ATLANTA — A study led by Professor Roberto Pacifici investigating the relationship between the gut microbiome and bone loss in primary hyperparathyroidism patients was published on May 25, 2026, in the journal Bone Research. Primary hyperparathyroidism is an endocrine disorder characterized by excessive secretion of parathyroid hormone.

Researchers analyzed stool samples, bone density measurements, and immune-cell profiles from 50 individuals diagnosed with the disorder. Gut microbiota from these patients, exhibiting varying bone densities, were transplanted into germ-free mice through fecal microbiota transfer.

Mice that received microbiota from osteoporotic patients developed greater bone loss and increased levels of inflammatory immune cells when compared to mice that received microbiota from patients with healthier bones. Higher levels of these immune cells were consistently associated with lower bone density in both the patients and the recipient mice.

Colonization with Bifidobacterium longum in germ-free mice stimulated the expansion of tumor necrosis factor-producing T cells and T helper 17 cells in their intestine and bone marrow. Bifidobacterium longum enhanced the migration of these immune cells from the gut to the bone marrow, where they released inflammatory factors. Statistical analyses revealed that an increased abundance of Bifidobacterium longum correlated with elevated expression of the inflammatory molecules TNF and IL-17.

Mice harboring Bifidobacterium longum experienced greater bone loss than control animals when exposed to elevated parathyroid hormone levels. Pacifici said, "We show that the extent to which primary hyperparathyroidism impacts the human skeleton correlated with the abundance of Bifidobacterium longum, a taxon that we show to induce the expansion of both intestinal and BM TNF + T cells and Th17 cells."

The study identified tumor necrosis factor-producing T cells and T helper 17 cells as mediators linking the gut microbiome to bone deterioration. Researchers found no differences in overall microbiome composition among patients with osteoporosis, osteopenia, or normal bone density. Pacifici added, "These findings confirmed that the presence of Bifidobacterium longum in the gut microbiome allows PTH to cause the expansion and migration of TNF + T cells and Th17 cells and to induce bone loss."

Susceptibility to bone loss depended on the abundance of specific bacterial species rather than broad changes in the microbial community. Researchers proposed that targeted microbiome interventions could help prevent or reduce bone loss in patients with the disorder.