741 Periodontal Defect in Hypophosphatemic Rickets Mice Model

Friday, March 23, 2012: 10:45 a.m. - 12:15 p.m.
Presentation Type: Oral Session
R. LIU, T. LEI, M. DALLAS, A. STERN, and L. YE, University of Missouri -Kansas City, Kansas City, MO
Objective: We have previously reported the early periodontal breakdown in the autosomal recessive hypophosphatemic rickets mouse model- Dentin Matrix Protein 1 (Dmp1) null mouse and that there is an increased prevalence of periodontitis in hypophosphatemic rickets adult patients. In this study, we sought to determine the mechanism for the periodontal defect by comparing two hypophosphatemic rickets mouse models: the Dmp1 null mouse and the Hyp mouse, and also investigate if loading is responsible for the periodontal bone loss in those mice.

Method: 1) Dmp1 null mice and Hyp mice were compared at different stages, 3-week, 6-week, and 3-month by histology and Micro-CT; 2) mechanical properties of Dmp1 null and Hyp bone were studied by 3-point bending test; 3) soft diet was used to decrease the occlusal loading in an attempt to rescue the periodontal bone loss in Dmp1 null mice.

Result: Although Dmp1 null mice and Hyp mice share some similarities in their tooth and long bone phenotypes, much less periodontal bone loss was observed in Hyp mice. However, 3-point bending test showed similar Young’s modulus in Dmp1 null bone and Hyp bone, suggesting that occlusal loading would lead to increased bone strain in both mice, compared with the wildtype control.  Lastly, soft diet from 3-week to 6-week significantly decreased the periodontal bone loss in Dmp1 null mice, but didn’t fully rescue the phenotype.

Conclusion: Both local and systemic effects of deleting DMP1 may be responsible for the periodontal bone loss in Dmp1 null mice.

This abstract is based on research that was funded entirely or partially by an outside source: NIDCR DE016977

Keywords: Bone and Loading
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