TY  - JOUR
AB  - Angiogenesis is critical in bone development and growth. Dense, large-scale, and multi-layered vascular networks formed by thin-walled sinusoidal vessels perfuse the plate bones and play an important role in bone repair. Yet, the intricate functional morphology of skull microvasculature remains poorly understood as it is difficult to visualize using existing intravital microscopy techniques. Here we introduced an intravital, fully-transcranial imaging approach based on hybrid optoacoustic and ultrasound bio-microscopy for large-scale observations and quantitative analysis of the vascular morphology, angiogenesis, vessel remodeling, and subsurface roughness in murine skulls. Our approach revealed radiation-inhibited angiogenesis in the skull bone. We also observed previously undocumented sinusoidal vascular networks spanning the entire skullcap, thus opening new vistas for studying the complex interactions between calvarial, pial, and cortical vascular systems.
AU  - Estrada, H.*
AU  - Rebling, J.*
AU  - Sivert, W.*
AU  - Hladik, D.
AU  - Hofmann, U.*
AU  - Gottschalk, S.*
AU  - Tapio, S.
AU  - Multhoff, G.*
AU  - Razansky, D.
C1  - 58195
C2  - 48186
CY  - Ste 800, 230 Park Ave, New York, Ny 10169 Usa
TI  - Intravital optoacoustic and ultrasound bio-microscopy reveal radiation-inhibited skull angiogenesis.
JO  - Bone
VL  - 133
PB  - Elsevier Science Inc
PY  - 2020
SN  - 8756-3282
ER  - 

TY  - JOUR
AB  - Hepatic osteodystrophy (HOD) denotes the alterations in bone morphology and metabolism frequently observed in patients with chronic liver diseases, in particular in case of cholestatic conditions. The molecular mechanisms underlying HOD are only partially understood. In the present study, we characterized the bone phenotypes of the ATP-binding cassette transporter B4 knockout mouse (Abcb4-/-), a well-established mouse model of chronic cholestatic liver disease, with the aim of identifying and characterizing a mouse model for HOD. Furthermore, we investigated the influence of vitamin D on bone quality in this model. The bone morphology analyses revealed reduced bone mineral contents as well as changes in trabecular bone architecture and decreased cortical bone densities in Abcb4-/- mice with severe liver fibrosis. We observed dysregulation of genes involved in bone remodeling (osteoprotegerin, osteocalcin, osteopontin) and vitamin D metabolism (7-dehydrocholesterol reductase, Gc-globulin, Cyp2r1, Cyp27a1) as well as alterations in calcium and vitamin D homeostasis. In addition, serum RANKL and TGF-β levels were increased in Abcb4-/- mice. Vitamin D dietary intervention did not restore the bone phenotypes of Abcb4-/- animals. We conclude that the Abcb4-/- mouse provides an experimental framework and a preclinical model to gain further insights into the molecular pathobiology of HOD and to study the systemic effects of therapeutic interventions.
AU  - Hochrath, K.*
AU  - Ehnert, S.*
AU  - Ackert-Bicknell, C.L.*
AU  - Lau, Y.*
AU  - Schmid, A.*
AU  - Krawczyk, M.*
AU  - Hengstler, J.G.*
AU  - Dunn, J.*
AU  - Hiththetiya, K.*
AU  - Rathkolb, B.
AU  - Micklich, K.*
AU  - Hans, W.
AU  - Fuchs, H.
AU  - Gailus-Durner, V.
AU  - Wolf, E.*
AU  - Hrabě de Angelis, M.
AU  - Dolley, S.*
AU  - Paigen, B.*
AU  - Wildemann, B.*
AU  - Lammert, F.*
AU  - Nüssler, A.K.*
C1  - 24745
C2  - 31658
SP  - 501-511
TI  - Modeling hepatic osteodystrophy in Abcb4 deficient mice.
JO  - Bone
VL  - 55
IS  - 2
PB  - Elsevier Science
PY  - 2013
SN  - 8756-3282
ER  - 

TY  - JOUR
AU  - Benet-Pagès, A.
AU  - Lorenz-Depiereux, B.
AU  - Zischka, H.
AU  - White, K.E.*
AU  - Econs, M.J.*
AU  - Strom, T.M.
C1  - 958
C2  - 22000
SP  - 455-462
TI  - FGF23 is processed by proprotein convertases but not by PHEX.
JO  - Bone
VL  - 35
PY  - 2004
SN  - 8756-3282
ER  - 

TY  - JOUR
AB  - Retrospective histologic analyses of bone biopsies and of post mortem samples from normal persons of different age groups, and of bone biopsies of age- and sex-matched groups of patients with primary osteoporosis and aplastic anemia show characteristic age dependent as well as pathologic changes including atrophy of osseous trabeculae and of hematopoiesis, and changes in the sinusoidal and arterial capillary compartments. These results indicate the possible role of a microvascular defect in the pathogenesis of osteoporosis and aplastic anemia.
AU  - Burkhardt, R.T.
AU  - Kettner, G.
AU  - Böhm, W.
AU  - Schmidmeier, M.
AU  - Schlag, R.*
AU  - Frisch, B.*
AU  - Mallmann, B.
AU  - Eisenmenger, W.J.*
AU  - Gilg, T.*
C1  - 33002
C2  - 38388
SP  - 157-164
TI  - Changes in trabecular bone, hematopoiesis and bone marrow vessels in aplastic anemia, primary osteoporosis, and old age: A comparative histomorphometric study.
JO  - Bone
VL  - 8
IS  - 3
PY  - 1987
SN  - 8756-3282
ER  -