Modelling neurofibromatosis type 1 tibial dysplasia and its treatment with lovastatin

doi:10.1186/1741-7015-6-21

BMC Medicine
Volume 6

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Kolanczyk M
Kühnisch J
Kossler N
Osswald M
Stumpp S
Thurisch B
Kornak U
Mundlos S

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Kolanczyk M
Kühnisch J
Kossler N
Osswald M
Stumpp S
Thurisch B
Kornak U
Mundlos S
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Research article

Modelling neurofibromatosis type 1 tibial dysplasia and its treatment with lovastatin

Mateusz Kolanczyk¹^,2^,3 , Jirko Kühnisch² , Nadine Kossler¹^,2 , Monika Osswald¹^,2 , Sabine Stumpp² , Boris Thurisch¹^,2 , Uwe Kornak¹^,2 and Stefan Mundlos¹^,2^,4

¹Max Planck Institute for Molecular Genetics, FG Development & Disease, Berlin, Germany

²Institute for Medical Genetics, Charité, Universitätsmedizin Berlin, Berlin, Germany

³In Silico Miners, ul. Chopina 13/10, 81-782 Sopot, Poland

⁴Berlin-Brandenburg Center for Regenerative Therapies (BCRT), Berlin, Germany

author email corresponding author email

BMC Medicine 2008, 6:21doi:10.1186/1741-7015-6-21


Published:	31 July 2008

Additional files

Additional file 1:

Progression of bone repair in control and Nf1Prx1 mice, longitudinal view. Toluidine/VonKossa stained longitudinal methacrylate sections of wild-type and Nf1Prx1 tibia 7 and 14 days post injury induction. Uninjured tibia is shown for comparison. The trabecular bone formed within the bone marrow cavity demarcates the injury site. Magnification of the cortical bone distant from the injury site shows normal mineralisation in uninjured animals and partial cortical bone demineralisation in mutant mice 7 and 14 days post injury (red frame, arrows).

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Additional file 2:

Progression of bone repair in control and Nf1Prx1 mice, 28 days post injury. Toluidine/VonKossa stained transverse sections of the cortical defect area. After 28 days post injury the cortical structure is regenerated in control mice (left). The cortical bone in mutant mice remains thinned and overlaid by a thick osteoid (red arrows). It is also excessively penetrated by blood vessels (white arrows).

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