Calcium transport in dentinogenesis. An experimental study in the rat incisor odontoblast.
Since cellular calcium transport mechanisms during biological calcification are less known, a series of experiments were performed by in vivo as well as in vitro methodologies in the dentinogenically active rat incisor. By means of micro-electrode technique, the pH and pCa (calcium ion activity) in predentin in situ were found to be 7.0 and 2.9, respectively. It was concluded that there exists a Ca2+ion concentrating mechanism over the odontoblast layer in direction towards the mineralization front. The kinetics of this calcium flow was determined in vivo by radiotracer technique. The time for 45Ca2+ uptake into the dentin mineral phase was determined to 10-15 min. Transmembraneous Ca2+ ion pumps and channels in odontoblasts were further analyzed. The resting membrane potential of rat incisor odontoblasts was determined to -24 mV. Using ion-specific mini-electrode technique as well as fluorescence spectrophotometry, calcium channels, Ca(2+)-ATPase and Na+/Ca2+ antiports, responsible for cellular Ca2+ uptake and extrusion, were identified in the odontoblast plasma membrane. Dissected odontoblasts were subjected to subcellular fractionation. An electrophoretic uniporter and a Na2+/Ca2+ exchanger, for Ca2+ release and uptake, respectively, were demonstrated in mitochondria, whereas a Ca(2+)-ATPase was present in the microsomal fraction. Mitochondria, microsomes and whole, digitonin-permeabilized odontoblasts, were able to maintain a steady state Ca2+ activity at pCa = 6.4-6.6 in vitro. In rats treated with colchicine, the incorporation of 45Ca2+ into dentin mineral was severely altered. Similarly, administration to rats of specific calcium channel blockers strongly inhibited 45Ca2+ incorporation. Together, the results indicate that a transcellular pathway is a major route for Ca2+ ion transport during dentinogenesis, and that this may be under a relatively strict cellular control.
Lundgren
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Department of Oral Biochemistry, University of Göteborg, Sweden.
D000818:Animals; D001692:Biological Transport; D002113:Calcification, Physiologic / Q000502:physiology; D002118:Calcium / Q000493:pharmacokinetics*; D015220:Calcium Channels / Q000378:metabolism; D002132:Calcium Radioisotopes; D000252:Calcium-Transporting ATPases / Q000378:metabolism; D002462:Cell Membrane / Q000378:metabolism; D003078:Colchicine / Q000494:pharmacology; D003804:Dentin / Q000378:metabolism; D003810:Dentinogenesis / Q000502:physiology*; D005260:Female; D006863:Hydrogen-Ion Concentration; D007180:Incisor; D017136:Ion Transport; D008297:Male; D008839:Microelectrodes; D008861:Microsomes / Q000378:metabolism; D008870:Microtubules / Q000378:metabolism; D008928:Mitochondria / Q000378:metabolism; D009804:Odontoblasts / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013050:Spectrometry, Fluorescence
D015220:Calcium Channels; D002132:Calcium Radioisotopes; D000252:Calcium-Transporting ATPases; D003078:Colchicine; D002118:Calcium