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J Oral Biosci. 2014 Nov 1;56(4):143-148.

Overexpressing the NH2-terminal fragment of dentin sialophosphoprotein (DSPP) aggravates the periodontal defects in Dspp knockout mice.

Author information

1
Department of Biomedical Sciences and Center for Craniofacial Research and Diagnosis, Texas A&M University Baylor College of Dentistry, 3302 Gaston Avenue, Dallas, TX 75246, USA.

Abstract

OBJECTIVE:

Previous studies have shown that dentin sialophosphoprotein (DSPP) is not only essential to the formation and mineralization of dentin but also plays an important role in forming and maintaining a healthy periodontium. Under physiological conditions, DSPP is proteolytically processed into the NH2-terminal and COOH-terminal fragments, and these fragments are believed to perform different functions in the mineralized tissues. Previous studies in our group have demonstrated that the NH2-terminal fragment of DSPP inhibits the formation and mineralization of dentin, while the role of this fragment in periodontium is unclear.

METHODS:

We analyzed the periodontal tissues of the transgenic mice overexpressing the NH2-terminal fragment of DSPP in the Dspp knockout background (referred to as "Dspp KO/DSP Tg" mice), in comparison with wild type mice and Dspp knockout mice. The approaches used in this study included histology, micro-computed tomography, back scattered scanning electron microscopy and resin-casted scanning electron microscopy.

RESULTS:

Dspp KO/DSP Tg mice exhibited a greater reduction of the alveolar bone, more remarkably altered canalicular systems around the osteocytes, less cementum, more radical migration of the epithelial attachment towards the apical direction, and more severe inflammation in molar furcation region, than in the Dspp knockout mice.

CONCLUSION:

Overexpressing the NH2-terminal fragment of DSPP worsened the periodontal defects in Dspp knockout mice, indicating that the NH2-terminal fragment of DSPP may exert an inhibitory role in the formation and mineralization of hard tissues in the periodontium.

KEYWORDS:

Bone biology; Cell biology; Cementum; Gene regulation; Periodontitis

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