Subject(s)
Cuspid/pathology , Tooth Eruption, Ectopic/therapy , Tooth Movement Techniques/methods , Tooth, Unerupted/therapy , Adolescent , Bicuspid/pathology , Child , Female , Humans , Incisor/pathology , Male , Mandible/pathology , Maxilla/pathology , Orthodontic Appliance Design , Orthodontic Brackets , Orthodontic Extrusion/instrumentation , Orthodontic Wires , Tooth Movement Techniques/instrumentationABSTRACT
OBJECTIVE: To investigate the time course of osteocyte death in a mouse model of orthodontic tooth movement (OTM) and its association to the caspase-3 activation pathway and osteoclast formation. MATERIALS AND METHODS: Twenty-five male wild type CD-1 mice (8-12 weeks old) were loaded with an orthodontic appliance. A spring delivering 10-12 g of force was placed between the right first molar and the incisor to displace the first molar mesially. The contralateral unloaded sides served as the control. The animals were equally divided into five different time points: 6, 12, 24, and 72 hours and 7 days of orthodontic loading. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay, caspase-3 immunostaining, and tartrate-resistant acid phosphatase (TRAP) staining was performed on histologic sections of the first molars. The labeling was quantified in osteocytes on the compression side of the alveolar bone at each time point. RESULTS: TUNEL labeling significantly increased at 12, 24, and 72 hours after orthodontic loading; the peak was observed at 24 hours. Elevated caspase-3 labeling was noted at 12, 24, and 72 hours and 7 days after loading, although the increase was not significant. Significant osteoclast formation was initially evident after 72 hours and progressively increased up to 7 days. CONCLUSIONS: Osteocyte death during OTM peaks at 24 hours, earlier than initial osteoclast activation. However, only a slight trend for increased caspase-3 activity suggests that other mechanisms might be involved in osteocyte death during OTM.
Subject(s)
Apoptosis/physiology , Osteocytes/pathology , Tooth Movement Techniques/methods , Acid Phosphatase/analysis , Alveolar Process/pathology , Animals , Biomechanical Phenomena , Caspase 3/analysis , Cell Count , Cell Death/physiology , Cell Differentiation/physiology , In Situ Nick-End Labeling , Isoenzymes/analysis , Male , Mice , Orthodontic Wires , Osteoclasts/pathology , Signal Transduction/physiology , Stress, Mechanical , Tartrate-Resistant Acid Phosphatase , Time Factors , Tooth Movement Techniques/instrumentationABSTRACT
Experiments were carried out to examine the effects of nitrogen source on nitrogen incorporation into cyanophycin during nitrogen limitation and repletion, both with or without inhibition of protein synthesis, in cyanobacteria grown on either nitrate or ammonium. The use of nitrate and ammonium, 14N labeled in the growth medium and 15N labeled in the repletion medium, allows the determination of the source of nitrogen in cyanophycin using proton nuclear magnetic resonance spectroscopy. The data suggest that nitrogen from both the breakdown of cellular protein (14N) and directly from the medium (15N) is incorporated into cyanophycin. Nitrogen is incorporated into cyanophycin at different rates and to different extents, depending on the source of nitrogen (ammonium or nitrate) and whether the cells are first starved for nitrogen. These differences appear to be related to the activity of nitrate reductase in cells and to the possible expression of cyanophycin synthetase during nitrogen starvation.
