title: Inactivation of Fam20C in cells expressing type I collagen causes periodontal disease in mice.
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.
  
  
  CONCLUSIONS
  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.
authors.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.
authors.forename: Peihong
authors.initials: P
authors.lastname: Liu
authors.affiliation: 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.
authors.forename: Hua
authors.initials: H
authors.lastname: Zhang
authors.affiliation: 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.
authors.forename: Chao
authors.initials: C
authors.lastname: Liu
authors.affiliation: 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.
authors.forename: Xiaofang
authors.initials: X
authors.lastname: Wang
authors.affiliation: Longjiang Scholar Laboratory, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, 150001, China.
authors.forename: Li
authors.initials: L
authors.lastname: Chen
authors.affiliation: 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.
authors.forename: Chunlin
authors.initials: C
authors.lastname: Qin
mesh_terms: D016301:Alveolar Bone Loss / Q000000981:diagnostic imaging / Q000235:genetics / Q000378:metabolism; D000818:Animals; D000943:Antigens, Differentiation / Q000096:biosynthesis* / Q000235:genetics; D002135:Calcium-Binding Proteins; D024042:Collagen Type I / Q000096:biosynthesis* / Q000235:genetics; D000090602:Collagen Type I, alpha 1 Chain; D016326:Extracellular Matrix Proteins; D051379:Mice; D018345:Mice, Knockout; D010011:Osteocytes / Q000378:metabolism* / Q000473:pathology; D011859:Radiography
chemical_list: D000943:Antigens, Differentiation; D002135:Calcium-Binding Proteins; D024042:Collagen Type I; D000090602:Collagen Type I, alpha 1 Chain; D016326:Extracellular Matrix Proteins; C509696:FAM20C protein, mouse