Periodontitis, the formal name given to inflammatory gum disease, is known to correlate to risk of a range of age-related conditions, including osteoporosis, the loss of bone mass and strength that occurs with age. A number of different mechanisms may be responsible for these correlations, and it remains a matter for debate as to which is most important. In the context of cardiovascular disease, researchers have focused on leakage of oral bacteria and inflammatory metabolites into the circulation via injured gums. Here, in the context of osteoporosis, researchers suggest that the oral bacteria responsible for periodontitis can alter the composition of the gut microbiome in ways that impair bone tissue maintenance, favoring the destruction of bone extracellular matrix by osteoclasts over matrix deposition by osteoblasts.
Epidemiological studies have highlighted an association between periodontitis and osteoporosis. However, the mechanism underlining this association remains unclear. Here, we revealed significant differences in the salivary microbiota between periodontally healthy individuals and periodontitis patients, with periodontitis patients exhibiting increased salivary microbiota diversity and an elevated abundance of pathogenic bacteria.
Using an ovariectomized (OVX) mouse model, we demonstrated that the salivary microbiota from periodontitis patients exacerbated bone destruction by modulating the gut microbiota. Metabolomic analysis revealed that the periodontitis-associated salivary microbiota suppressed tryptophan metabolism. The tryptophan metabolite indole-3-lactic acid (ILA) directly inhibited osteoclast formation and differentiation. In OVX mice treated with periodontitis salivary microbiota, supplementation with ILA effectively suppressed osteoclastogenesis and alleviated the detrimental effects of periodontitis-associated salivary microbiota on systemic bones.
In summary, our data demonstrate that periodontitis can affect systemic bone metabolism via the oral-gut axis and that ILA supplementation serves as a potential therapeutic option to mitigate these adverse effects.
Link: https://doi.org/10.1038/s41368-025-00415-2
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