Rivan Sidaly1, Steinar Risnes2, Qalb-E-Saleem Khan2, Tom Stiris3, Amer Sehic2. 1. Department of Biomaterials, Faculty of Dentistry, University of Oslo, Norway. Electronic address: rivan.sidaly@odont.uio.no. 2. Department of Oral Biology, Faculty of Dentistry, University of Oslo, Norway. 3. Department of Neonatology, Oslo University Hospital, Norway.
Abstract
OBJECTIVE: The permanently growing mouse incisors exhibit all stages of tooth development along their inciso-apical axis at any time. Any disturbance or injury of the ameloblasts during enamel formation or maturation may result in permanent defects in the finished enamel since the enamel does not undergo repair or remodeling after formation. In order to increase our understanding of how hypoxia affects enamel formation, we induced severe acute hypoxia in adult mice and observed its effects on the enamel in incisors. DESIGN: Incisors from hypoxic mice were obtained 5 and 49 days after the hypoxic insult. Hypoxic and control incisors were dissected out and observed by scanning electron microscopy (SEM). Incisors were subsequently ground longitudinally or transversely, etched, and observed again by SEM. The nature and position of defects were considered in relation to the configuration and dynamics of the incisors. RESULTS: The effect of hypoxia varied considerably, among mice, among incisors, and among ameloblasts. Affected enamel showed hypoplasia with hypomineralization or hypomineralization without hypoplasia. Vascular endothelial growth factor (VEGF) showed considerably stronger labeling in hypoxic compared to control ameloblasts. CONCLUSIONS: The present study demonstrates quantitative and qualitative defects in the enamel reflecting the vulnerability of ameloblasts toward severe acute hypoxia in mouse incisors.
OBJECTIVE: The permanently growing mouse incisors exhibit all stages of tooth development along their inciso-apical axis at any time. Any disturbance or injury of the ameloblasts during enamel formation or maturation may result in permanent defects in the finished enamel since the enamel does not undergo repair or remodeling after formation. In order to increase our understanding of how hypoxia affects enamel formation, we induced severe acute hypoxia in adult mice and observed its effects on the enamel in incisors. DESIGN: Incisors from hypoxicmice were obtained 5 and 49 days after the hypoxic insult. Hypoxic and control incisors were dissected out and observed by scanning electron microscopy (SEM). Incisors were subsequently ground longitudinally or transversely, etched, and observed again by SEM. The nature and position of defects were considered in relation to the configuration and dynamics of the incisors. RESULTS: The effect of hypoxia varied considerably, among mice, among incisors, and among ameloblasts. Affected enamel showed hypoplasia with hypomineralization or hypomineralization without hypoplasia. Vascular endothelial growth factor (VEGF) showed considerably stronger labeling in hypoxic compared to control ameloblasts. CONCLUSIONS: The present study demonstrates quantitative and qualitative defects in the enamel reflecting the vulnerability of ameloblasts toward severe acute hypoxia in mouse incisors.
Authors: Roshan Noor Mohamed; Sakeenabi Basha; Yousef Al-Thomali; Fatma Salem Al Zahrani; Amal Adnan Ashour; Ammar Saleh Al Shamrani; Nada Eid Almutair Journal: Ann Saudi Med Date: 2021-08-22 Impact factor: 1.526
Authors: Rivan Sidaly; Andreas Schmalfuss; Anne B Skaare; Amer Sehic; Tom Stiris; Ivar Espelid Journal: BMC Oral Health Date: 2016-07-22 Impact factor: 2.757