The Lyme Disease Pathogen Borrelia burgdorferi Infects Murine Bone and Induces Trabecular Bone Loss.

Authors:
Tian Tian Tang
Tian Tian Tang
University of Toronto
Toronto | Canada
Lucia Zhang
Lucia Zhang
University of Toronto
Anil Bansal
Anil Bansal
University of Toronto
Marc Grynpas
Marc Grynpas
University of Toronto
Canada
Tara J Moriarty
Tara J Moriarty
University of Toronto
Toronto | Canada

Infect Immun 2017 02 26;85(2). Epub 2017 Jan 26.

Matrix Dynamics Group, Faculty of Dentistry, University of Toronto, Toronto, ON, Canada

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 reductions in areal and trabecular volumetric BMDs. Trabecular regions of femora exhibited significant, copy number-correlated microarchitectural disruption, but BMD, microarchitectural, and 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 it 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.

Download full-text PDF

Source
http://iai.asm.org/lookup/doi/10.1128/IAI.00781-16
Publisher Site
http://dx.doi.org/10.1128/IAI.00781-16DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5278181PMC

Still can't find the full text of the article?

We can help you send a request to the authors directly.
February 2017
23 Reads

Publication Analysis

Top Keywords

bone
16
bone loss
16
burgdorferi dna
12
burgdorferi infection
12
lyme disease
12
burgdorferi
9
bone building
8
trabecular bone
8
long bones
8
infection bone
8
biomechanical properties
8
reduced osteoblast
8
borrelia burgdorferi
8
infection
5
exhibited copy
4
microarchitectural biomechanical
4
femora exhibited
4
disruption bmd
4
number-correlated microarchitectural
4
microarchitectural disruption
4

Similar Publications