Background Despite many potential effects of the oral microbiome on oral and systemic health, scant information is available regarding the associations between diet and the oral microbiome. Methods Oral rinse DNA samples from 182 participants in a population-based case–control study for colorectal cancer were used to amplify a V3–V4 region of bacterial 16S rRNA gene. The amplicons were sequenced using Illumina MiSeq paired end chemistry on 2 runs, yielding approximately 33 million filtered reads that were assigned to bacterial classes. Relative abundances of each class and family as well microbial diversity/richness indices were correlated with selected dietary intakes from a food frequency questionnaire. Results Saturated fatty acids (SFAs) and vitamin C intakes were consistently correlated with alpha (within-subjects) diversity indexes in both richness and diversity. SFA intake was positively correlated with relative abundance of betaproteobacteria and fusobacteria. Vitamin C and other vitamins with correlated intakes—for example, the B vitamins and vitamin E—exhibited positive correlations with fusobacteria class, its family Leptotrichiaceae and a clostridia family Lachnospiraceae. In addition, glycemic load was positively correlated with Lactobacillaceae abundance. Conclusion The observed associations in this study were modest. However, the results suggest that the effects of diets are likely to be habitat specific, and observations from the gut microbiome are not transferrable to the oral microbiome. Further studies are warranted, incorporating a range of host biomarkers, such as cytohistological, molecular, or biochemical measurements, in order to address biological consequences of these dietary intakes in human oral health.
Background The equilibrium of oral microbiome may be altered by environmental factors, including cigarette smoking. Several recent studies also suggest that oral pathogens causing periodontal disease, such as Fusobacterium nucleatum, are involved in pathogenesis of colorectal cancer. Methods For this study oral rinse DNA samples from 190 participants in a population-based case-control study for colorectal cancer were used to amplify a V3-V4 region of bacterial 16S rRNA gene. The amplicons were sequenced using Illumina MiSeq paired end chemistry on two runs, yielding approximately 35 million filtered reads which were assigned to bacterial phyla. Results No association was found between Fusobacterium abundance or presence and colorectal cancer. However, adjusted for age and experimental batch, colorectal cancer history was associated with increased presence of genus Lactobacillus and increased relative abundance of Rothia by 28% and current smoking was associated with a 33% decrease in relative counts of Betaproteobacteria (primarily Neisseria) and 23% increase in relative abundance of Veillonellaceae family. We also found that smoking had significant effects on the 2nd component scores and 2nd coordinate distances in principal component and coordinate analyses. Conclusions It remains to be elucidated whether the observed differences can be translated into biochemical changes in oral environment, thus potentially affecting oral health.
In spite of recent scientific advances, treatment and repair of cartilage using tissue engineering techniques remains challenging. The major constraint is the limited proliferative capacity of mature autologous chondrocytes used in the tissue engineering approach. This problem can be addressed by using stem cells, which can self-renew with greater proliferative potential. Cartilage tissue engineering using adult mesenchymal stem cells derived from bone marrows has met with limited success. In this study we explored cartilage tissue generation from embryonic stem cells (ESCs). ESCs were induced to differentiate into chondroprogenitors, capable of proliferating and subsequently differentiating into cartilage-producing cells. The chondrogenic cells expressed chondrocyte-specific markers and deposited extracellular matrix proteins, proteoglycans. ESC-derived chondrogenic cells and polycaprolactone scaffolds seeded with these cells implanted in mice (129 SvImJ) generated cartilage tissue in vivo. Postimplant analysis of the retrieved tissues demonstrated cartilage-like tissue formation in 3-4 weeks. The cells of retrieved tissues also expressed the chondrocyte-specific marker collagen II. These findings suggest that ESCs can be used for tissue engineering and cultivation of cartilage tissues.
Stem cell therapy may be used potentially to treat retinal degeneration and restore vision. Since embryonic stem cells (ESCs) can differentiate into almost any cell types, including those found in the eye, they can be transplanted to repair or replace damaged or injured retinal tissue resulting from inherited diseases or traumas. In this investigation, we explored the potential of ESCs and ESC-derived neuroprogenitors to proliferate and integrate into the diseased retinal tissue of rd12 mice. These rd12 mice mimic the slow and progressive retinal degeneration seen in humans. Both ESCs and ESC-derived neuroprogenitors from ESCs survived and proliferated as evidenced from an increase in yellow fluorescent protein fluorescence. Quantification analysis of cryosectioned retinal tissue initially revealed that both ESCs and neuroprogenitors differentiated into cells expressing neural markers. However, ESC proliferation was robust and resulted in the disruption of the retinal structure and the eventual formation of teratomas beyond 6 weeks postimplantation. In contrast, the neuroprogenitors proliferated slowly, but differentiated further and integrated into the retinal layers of the eye. The differentiation of neuroprogenitors represented various retinal cell types, as judged from the expression of cell-specific markers including Nestin, Olig1, and glial fibrillary acidic protein. These results suggest that ESC-derived neuroprogenitors can survive, proliferate, and differentiate when implanted into the eyes of experimental mice and may be used potentially as cell therapy for treating degenerated or damaged retinal tissue.
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