Fractures and the gut microbiome

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Abstract

Purpose of review

The role of the gut microbiome in the pathogenesis of several inflammatory, non-AIDS comorbidities, such as cardiovascular disease, cognitive impairment and liver disease has become a focus of recent research. Low bone mineral density (BMD) and increased fracture incidence in people living with HIV (PLWH) is also widely reported, however, the relationship between alterations in the gut microbiome and bone disease in PLWH has not been previously reviewed.

Recent findings

Murine models that manipulate the gut microbiome, either through breeding of ‘germ-free’ mice or antibiotic-depleted gut microbiome, show differences in bone mineral density and bone mass in those with altered gut microbiome. This effect is reported to be driven via changes in the gut–immune–skeletal axis, with changes favouring bone resorption. Several inflammatory conditions wherever bone loss is a prominent feature, such as rheumatoid arthritis and inflammatory bowel disease, have also reported alterations in the gut microbiome, which are associated with bone loss, again through changes in the gut–immune–skeletal axis.

Summary

The interplay between the gut microbiome and the immune–skeletal axis in HIV represents a complex relationship. Alterations in the gut microbiome, which induce an activated immune phenotype and inflammatory milieu are associated with non-AIDS comorbidities in PLWH and bone loss in several other conditions characterized by chronic immune activation and inflammation. It is, therefore, likely that there are comparable effects between altered gut microbiome and bone loss in HIV, however, further research is required to better define this relationship in populations of PLWH.

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