Lyme disease is caused by members of the Borrelia burgdorferi sensu lato species complex. Arthritis is a well-known late-stage pathology of Lyme disease, but the effects of B. burgdorferi infection on bone at sites other than articular surfaces are largely unknown. In this study, we investigated whether B. burgdorferi infection affects bone health in mice.
In mice inoculated with B. burgdorferi or vehicle (mock infection), we
measured the presence of B. burgdorferi DNA in bones, bone mineral
density (BMD), bone formation rates, biomechanical properties, cellular
composition, and two- and three-dimensional features of bone
microarchitecture. B. burgdorferi DNA was detected in bone. In the
long bones, increasing B. burgdorferi DNA copy number correlated with
reduction in areal and trabecular volumetric BMD. Trabecular regions of
femora exhibited significant, copy number-correlated microarchitectural
disruption, but BMD, microarchitectural, or biomechanical properties of
cortical bone were not affected.
Bone loss in tibiae was not due to increased osteoclast numbers or
bone-resorbing surface area, but was associated with reduced osteoblast numbers, implying that bone loss in long bones was due to impaired bone building. Osteoid-producing and mineralization activities of existing osteoblasts were unaffected by infection. Therefore, deterioration of trabecular bone was not dependent on inhibition of osteoblast function, but was more likely caused by blockade of osteoblastogenesis, reduced osteoblast survival, and/or induction of osteoblast death.
Together, these data represent the first evidence that B. burgdorferi infection induces bone loss in mice, and suggest that this phenotype results from inhibition of bone building rather than increased bone resorption.