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Inactivation of Fam20C in cells expressing type I collagen causes periodontal disease in mice.

Liu P, Zhang H, Liu C, Wang X, Chen L, Qin C - PLoS ONE (2014)

Bottom Line: Previous studies have shown that FAM20C plays an essential role in the formation and mineralization of bone, dentin and enamel.The levels of bone sialoprotein, osteopontin, dentin matrix protein 1 and dentin sialoprotein were reduced in the Fam20C-deficient alveolar bone and/or cementum, while periostin and fibrillin-1 were decreased in the periodontal ligament of the cKO mice.The reduced levels of bone sialoprotein, osteopontin, dentin matrix protein 1, dentin sialoprotein, periostin and fibrillin-1 may contribute to the periodontal defects in the Fam20C-deficient mice.

View Article: PubMed Central - PubMed

Affiliation: Department of Periodontics, Harbin Medical University School of Stomatology, Harbin, Heilongjiang, 150001, China; Department of Biomedical Sciences and Center for Craniofacial Research and Diagnosis, Texas A&M University Baylor College of Dentistry, Dallas, Texas, 75246, United States of America.

ABSTRACT

Background: FAM20C is a kinase that phosphorylates secretory proteins. Previous studies have shown that FAM20C plays an essential role in the formation and mineralization of bone, dentin and enamel. The present study analyzed the loss-of-function effects of FAM20C on the health of mouse periodontal tissues.

Methods: By crossbreeding 2.3 kb Col 1a1-Cre mice with Fam20Cfl/fl mice, we created 2.3 kb Col 1a1-Cre;Fam20Cfl/fl (cKO) mice, in which Fam20C was inactivated in the cells that express Type I collagen. We analyzed the periodontal tissues in the cKO mice using X-ray radiography, histology, scanning electron microscopy and immunohistochemistry approaches.

Results: The cKO mice underwent a remarkable loss of alveolar bone and cementum, along with inflammation of the periodontal ligament and formation of periodontal pockets. The osteocytes and lacuno-canalicular networks in the alveolar bone of the cKO mice showed dramatic abnormalities. The levels of bone sialoprotein, osteopontin, dentin matrix protein 1 and dentin sialoprotein were reduced in the Fam20C-deficient alveolar bone and/or cementum, while periostin and fibrillin-1 were decreased in the periodontal ligament of the cKO mice.

Conclusion: Loss of Fam20C function leads to periodontal disease in mice. The reduced levels of bone sialoprotein, osteopontin, dentin matrix protein 1, dentin sialoprotein, periostin and fibrillin-1 may contribute to the periodontal defects in the Fam20C-deficient mice.

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Plain X-ray radiography analyses of 4-, 12- and 24-week-old mice.The mandibles dissected from the 4-, 12- and 24-week-old normal mice (images in the upper portion) and cKO mice (lower portion) were examined by X-ray radiography. At 4 weeks, the furcation region between the mesial and distal roots of the first mandibular molars in the cKO mice had apparent radiolucency compared with the same area of the normal mice (a, arrows). At 12 weeks, the interdental region between the first and second mandibular molars in the cKO mice revealed remarkable bone loss compared with the normal mice (b). At 24 weeks, alveolar bone in the furcation and interdental regions of the cKO mice showed dramatically lower radiopacity than the normal mice (c).
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pone-0114396-g001: Plain X-ray radiography analyses of 4-, 12- and 24-week-old mice.The mandibles dissected from the 4-, 12- and 24-week-old normal mice (images in the upper portion) and cKO mice (lower portion) were examined by X-ray radiography. At 4 weeks, the furcation region between the mesial and distal roots of the first mandibular molars in the cKO mice had apparent radiolucency compared with the same area of the normal mice (a, arrows). At 12 weeks, the interdental region between the first and second mandibular molars in the cKO mice revealed remarkable bone loss compared with the normal mice (b). At 24 weeks, alveolar bone in the furcation and interdental regions of the cKO mice showed dramatically lower radiopacity than the normal mice (c).

Mentions: At 4 weeks after birth, plain X-ray examinations showed radiolucency in the furcation region between the first and second mandibular molars of the cKO mice, while the height of the interdental alveolar bone appeared similar in the normal (control) and cKO mice (Figure 1a). At 12 weeks, the interdental region between the first and second mandibular molars in the cKO mice had remarkable bone loss compared with the normal mice (Figure 1b). At 24 weeks, very little alveolar bone remained in the interdental region, and the remaining alveolar bone in the cKO mice had a much lower radiopacity than the normal mice (Figure 1c).


Inactivation of Fam20C in cells expressing type I collagen causes periodontal disease in mice.

Liu P, Zhang H, Liu C, Wang X, Chen L, Qin C - PLoS ONE (2014)

Plain X-ray radiography analyses of 4-, 12- and 24-week-old mice.The mandibles dissected from the 4-, 12- and 24-week-old normal mice (images in the upper portion) and cKO mice (lower portion) were examined by X-ray radiography. At 4 weeks, the furcation region between the mesial and distal roots of the first mandibular molars in the cKO mice had apparent radiolucency compared with the same area of the normal mice (a, arrows). At 12 weeks, the interdental region between the first and second mandibular molars in the cKO mice revealed remarkable bone loss compared with the normal mice (b). At 24 weeks, alveolar bone in the furcation and interdental regions of the cKO mice showed dramatically lower radiopacity than the normal mice (c).
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4257665&req=5

pone-0114396-g001: Plain X-ray radiography analyses of 4-, 12- and 24-week-old mice.The mandibles dissected from the 4-, 12- and 24-week-old normal mice (images in the upper portion) and cKO mice (lower portion) were examined by X-ray radiography. At 4 weeks, the furcation region between the mesial and distal roots of the first mandibular molars in the cKO mice had apparent radiolucency compared with the same area of the normal mice (a, arrows). At 12 weeks, the interdental region between the first and second mandibular molars in the cKO mice revealed remarkable bone loss compared with the normal mice (b). At 24 weeks, alveolar bone in the furcation and interdental regions of the cKO mice showed dramatically lower radiopacity than the normal mice (c).
Mentions: At 4 weeks after birth, plain X-ray examinations showed radiolucency in the furcation region between the first and second mandibular molars of the cKO mice, while the height of the interdental alveolar bone appeared similar in the normal (control) and cKO mice (Figure 1a). At 12 weeks, the interdental region between the first and second mandibular molars in the cKO mice had remarkable bone loss compared with the normal mice (Figure 1b). At 24 weeks, very little alveolar bone remained in the interdental region, and the remaining alveolar bone in the cKO mice had a much lower radiopacity than the normal mice (Figure 1c).

Bottom Line: Previous studies have shown that FAM20C plays an essential role in the formation and mineralization of bone, dentin and enamel.The levels of bone sialoprotein, osteopontin, dentin matrix protein 1 and dentin sialoprotein were reduced in the Fam20C-deficient alveolar bone and/or cementum, while periostin and fibrillin-1 were decreased in the periodontal ligament of the cKO mice.The reduced levels of bone sialoprotein, osteopontin, dentin matrix protein 1, dentin sialoprotein, periostin and fibrillin-1 may contribute to the periodontal defects in the Fam20C-deficient mice.

View Article: PubMed Central - PubMed

Affiliation: Department of Periodontics, Harbin Medical University School of Stomatology, Harbin, Heilongjiang, 150001, China; Department of Biomedical Sciences and Center for Craniofacial Research and Diagnosis, Texas A&M University Baylor College of Dentistry, Dallas, Texas, 75246, United States of America.

ABSTRACT

Background: FAM20C is a kinase that phosphorylates secretory proteins. Previous studies have shown that FAM20C plays an essential role in the formation and mineralization of bone, dentin and enamel. The present study analyzed the loss-of-function effects of FAM20C on the health of mouse periodontal tissues.

Methods: By crossbreeding 2.3 kb Col 1a1-Cre mice with Fam20Cfl/fl mice, we created 2.3 kb Col 1a1-Cre;Fam20Cfl/fl (cKO) mice, in which Fam20C was inactivated in the cells that express Type I collagen. We analyzed the periodontal tissues in the cKO mice using X-ray radiography, histology, scanning electron microscopy and immunohistochemistry approaches.

Results: The cKO mice underwent a remarkable loss of alveolar bone and cementum, along with inflammation of the periodontal ligament and formation of periodontal pockets. The osteocytes and lacuno-canalicular networks in the alveolar bone of the cKO mice showed dramatic abnormalities. The levels of bone sialoprotein, osteopontin, dentin matrix protein 1 and dentin sialoprotein were reduced in the Fam20C-deficient alveolar bone and/or cementum, while periostin and fibrillin-1 were decreased in the periodontal ligament of the cKO mice.

Conclusion: Loss of Fam20C function leads to periodontal disease in mice. The reduced levels of bone sialoprotein, osteopontin, dentin matrix protein 1, dentin sialoprotein, periostin and fibrillin-1 may contribute to the periodontal defects in the Fam20C-deficient mice.

Show MeSH
Related in: MedlinePlus