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Acidosis inhibits osteoblastic and stimulates osteoclastic activity in vitro
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1992
Year
Acidosis JcaCellular PhysiologyOsteoporosisOsteoarthritisOsteoclastic ActivityBone HomeostasisMetabolic SignalingMineral MetabolismHealth SciencesMolecular PhysiologyBiochemistryBone MetabolismEnergy MetabolismPhysiologyCollagen SynthesisMetabolic AcidosisCellular BiochemistryMetabolismMedicineExtracellular Matrix
Metabolic acidosis drives net calcium flux from cultured neonatal mouse calvariae via physicochemical and cell‑mediated mechanisms. The study aimed to determine how osteoblasts and osteoclasts contribute to acid‑induced calcium flux. Collagen synthesis and alkaline phosphatase activity were measured in calvariae under metabolic acidosis and compared with controls, while osteoclastic beta‑glucuronidase activity was assessed with and without calcitonin. Acidosis reduced collagen synthesis and alkaline phosphatase, increased beta‑glucuronidase, and the calcium flux correlated inversely with osteoblastic markers and directly with osteoclastic activity, indicating that inhibited osteoblasts and stimulated osteoclasts mediate the cell‑dependent component of calcium flux.
Metabolic acidosis induces net calcium flux (JCa) from cultured neonatal mouse calvariae through physicochemical and cell-mediated mechanisms. To determine the role of osteoblasts in acid-induced JCa, collagen synthesis and alkaline phosphatase activity were assessed in calvariae incubated in reduced pH and bicarbonate medium, a model of metabolic acidosis (Met), and compared with controls (Ctl). Collagen synthesis fell from 30.5 +/- 1.1 in Ctl to 25.1 +/- 0.4% with Met, and alkaline phosphatase decreased from 403 +/- 25 in Ctl to 298 +/- 21 nmol Pi.min-1.mg protein-1 with Met. During acidosis JCa was correlated inversely with percent collagen synthesis (r = -0.743, n = 11, P = 0.009) and with alkaline phosphatase activity (r = -0.453, n = 22, P = 0.034). To determine the role of osteoclasts in acid-induced JCa, osteoclastic beta-glucuronidase activity was determined in Ctl and Met in the absence or presence of the osteoclastic inhibitor calcitonin (CT, 3 x 10(-9) M). Met increased beta-glucuronidase (5.9 +/- 0.2) compared with Ctl (4.6 +/- 0.3 micrograms phenolphthalein released.bone-1.h-1), whereas CT inhibited beta-glucuronidase in both Ctl and Met (3.1 +/- 0.2 and 3.5 +/- 0.3, respectively). During acidosis JCa was correlated directly with beta-glucuronidase activity (r = 0.683, n = 42, P less than 0.001). Thus the cell-mediated component of JCa during acidosis in vitro appears to result from a combination of inhibited osteoblastic and stimulated osteoclastic activity.