作者: Tian Tian Tang , Lucia Zhang , Anil Bansal , Marc Grynpas , Tara J. Moriarty
DOI: 10.1128/IAI.00781-16
关键词: Bone mineral 、 Immunology 、 Biology 、 Cortical bone 、 Pathology 、 Osteolysis 、 Arthritis 、 Borrelia burgdorferi 、 Osteoblast 、 Osteoclast 、 Osteopenia
摘要: Lyme disease is caused by members of the Borrelia burgdorferi sensu lato species complex. Arthritis a well-known late-stage pathology disease, but effects B. infection on bone at sites other than articular surfaces are largely unknown. In this study, we investigated whether affects health in mice. mice inoculated with or vehicle (mock infection), measured presence DNA bones, mineral density (BMD), formation rates, biomechanical properties, cellular composition, and two- three-dimensional features microarchitecture. was detected bone. long increasing copy number correlated reductions areal trabecular volumetric BMDs. Trabecular regions femora exhibited significant, number-correlated microarchitectural disruption, BMD, microarchitectural, properties cortical were not affected. Bone loss tibiae due to increased osteoclast numbers bone-resorbing surface area, it associated reduced osteoblast numbers, implying that bones impaired building. Osteoid-producing mineralization activities existing osteoblasts unaffected infection. Therefore, deterioration dependent inhibition function more likely blockade osteoblastogenesis, survival, and/or induction death. Together, these data represent first evidence induces suggest phenotype results from building rather resorption.