Effects of osteoclastic resorption on bone surface ion composition

Abstract

Osteoclasts are responsible for resorption of bone mineral. To determine how osteoclasts alter bone surface ion composition, neonatal mouse bone cells were isolated and cultured in the presence of parathyroid hormone (PTH) on bovine cortical bone. Surface ion composition of the resulting osteoclastic resorption pits was compared with that of unresorbed bone, utilizing a high-resolution scanning ion microprobe. Cortical bone cultured with cells in the presence of PTH had numerous resorption pits. The unresorbed area adjacent to the pits had a ratio of surface 23Na/40Ca of 18.7 + 1.6 (mean counts per second of detected secondary ions +95% confidence interval) and 39K/40Ca of 2.3 + 2.2. At the base of the pits, the ratio of 23Na/40Ca was 1.0 + 2.0 and 39K/40Ca was 0.1 + 1.0 (each different from area adjacent to the pit, P < 0.001). The ratio of 23Na/39K in the unresorbed area was not different from that at the base of the pit. Thus osteoclasts induce a decrease in the ratio of surface ion composition of both 23Na/40Ca and 39K/40Ca but not 23Na/39K in bovine cortical bone. The elevated ratios of 23Na/40Ca and 39K/40Ca on the surface, but not at the base of the pits, indicate adsorption of medium ions onto the mineral. Because osteoclasts foster the release of bone Ca, these results indicate that osteoclastic resorption causes a greater, and approximately equal, release of both 23Na and 39K compared with 40Ca from bone mineral. Osteoclasts appear to remove nonselectively the surface mineral that had been exposed to the medium, uncovering underlying mineral.

Metabolic, but not respiratory, acidosis increases bone PGE2levels and calcium release

“…24-48 H. Although acid-induced calcium efflux during the first 24 h is due primarily to physicochemical calcium release (6,20,23,29,38), we have previously shown that calcium efflux in more prolonged incubations is due, primarily, to cell-mediated mechanisms (7,11,13,14,19,25,36,37,47,70). At the conclusion of the subsequent 24-h incubation, incubation in Met led to a marked increase in net calcium efflux (P Ͻ 0.001) and an increase in medium PGE 2 concentration (P Ͻ 0.001) compared with culture in Ntl (Fig.…”

Acid–Base Balance and Bone Health

“…Calvariae cultured in acidic medium exhibit proton-dependent net calcium efflux during both acute (3 h) and more chronic (>24-99 h) incubations [2,3,9,23,24,26,30,32,[69][70][71]. During acute incubations there was net calcium efflux from the calvariae when medium pH was decreased to less than the physiologic normal of 7.40 by decreasing the [HCO 3 − ], no net flux at a neutral physiologic pH and an influx of calcium into bone when pH was greater than 7.40 [24] (Fig.…”

“…The in vitro evidence for proton buffering by bone is derived from studies of acidosis-induced proton influx into bone [22][23][24] and microprobe evidence for a depletion of bone sodium and potassium during acidosis [25,26,30,31,89]. When calvariae are cultured in medium acidified by a decrease in the concentration of bicarbonate (metabolic acidosis), there is a net influx of protons into the bone, decreasing the medium proton concentration and indicating that the additional hydrogen ions are being buffered by bone [22][23][24] (Fig.…”

“…After incubation in acidic medium there is loss of surface sodium and potassium relative to calcium [25,26,30,31,89] in conjunction with buffering of the additional protons, suggesting sodium and potassium exchange for hydrogen ions on the bone surface resulting in a decrease in medium acidity [25,27,28]. When osteoclastic function is inhibited with calcitonin, microprobe analysis indicates that physicochemical proton buffering by bone causes relatively equal calcium and sodium loss [26].…”

“…Studies to date have shown that the calvarial surface is rich in sodium and potassium relative to calcium [25,26,30,31,[89][90][91][92]133]. The excess bone potassium is maintained through cell-mediated processes [91].…”