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Journal of Dental Research, Vol. 87, No. 7, 624-629 (2008)
DOI: 10.1177/154405910808700708

RAPID COMMUNICATION

Periodontal Breakdown in the Dmp1 Null Mouse Model of Hypophosphatemic Rickets

L. Ye1,*, S. Zhang1, H. Ke2, L. F. Bonewald1 and JQ. Feng3,*

1 Oral Biology, School of Dentistry, University of Missouri-Kansas City, 650 E 25th Street, Kansas City, MO 64108, USA;
2 Amgen, Amgen Center Drive, Thousand Oaks, CA 91320, USA; and
3 Department of Biomedical Sciences, Baylor College of Dentistry, Dallas, TX 75246, USA

Correspondence: * corresponding author, yeling{at}umkc.edu or jfeng{at}bcd.tamhsc.edu

Dentin Matrix Protein 1 (DMP1) is highly expressed in alveolar bone and cementum, which are important components of the periodontium. Therefore, we hypothesized that Dmp1 is critical for the integrity of the periodontium, and that deletion may lead to increased susceptibility to disease. An early-onset periodontal defect was observed in the Dmp1 null mouse, a mouse model of hypophosphatemic rickets. The alveolar bone is porous, with increased proteoglycan expression. The cementum is also defective, as characterized by irregular, punctate fluorochrome labeling and elevated proteoglycan. The osteocyte and cementocyte lacuno-canalicular system of both alveolar bone and cementum is abnormal, with irregular lacunar walls and fewer canaliculi. As a consequence, there is significant interproximal alveolar bone loss, combined with detachment between the periodontal ligament (PDL) and cementum. We propose that defective alveolar bone and cementum may account for the periodontal breakdown and increased susceptibility to bacterial infection in Dmp1 null mice.

Key Words: DMP1 • PDL • cementum • hypophosphatemic rickets • alveolar bone


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