Deficiency in Acellular Cementum and Periodontal Attachment in Bsp Null Mice

Author:

Foster B.L.1,Soenjaya Y.2,Nociti F.H.13,Holm E.4,Zerfas P.M.5,Wimer H.F.6,Holdsworth D.W.7,Aubin J.E.8,Hunter G.K.249,Goldberg H.A.249,Somerman M.J.1

Affiliation:

1. National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), National Institutes of Health (NIH), Bethesda, MD, USA

2. Biomedical Engineering Program, Schulich School of Medicine & Dentistry, University of Western Ontario, London, ON, Canada

3. Department of Prosthodontics and Periodontics, Division of Periodontics, School of Dentistry, Campinas State University, Piracicaba, SP, Brazil

4. Department of Biochemistry, Schulich School of Medicine & Dentistry, University of Western Ontario, London, ON, Canada

5. Division of Veterinary Resources, Office of Research Services, National Institutes of Health (NIH), Bethesda, MD, USA

6. Department of Vertebrate Zoology, National Museum of Natural History, Smithsonian Institution, Washington, DC, USA

7. Imaging Research Laboratories, Robarts Research Institute, London, ON, Canada

8. Department of Molecular Genetics and Faculty of Dentistry, University of Toronto, Toronto, ON, Canada

9. School of Dentistry, Schulich School of Medicine & Dentistry, University of Western Ontario, London, ON, Canada

Abstract

Bone sialoprotein (BSP) is an extracellular matrix protein found in mineralized tissues of the skeleton and dentition. BSP is multifunctional, affecting cell attachment and signaling through an RGD integrin-binding region, and acting as a positive regulator for mineral precipitation by nucleating hydroxyapatite crystals. BSP is present in cementum, the hard tissue covering the tooth root that anchors periodontal ligament (PDL) attachment. To test our hypothesis that BSP plays an important role in cementogenesis, we analyzed tooth development in a Bsp null (-/-) mouse model. Developmental analysis by histology, histochemistry, and SEM revealed a significant reduction in acellular cementum formation on Bsp-/- mouse molar and incisor roots, and the cementum deposited appeared hypomineralized. Structural defects in cementum-PDL interfaces in Bsp-/- mice caused PDL detachment, likely contributing to the high incidence of incisor malocclusion. Loss of BSP caused progressively disorganized PDL and significantly increased epithelial down-growth with aging. Bsp-/- mice displayed extensive root and alveolar bone resorption, mediated by increased RANKL and the presence of osteoclasts. Results collected here suggest that BSP plays a non-redundant role in acellular cementum formation, likely involved in initiating mineralization on the root surface. Through its importance to cementum integrity, BSP is essential for periodontal function.

Publisher

SAGE Publications

Subject

General Dentistry

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