Absence of bone sialoprotein (BSP) impairs cortical defect repair in mouse long bone

• Published in: Bone (New York, N.Y.) Vol. 45; no. 5; pp. 853 - 861
• Main Authors: Malaval, Luc, Monfoulet, Laurent, Fabre, Thierry, Pothuaud, Laurent, Bareille, Reine, Miraux, Sylvain, Thiaudiere, Eric, Raffard, Gerard, Franconi, Jean-Michel, Lafage-Proust, Marie-Hélène, Aubin, Jane E, Vico, Laurence, Amédée, Joëlle
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier Inc 01.11.2009; Elsevier
• Subjects: Animals; Biological and medical sciences; Bone and Bones - diagnostic imaging; Bone and Bones - pathology; Bone and Bones - surgery; Bone Remodeling; Bone sialoprotein; Cortical defect; Fundamental and applied biological sciences. Psychology; Integrin-Binding Sialoprotein; Magnetic Resonance Imaging; Mice; Orthopedics; Osteoblast; Osteoclast; Sialoglycoproteins - deficiency; Sialoglycoproteins - metabolism; SIBLINGs; Vertebrates: anatomy and physiology, studies on body, several organs or systems; Wound Healing; X-Ray Microtomography; magnetic resonance imaging; μCT; MRI; Cortical defect; region of interest; SIBLINGs; Osteoblast; Bone sialoprotein; microcomputed tomography; Osteoclast; ROI; Diseases of the osteoarticular system; Rodentia; Sibling; Vertebrata; Mammalia; Sialoproteins; Mouse; Animal; Morphology; Bone defect; Repair; Long bone
• ISSN: 8756-3282; 1873-2763
• DOI: 10.1016/j.bone.2009.06.005

Abstract Matrix proteins of the SIBLING family interact with bone cells and with bone mineral and are thus in a key position to regulate bone development, remodeling and repair. Within this family, bone sialoprotein (BSP) is highly expressed by osteoblasts, hypertrophic chondrocytes and osteoclasts. We recently reported that mice lacking BSP (BSP−/−) have very low trabecular bone turnover. In the present study, we set up an experimental model of bone repair by drilling a 1 mm diameter hole in the cortical bone of femurs in both BSP−/− and +/+ mice. A non-invasive MRI imaging and bone quantification procedure was designed to follow bone regeneration, and these data were extended by μCT imaging and histomorphometry on undecalcified sections for analysis at cellular level. These combined approaches revealed that the repair process as reflected in defect-refilling in the cortical area was significantly delayed in BSP−/− mice compared to +/+ mice. Concomitantly, histomorphometry showed that formation, mineralization and remodeling of repair (primary) bone in the medulla were delayed in BSP−/− mice, with lower osteoid and osteoclast surfaces at day 15. In conclusion, the absence of BSP delays bone repair at least in part by impairing both new bone formation and osteoclast activity.