Inhibition ofBoneMiatrix Formation, Mineralization, andResorption in Thyroparathyroidectomized Rats

ratsdeveloped hypocalcemia andanimpairment ofboneformation and mineralization. Thepresent studyofthyroparathyroidectomized (TPTX)ratswasundertaken todetermine theeffect ofhypocalcemia without secondary hyperparathyroidism. TPTX ratsfedanormaldietdeveloped hypocalcemia andhyperphosphatemia inassociation with impairment ofosteoblastic bonematrix formation andof mineralization ofnewlyformedmatrix. TheserumcalciumX phosphorus product wasnotdecreased. Thedecreased formation waslargely duetoa reduction in matrix apposition indicating decreased synthetic activity ofindividual osteoblasts. Incontrast totheabove results, whenTPTX ratswerefedahigh-calcium diet topreventhypocalcemia, noimpairment ofeither formation or mineralization wasfound. Fromtheresults ofthese two experiments, itisreasonably certain thathypocalcemia wasresponsible fortheinhibition offormation andmineralization. Moreover, basedonthemagnitude ofthe changes inserumcalcium andboneparameters inTPTX rats, hypocalcemia could haveaccounted fortheinhibition offormation andmineralization incalcium-deficient aswellasvitamin D-deficient rats. InTPTX ratsthemineralization defect wasmanifested bydecreases inboththerateofosteoid maturation(indicating adelayed onsetofmineralization) and therateofmineralization. A strongcorrelation (r= 0.95, P<0.001) wasobserved between these tworates suggesting a tight coupling ofthesetwo aspects of mineralization. TPTX ratsalsohadlowerboneresorption ratesand higher serumphosphorus levels thansham-operated aniA preliminary report ofthis workwaspublished inab-.