Figure 2
From: Modelling neurofibromatosis type 1 tibial dysplasia and its treatment with lovastatin
Progression of cortical bone repair in control and Nf1Prx1 mice. Toluidine/VonKossa stained transverse sections of the drill channel entry site 7 and 14 days post injury induction. (A), (B) Trabecular bone formation is delayed within the injury site in mutant mice as compared with controls at day 7. (C) Lovastatin treatment accelerates the formation of new mineralised bone by preventing fibro-cartilaginous tissue accumulation. (D), (E) Unlike in control mice, at day 14 post injury trabecular bone within the drill channel is covered by thick osteoid (arrows) in the mutant mice and the cartilaginous tissue persists (*). (F) Lovastatin treatment improves trabecular bone formation and extracellular matrix mineralisation. In addition, a marked reduction of the osteoid occurs.