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Journal of Dental Research, Vol. 87, No. 7,
624-629 (2008)
DOI: 10.1177/154405910808700708
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
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Figure 1. Dmp1 null mice develop early periodontal breakdown. (A) Histological pictures of interproximal areas between the first and second lower molars at different stages (3 wks, 3 and 6 mos). At 3 wks of age, the periodontal attachment is intact in the Dmp1 null mice. At 3 mos, the alveolar bone defect becomes evident, accompanied by detachment between the PDL and cementum, compared with the healthy periodontal tissue in WT control mice. At 6 mos, the periodontal defect becomes more severe in the KO mice. (B) Quantitative analyses of alveolar bone width and alveolar bone area between the first and second molars from ages of 3 wks to 3 mos, showing decreases with age. +/+, WT; –/–, KO; n = 5; *P < 0.05; **P < 0.01, data represent mean ± SD.(AQ)
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Figure 2. Dmp1 null mice have defective alveolar bone. (A) Representative radiographs of mandibles from three-week-, three-month-, and six-month-old mice (WT in upper panels, and KO in lower panels). The porous alveolar bone in the null animals is evident by the ages of 3 and 6 mos (arrows). (B) Representative micro-CT reconstructions of mandibles from 12-month-old animals. Note that there is severe bone loss in KO mice.
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Figure 3. Elevated proteoglycan expression and defective lacuno-canalicular morphology in Dmp1 null alveolar bone. (A) Immunostaining for biglycan and decorin on sections of alveolar bones from three-week- and three-month-old animals (WT in the upper panels, and KO in the lower panels). The increased staining of biglycan and decorin is evident (white asterisks). (B) SEM images of resin-infiltrated, acid-etched alveolar bone from three-week-old WT (left panels) and KO mice (right panels). Osteocyte lacunae were filled with resin, and the mineral was removed by 37% phosphoric acid and 5% sodium hypochlorite. The smooth canalicular walls from a representative lacuna are indicated with red arrows (lower left panel), while rough canalicular walls from a lacuna in KO bone are indicated by arrowheads (lower right panel). Note that the WT osteocyte lacuno-canalicular system is evenly distributed, but the KO osteocyte lacuno-canalicular system is disorganized, and lacunae are clustered. There is also a large amount of osteoid present in the matrix.
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Figure 4. Cementum and PDL in the Dmp1 null mouse are malformed. (A) H&E staining of section containing cementum, cementoblasts, PDL. The cuboidal cementoblasts aligned along the surface of the cementum in the WT (left panel), as indicated by the red arrows, are absent in the KO (right panel). Note that the cells in the WT PDL are mixed, with few spindle-like shapes (left panel), whereas the majority of the KO PDL cells are spindle-shaped (right panel). (B) Immunostaining of a one-month-old mandible for DMP1. Brown signal for DMP1 immunostaining in the acellular layer is indicated by a red arrowhead, and in the cellular layer by a red arrow. (C) Immunostaining with polyclonal antibodies against biglycan and decorin in cellular cementum. The increased expression of biglycan and decorin in KO cellular cementum is indicated by white asterisks in both ages of 3 wks and 3 mos.
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