title: Histochemical evidences on the chronological alterations of the hypertrophic zone of mandibular condylar cartilage.
abstract: The hypertrophic chondrocytes lack the ability to proliferate, thus permitting matrix mineralization as well as vascular invasion from the bone in both the mandibular condyle and the epiphyseal cartilage. This study attempted to verify whether the histological appearance of the hypertrophic chondrocytes is in a steady state during postnatal development of the mouse mandibular condyle. Type X collagen immunohistochemistry apparently distinguished the fibrous layer described previously as the "articular zone," "articular layer," and "resting zone" from the hypertrophic zone. Interestingly, the ratio of the type X collagen-positive hypertrophic zone in the entire condyle seemed higher in the early stages but decreased in the later stages. Some apparently compacted cells in the hypertrophic zone showed proliferating cell nuclear antigen (PCNA) immunoreaction, indicating the potential for cell proliferation at the early stages. As the mice matured, in contrast, they further enlarged and assumed typical features of hypertrophic chondrocytes. Apoptotic cells were also discernible in the hypertrophic zone at the early but not later stages. Consistent with morphological configurations of hypertrophic chondrocytes, immunoreactions for alkaline phosphatase, osteopontin, and type I collagen were prominent at the later stage, but not the early stage. Cartilaginous matrices demonstrated scattered patches of mineralization at the early stage, but increased in their volume and connectivity at the later stage. Thus, the spatial and temporal occurrence of these immunoreactions as well as apoptosis likely reflect the prematurity of hypertrophying cells at the early stage, and imply a physiological relevance during the early development of the mandibular condyles.
authors.affiliation: Division of Oral and Maxillofacial Surgery, Department of Oral Health Science, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
authors.forename: Kazi Sazzad
authors.initials: KS
authors.lastname: Hossain
authors.forename: Norio
authors.initials: N
authors.lastname: Amizuka
authors.forename: Nobuyki
authors.initials: N
authors.lastname: Ikeda
authors.forename: Kayoko
authors.initials: K
authors.lastname: Nozawa-Inoue
authors.forename: Akiko
authors.initials: A
authors.lastname: Suzuki
authors.forename: Minqi
authors.initials: M
authors.lastname: Li
authors.forename: Kiichi
authors.initials: K
authors.lastname: Takeuchi
authors.forename: Megumi
authors.initials: M
authors.lastname: Aita
authors.forename: Yoshiro
authors.initials: Y
authors.lastname: Kawano
authors.forename: Masaaki
authors.initials: M
authors.lastname: Hoshino
authors.forename: Kimimitsu
authors.initials: K
authors.lastname: Oda
authors.forename: Ritsuo
authors.initials: R
authors.lastname: Takagi
authors.forename: Takeyasu
authors.initials: T
authors.lastname: Maeda
mesh_terms: D000469:Alkaline Phosphatase / Q000032:analysis; D000818:Animals; D017209:Apoptosis; D002113:Calcification, Physiologic; D002356:Cartilage / Q000166:cytology* / Q000502:physiology / Q000648:ultrastructure*; D019902:Chondrocytes / Q000166:cytology* / Q000648:ultrastructure*; D024042:Collagen Type I / Q000032:analysis; D024121:Collagen Type X / Q000032:analysis; D006651:Histocytochemistry; D008335:Mandibular Condyle / Q000166:cytology* / Q000502:physiology / Q000648:ultrastructure*; D051379:Mice; D046529:Microscopy, Electron, Transmission; D009024:Morphogenesis; D053495:Osteopontin; D018809:Proliferating Cell Nuclear Antigen / Q000032:analysis; D012795:Sialoglycoproteins / Q000032:analysis; D013997:Time Factors
chemical_list: D024042:Collagen Type I; D024121:Collagen Type X; D018809:Proliferating Cell Nuclear Antigen; D012795:Sialoglycoproteins; C506896:Spp1 protein, mouse; D053495:Osteopontin; D000469:Alkaline Phosphatase