title: Tissue interaction is required for glenoid fossa development during temporomandibular joint formation.
abstract: The mammalian temporomandibular joint (TMJ) develops from two distinct mesenchymal condensations that grow toward each other and ossify through different mechanisms, with the glenoid fossa undergoing intramembranous ossification while the condyle being endochondral in origin. In this study, we used various genetically modified mouse models to investigate tissue interaction between the condyle and glenoid fossa during TMJ formation in mice. We report that either absence or dislocation of the condyle results in an arrested glenoid fossa development. In both cases, glenoid fossa development was initiated, but failed to sustain, and became regressed subsequently. However, condyle development appears to be independent upon the presence of the forming glenoid fossa. In addition, we show that substitution of condyle by Meckel's cartilage is able to sustain glenoid fossa development. These observations suggest that proper signals from the developing condyle or Meckel's cartilage are required to sustain the glenoid fossa development.
authors.affiliation: Department of Operative Dentistry and Endodontics, College of Stomatology, The Fourth Military Medical University, Xi'an, Shaanxi, P R China.
authors.forename: Ying
authors.initials: Y
authors.lastname: Wang
authors.forename: Chao
authors.initials: C
authors.lastname: Liu
authors.forename: Joseph
authors.initials: J
authors.lastname: Rohr
authors.forename: Hongbing
authors.initials: H
authors.lastname: Liu
authors.forename: Fenglei
authors.initials: F
authors.lastname: He
authors.forename: Jian
authors.initials: J
authors.lastname: Yu
authors.forename: Cheng
authors.initials: C
authors.lastname: Sun
authors.forename: Lu
authors.initials: L
authors.lastname: Li
authors.forename: Shuping
authors.initials: S
authors.lastname: Gu
authors.forename: YiPing
authors.initials: Y
authors.lastname: Chen
mesh_terms: D000818:Animals; D002356:Cartilage / Q000002:abnormalities / Q000196:embryology / Q000378:metabolism / Q000473:pathology; D002450:Cell Communication / Q000235:genetics / Q000502:physiology*; D050659:Core Binding Factor Alpha 1 Subunit / Q000235:genetics / Q000378:metabolism; D019465:Craniofacial Abnormalities / Q000235:genetics; D004622:Embryo, Mammalian; D020868:Gene Silencing; D061165:Glenoid Cavity / Q000196:embryology* / Q000254:growth & development; D008335:Mandibular Condyle / Q000196:embryology* / Q000254:growth & development; D051379:Mice; D008822:Mice, Transgenic; D009432:Neural Crest / Q000378:metabolism; D055758:SOX9 Transcription Factor / Q000235:genetics / Q000378:metabolism; D013704:Temporomandibular Joint / Q000196:embryology* / Q000254:growth & development
chemical_list: D050659:Core Binding Factor Alpha 1 Subunit; C493716:Runx2 protein, mouse; D055758:SOX9 Transcription Factor; C527933:Sox9 protein, mouse