Objective　To investigate whether the osteocyte apoptosis exists in orbital bones and to discuss its effect on the orbital development.Methods　Seven young Newzealand white rabbits were selected as experimental animals.At two-month-old ,all rabbits were killed and then zygomas were made into paraffin and electron microscope sections after they were decalcified.Apoptosis of osteocytes was observed by light microscope and transmission electron microscopes and detected by TUNEL staining.Results　The classical apoptosis of osteocytes was found under light and transmission electron microscopes.Apoptosis of osteocytes was diffused irregularly in the zygomatic tissue.　Conclusion　Osteocyte can apoptosis and it may participate in the development of the bony orbit.

Elevated oxidative stress (OS) during aging leads to bone loss. OS increases intracellular Ca2+ ([Ca2+]i), resulting in cellular damage and death. We show earlier that Cx43 hemichannels open in response to OS, which serves as a protective mechanism for osteocytes. However, the underlying mechanism is unknown. Here, we found that treatment with H2O2 increased [Ca2+]i in osteocytes with [Ca2+]i being primarily derived from an extracellular Ca2+source. Hemichannel opening induced by OS was inhibited by the depletion of [Ca2+]i with BAPTA-AM, a Ca2+chelator, suggesting that [Ca2+]i influenced the activity of Cx43 hemichannels. Conversely, blockade of hemichannels had no effect on [Ca2+]i. A biotinylation assay showed that cell surface-expressed Cx43 was increased by OS, which could be inhibited by BAPTA-AM, suggesting that [Ca2+]i is necessary for Cx43 migration to the cell surface in response to OS. Together, these data suggest that increased hemichannel activity induced by OS was likely to be caused by elevated [Ca2+]i through increased Cx43 on the cell surface.