摘要
The vital role of oral microbiome in the well-being of humans is only beginning to be unraveled. Employing a rigorous analysis of PCR-restriction fragment length polymorphisms (PCR-RFLP) and DNA fingerprints from denatured gradient gel electrophoresis (PCR-DGGE) of the 16S rDNA gene in metagenomic samples, this study evaluated the stability of the oral microbiome and contrasted the PCR-DGGE profiles of subjects belonging to three groups—healthy, smokers and oral diseases;in search of distinctive patterns predictive of each group. The DNA band size, intensity and profile generated by three restriction enzymes from a 1500 bp amplicon showed a fairly stable microbial community structure (P H' = 0.99 ± 0.12;S = 2.87 ± 0.75) and oral disease mouths (H' = 1.06 ± 0.085;S = 2.86 ± 0.31), than in healthy subjects (H' = 0.926 ± 0.07;S = 1.79 ± 0.56) suggesting that smoking is associated with a microbial community shift towards the structure found in poor oral health. It is clear that the human oral bacteria symbionts are not all random colonizers. Rather some of them constitute a fragile stable dynamic community whose disturbance could lead to disease or be indicative of disease. Understanding the dynamics of the bacterial community structure in health and disease states is a prerequisite to developing effective preventive healthcare and rapid diagnosis of diseases.
The vital role of oral microbiome in the well-being of humans is only beginning to be unraveled. Employing a rigorous analysis of PCR-restriction fragment length polymorphisms (PCR-RFLP) and DNA fingerprints from denatured gradient gel electrophoresis (PCR-DGGE) of the 16S rDNA gene in metagenomic samples, this study evaluated the stability of the oral microbiome and contrasted the PCR-DGGE profiles of subjects belonging to three groups—healthy, smokers and oral diseases;in search of distinctive patterns predictive of each group. The DNA band size, intensity and profile generated by three restriction enzymes from a 1500 bp amplicon showed a fairly stable microbial community structure (P H' = 0.99 ± 0.12;S = 2.87 ± 0.75) and oral disease mouths (H' = 1.06 ± 0.085;S = 2.86 ± 0.31), than in healthy subjects (H' = 0.926 ± 0.07;S = 1.79 ± 0.56) suggesting that smoking is associated with a microbial community shift towards the structure found in poor oral health. It is clear that the human oral bacteria symbionts are not all random colonizers. Rather some of them constitute a fragile stable dynamic community whose disturbance could lead to disease or be indicative of disease. Understanding the dynamics of the bacterial community structure in health and disease states is a prerequisite to developing effective preventive healthcare and rapid diagnosis of diseases.
