IADR Abstract Archives
Investigation of the microbiome of oral leukoplakia (OLK)
Objectives: This study was undertaken to investigate the microbiome of oral leukoplakia (OLK), the most common of the 11 recognised oral potentially malignant disorders and establish if it differs from that of normal healthy mucosa. The secondary aim was to examine whether the degree of dysplasia on biopsy, currently the most accurate predictor of malignant transformation risk, influences the microbial community of OLK and whether the microbiome may therefore have a role to play in the malignant transformation of OLK
Methods: Mucosal swabs of disease and contralateral normal sites were collected from 203 patients with OLK attending Oral Medicine and Dysplasia clinics in the Dublin Dental University Hospital. Exclusion criteria included no available histology report, certain systemic diseases, and any immunosuppressant, antibiotic or steroid use in the previous two months. DNA was extracted from the swab samples, the V1-V3 region of the 16S rRNA gene was sequenced using the Illumina MiSeq and the data analysed using RStudio.
Results: 226 disease and 202 contralateral normal site samples from 192 patients were available for analysis. Five core taxa, Bergeyella sp. HMT322, Leptotrichia sp. HMT215, Streptococcus australis infantis clade 431, Gemella morbillorum, and Leptotrichia sp. HMT392, were consistently associated with OLK after adjusting for multiple variables, including smoking and oral site. Two species, Gemella morbillorum and Mogibacterium diversum were associated with no and mild dysplasia while three taxa, Bergeyella sp. HMT322, Streptococcus australis infantis clade 431 and Leptotrichia sp. HMT215 were associated with moderate and severe dysplasia, with Bergeyella sp. HMT322 appearing to be an independent marker for severe dysplasia
Conclusions: We have identified a core microbiome consistently associated with OLK. We have also demonstrated for the first time that OLKs with different degrees of dysplasia display different microbial communities, suggesting that the microbiome may play a role in the pathogenesis of OLK.
Methods: Mucosal swabs of disease and contralateral normal sites were collected from 203 patients with OLK attending Oral Medicine and Dysplasia clinics in the Dublin Dental University Hospital. Exclusion criteria included no available histology report, certain systemic diseases, and any immunosuppressant, antibiotic or steroid use in the previous two months. DNA was extracted from the swab samples, the V1-V3 region of the 16S rRNA gene was sequenced using the Illumina MiSeq and the data analysed using RStudio.
Results: 226 disease and 202 contralateral normal site samples from 192 patients were available for analysis. Five core taxa, Bergeyella sp. HMT322, Leptotrichia sp. HMT215, Streptococcus australis infantis clade 431, Gemella morbillorum, and Leptotrichia sp. HMT392, were consistently associated with OLK after adjusting for multiple variables, including smoking and oral site. Two species, Gemella morbillorum and Mogibacterium diversum were associated with no and mild dysplasia while three taxa, Bergeyella sp. HMT322, Streptococcus australis infantis clade 431 and Leptotrichia sp. HMT215 were associated with moderate and severe dysplasia, with Bergeyella sp. HMT322 appearing to be an independent marker for severe dysplasia
Conclusions: We have identified a core microbiome consistently associated with OLK. We have also demonstrated for the first time that OLKs with different degrees of dysplasia display different microbial communities, suggesting that the microbiome may play a role in the pathogenesis of OLK.