells, present in an infected and inflamed oral environment, show different DNA methylation status from those present in a healthy oral environment, regarding the SOCS1 and LINE-1. In addition, the investigation allows detecting alterations in the DNA in a non-limited manner, since the results observed might reflect a generalized condition of the oral epithelial cells, besides reflecting the condition of the gingival epithelium cells.
Department of Morphology, Division of Histology, School of Dentistry at Piracicaba, University of Campinas, Piracicaba, São Paulo, Brazil.
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Baptista
Department of Morphology, Division of Histology, School of Dentistry at Piracicaba, University of Campinas, Piracicaba, São Paulo, Brazil.
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Portinho
Department of Prosthodontics and Periodontics, Division of Periodontics, School of Dentistry at Piracicaba, University of Campinas, Piracicaba, São Paulo, Brazil.
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Casarin
Department of Prosthodontics and Periodontics, Division of Periodontics, School of Dentistry at Piracicaba, University of Campinas, Piracicaba, São Paulo, Brazil.
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Vale
Department of Prosthodontics and Periodontics, Division of Periodontics, School of Dentistry at Piracicaba, University of Campinas, Piracicaba, São Paulo, Brazil.
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MZ
Casati
Department of Morphology, Division of Histology, School of Dentistry at Piracicaba, University of Campinas, Piracicaba, São Paulo, Brazil.
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De Souza
Department of Morphology, Division of Histology, School of Dentistry at Piracicaba, University of Campinas, Piracicaba, São Paulo, Brazil. Electronic address: denise@andia.com.br.
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Andia
D000328:Adult; D010520:Aggressive Periodontitis / Q000235:genetics*; D016022:Case-Control Studies; D019175:DNA Methylation; D005260:Female; D020022:Genetic Predisposition to Disease; D006801:Humans; D020084:Long Interspersed Nucleotide Elements / Q000235:genetics*; D008297:Male; D050826:Suppressor of Cytokine Signaling Proteins / Q000235:genetics*
D050826:Suppressor of Cytokine Signaling Proteins
Aggressive periodontitis; DNA methylation; Long interspersed nuclear elements; Suppressor of cytokine signalling proteins