D-galactose and the oral prebiotic idea
The research behind a microbiome-minded ingredient
By Jennifer C. Sullivan, periodontist and founder of Galacxy™
The mouth is home to a diverse community of microorganisms. Some help maintain a healthy oral environment; others can contribute to plaque formation and acid production. A prebiotic approach asks whether an ingredient can help shape that community in a favorable direction. D-galactose is a sugar substrate that oral bacteria can use, and researchers are exploring its potential as a biofilm regulator because different species respond to it differently in laboratory studies. [1, 4, 9]
Why researchers are exploring its prebiotic potential
A slower fuel for S. mutans
S. mutans can metabolize D-galactose, but a 2004 laboratory study found that it grew more slowly on galactose than on glucose or lactose. In the strain tested, the doubling time was about 157 minutes with galactose versus 71 minutes with either glucose or lactose. Disrupting a key galactose-metabolism gene, galK, left the bacterium with only marginal growth on galactose. This distinctive metabolic response adds to the rationale for studying galactose as an oral prebiotic substrate. [9]
Different effects on oral biofilms
In a 2020 laboratory study, Ryu and colleagues grew Streptococcus mutans—a bacterium associated with tooth decay—alongside S. oralis and S. mitis on saliva-coated surfaces. D-galactose reduced S. mutans biofilm formation in the conditions tested, while increasing biofilm formation by the other two species at some concentrations. This different response across species is central to the oral prebiotic hypothesis. The researchers also observed changes in genes involved in glucan production. When they briefly applied a D-galactose solution or paste to bovine teeth before laboratory incubation, less S. mutans biofilm formed than on control surfaces. [1]
In a 2016 laboratory study, Ryu and colleagues found that D-galactose reduced AI-2 signaling activity and biofilm formation involving Fusobacterium nucleatum, Porphyromonas gingivalis, and Tannerella forsythia under the conditions tested. The researchers examined bacteria grown on glass surfaces and in a two-chamber laboratory culture system. [2]
An earlier adhesion study identified a galactose-binding protein on one F. nucleatum strain. In those experiments, soluble galactose interfered with the strain’s attachment to mammalian cells and with its coaggregation with P. gingivalis and Aggregatibacter actinomycetemcomitans. This suggests a competing-binding, or decoy, mechanism for that strain. [6]
In a separate 2018 study comparing carbohydrate sources, S. mutans clinical isolates formed the most biofilm with sucrose and the least with galactose in the laboratory conditions tested. The investigators also examined how galactose and sucrose affected a multi-species biofilm community. [5]
A short human plaque study
In a small 1982 crossover study, 26 young adults rinsed with 9% D-galactose or a comparison rinse three times daily for three days while regular oral hygiene was suspended. Plaque scores were lower during the galactose-rinse period. The authors also reported that 0.9% and 4.5% galactose solutions did not prevent plaque formation in their preliminary observations. [3]
Galactose and plaque pH
It can. In a 1992 comparison, galactose generally caused a smaller plaque-pH drop than glucose. Responses differed across oral bacteria and experimental conditions. [4]
The oral–gut connection
The mouth is a major habitat for F. nucleatum, a bacterium also found in some colorectal tumors. Researchers have begun tracing whether oral strains can appear farther along the digestive tract. In one study of 14 people with colorectal cancer, investigators identified matching F. nucleatum strains in saliva and tumor tissue in six people. This offers a concrete reason to study the mouth as a possible source of bacteria detected beyond it. [7]
Laboratory research also offers a clue about how F. nucleatum can attach to colorectal tumor cells. A bacterial surface protein called Fap2 recognizes Gal-GalNAc, a sugar structure displayed on those cells. This is a different setting from the oral experiments in which free D-galactose interfered with attachment by one F. nucleatum strain. Together, the findings make bacterial attachment in the mouth and farther along the oral–gut route an interesting area of research. [6, 8]
Looking ahead
Together, these findings offer a promising scientific foundation for exploring D-galactose as part of an oral prebiotic approach. Its different effects on oral bacteria in laboratory studies make it especially interesting to investigate. If an oral-care approach can reduce an oral reservoir of F. nucleatum, it may also reduce opportunities for that organism to travel beyond the mouth. Whether D-galactose toothpaste achieves either effect, or changes any gut or cancer outcome, remains to be studied.
References
1. Ryu E-J, An S-J, Sim J, et al. Use of D-galactose to regulate biofilm growth of oral streptococci. Archives of Oral Biology. 2020;111:104666. doi:10.1016/j.archoralbio.2020.104666.
2. Ryu E-J, Sim J, Sim J, Lee J, Choi B-K. D-Galactose as an autoinducer 2 inhibitor to control the biofilm formation of periodontopathogens. Journal of Microbiology. 2016;54(9):632–637. doi:10.1007/s12275-016-6345-8.
3. Nagata K, Shibata S, Inoshita E, et al. The effect of daily mouth rinsing with galactose on dental plaque formation. Journal of Dental Health (Japan). 1982;32(4). Clinical study supplied for this review.
4. Salako NO, Kleinberg I. Comparison of the effects of galactose and glucose on the pH responses of human dental plaque, salivary sediment and pure cultures of oral bacteria. Archives of Oral Biology. 1992;37(10):821–829. doi:10.1016/0003-9969(92)90116-P.
5. Zhou Y, Millhouse E, Shaw T, et al. Evaluating Streptococcus mutans strain dependent characteristics in a polymicrobial biofilm community. Frontiers in Microbiology. 2018;9:1498. doi:10.3389/fmicb.2018.01498.
6. Weiss EI, Shaniztki B, Dotan M, et al. Attachment of Fusobacterium nucleatum PK1594 to mammalian cells and its coaggregation with periodontopathogenic bacteria are mediated by the same galactose-binding adhesin. Oral Microbiology and Immunology. 2000;15(6):371–377. doi:10.1034/j.1399-302X.2000.150606.x.
7. Komiya Y, Shimomura Y, Higurashi T, et al. Patients with colorectal cancer have identical strains of Fusobacterium nucleatum in their colorectal cancer and oral cavity. Gut. 2019;68(7):1335–1337. doi:10.1136/gutjnl-2018-316661.
8. Abed J, Emgård JEM, Zamir G, et al. Fap2 mediates Fusobacterium nucleatum colorectal adenocarcinoma enrichment by binding to tumor-expressed Gal-GalNAc. Cell Host & Microbe. 2016;20(2):215–225. doi:10.1016/j.chom.2016.07.006.
9. Abranches J, Chen Y-YM, Burne RA. Galactose metabolism by Streptococcus mutans. Applied and Environmental Microbiology. 2004;70(10):6047–6052. doi:10.1128/AEM.70.10.6047-6052.2004.
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