Streptococcus mitis and Prevotella melaninogenica Influence Gene Expression Changes in Oral Mucosal Lesions in Periodontitis Patients

Author:

Tomic Uros1ORCID,Nikolic Nadja2ORCID,Carkic Jelena2,Mihailovic Djordje3,Jelovac Drago4,Milasin Jelena2ORCID,Pucar Ana1ORCID

Affiliation:

1. Clinic for Periodontology and Oral Medicine, School of Dental Medicine, University of Belgrade, 11000 Belgrade, Serbia

2. Department of Human Genetics, School of Dental Medicine, University of Belgrade, 11000 Belgrade, Serbia

3. Department of Dentistry, Faculty of Medical Sciences Pristina, University of Pristina, 38220 Kosovska Mitrovica, Serbia

4. Clinic for Maxillofacial Surgery, School of Dental Medicine, University of Belgrade, 11000 Belgrade, Serbia

Abstract

Oral microbiome disruptions in periodontitis are related to the chronic inflammatory reactions that could in turn lead to the development of multiple oral diseases. The objective of the study was to assess the frequencies of Streptococcus mitis, Prevotella melaninogenica, and Prevotella intermedia in oral benign lesions, oral potentially malignant disorders (OPMDs), and oral squamous cell carcinomas (OSCCs) and investigate the impact of these bacteria on the expression patterns of the selected (potential) target genes (PI3CA/AKT2/mTOR, DUSP16/MAPK14, and COX2). After sample collection (25 benign lesions, 30 OPMDs, and 35 OSCCs) and DNA/RNA extraction, quantitative real-time polymerase chain reaction (qPCR) was performed to detect bacterial presence and assess relative gene expression levels in different lesion groups. Prevotella melaninogenica was the most prevalent of the three analyzed bacteria, with the frequency being 60% in benign lesions, 87% in OPMDs (p = 0.024), and 77% in OSCC. The OPMD tissues in which Prevotella melaninogenica was present exhibited a higher expression level of AKT2 (p = 0.042). Significantly lower expression of DUSP16 was observed in OSCC tissues containing Streptococcus mitis (p = 0.011). The obtained results indicate a substantial contribution of P. melaninogenica and Str. mitis in the pathogenesis of oral mucosal lesions, possibly via AKT2 upregulation and DUSP16 downregulation.

Funder

Science Fund of the Republic of Serbia

Eklund Foundation for Odontological Research and Education

Publisher

MDPI AG

Subject

Infectious Diseases,Microbiology (medical),General Immunology and Microbiology,Molecular Biology,Immunology and Allergy

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