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The major physiological function of parathyroid hormone (PTH) is the maintenance of Ca2+/Pi homeostasis via the parathyroid hormone/parathyroid hormone-related protein receptor (PTHR) in kidney and bone. An important consequence of PTHR activation in bone is enhanced local acidification of the extracellular space. Agonist activation of some seven transmembrane-domain receptors increases the extracellular acidification rate (ECAR). We utilized microphysiometry to investigate PTH-stimulated, receptor-mediated increases in ECAR in human osteoblast-like SaOS-2 cells. PTH-(1-34) elicited a large, acute, dose-dependent increase in ECAR with an EC50 of about 2 nM. The PTH-induced increase in ECAR was specific to cells expressing the PTHR and was inhibited by PTHR antagonists. Rapid, partial, homologous desensitization of the PTH-induced increase in ECAR was observed. Incubation of SaOS-2 cells with 8-bromo-cyclic AMP neither mimicked nor abrogated the PTH effect, and PTH stimulated an acute increase in ECAR in cAMP-resistant SaOS-2 Ca#4A cells. Stimulation of ECAR by PTH was independent of transient increases in cytosolic free calcium. Both inhibition and down-regulation of PKC reduced the PTH-induced increase in ECAR. Inhibition of Na+/H+ exchange did not affect the PTH-induced ECAR response. We conclude that PTH caused a receptor-mediated, concentration-dependent, increase in ECAR, which was not dependent on the cAMP/PKA signaling pathway or the Na+/H+ exchanger but involved the action of PKC. Thus, acid production in bone, a physiologically important action of PTH, is not confined to osteoclasts as previously considered but is also mediated by osteoblasts.

This study compares the bond strength and durability of three metal surface treatments subjected to two types of environmental stress for both short- and long-term exposures. The luting resins Panavia and Comspan were applied to alumina-blasted, non-beryllium, nickel-chromium alloy coupons. Metal surface treatments consisted of either microscopic roughening by electrochemical etching, or one of two types of adhesives: a silanated silica coating (Silicoating) or a phosphate ester monomer (a component in the Panavia liquid). Shear bond strength was determined following short- or long-term exposure to either thermocycling in 6-60 degrees C water (2,672 cycles/7 days or 10,584 cycles/42 days) or storage in 37 degrees C water (7 or 42 days). Three-way ANOVA showed that both the type of environmental stress and the exposure time affected the bond strength of electroetched surfaces, but that only exposure time affected the two chemical adhesives (P0.05), regardless of the environmental stress used. In the short-term, the silica/silane coated surfaces produced and maintained the higher shear bond strengths (15.9 +/- 2.3 MPa). However, after 42 days the silica/silane bonds decreased 30% (to 11.3 +/- 2.2 MPa), while the phosphate ester bonds were essentially unchanged (11.4 +/- 3.0 at 4 days, 10.4 +/- 2.2 MPa at 42 days). Electroetched bonds were the weakest and decreased by 18% between 7 and 42 days in water (8.8 +/- 1.2 to 7.2 +/- 3.0 MPa) and 27% after 42 days of thermocycling (7.2 +/- 2.8 to 5.3 +/- 1.8 MPa).