Removal of osteoclast bone resorption products by transcytosis.

Osteoclasts are multinucleated cells responsible for bone resorption. During the resorption cycle, osteoclasts undergo dramatic changes in their polarity, and resorbing cells reveal four functionally and structurally different membrane domains. Bone degradation products, both organic and inorganic, were endocytosed from the ruffled border membrane. They were then found to be transported in vesicles through the cell to the plasma membrane domain, located in the middle of the basal membrane, where they were liberated into the extracellular space. These results explain how resorbing osteoclasts can simultaneously remove large amounts of matrix degradation products and penetrate into bone.

[1]  J. Salo,et al.  Bone-resorbing osteoclasts reveal a dynamic division of basal plasma membrane into two different domains. , 1996, Journal of cell science.

[2]  M Horton,et al.  The osteoclast clear zone is a specialized cell-extracellular matrix adhesion structure. , 1995, Journal of cell science.

[3]  L. Golub,et al.  Modulation of Bone Resorption by Tetracyclines a , 1994, Annals of the New York Academy of Sciences.

[4]  T. Yoneda,et al.  Osteopetrosis in Src-deficient mice is due to an autonomous defect of osteoclasts. , 1993, Proceedings of the National Academy of Sciences of the United States of America.

[5]  K. Väänänen,et al.  Kinetics of the osteoclast cytoskeleton during the resorption cycle in vitro , 1991, Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research.

[6]  Allan Bradley,et al.  Targeted disruption of the c-src proto-oncogene leads to osteopetrosis in mice , 1991, Cell.

[7]  B. Gomperts,et al.  Changes in the state of actin during the exocytotic reaction of permeabilized rat mast cells , 1990, The Journal of cell biology.

[8]  J. Tuukkanen,et al.  Evidence for the presence of a proton pump of the vacuolar H(+)-ATPase type in the ruffled borders of osteoclasts , 1990, The Journal of cell biology.

[9]  S. Nishikawa,et al.  The murine mutation osteopetrosis is in the coding region of the macrophage colony stimulating factor gene , 1990, Nature.

[10]  S. Teitelbaum,et al.  Osteoclastic bone resorption by a polarized vacuolar proton pump. , 1989, Science.

[11]  I A Silver,et al.  Microelectrode studies on the acid microenvironment beneath adherent macrophages and osteoclasts. , 1988, Experimental cell research.

[12]  A. Boyde,et al.  Early scanning electron microscopic studies of hard tissue resorption: their relation to current concepts reviewed. , 1987, Scanning microscopy.

[13]  A. Boyde,et al.  Resorption of dentine by isolated osteoclasts in vitro , 1984, British Dental Journal.

[14]  P. Revell,et al.  Resorption of bone by isolated rabbit osteoclasts. , 1984, Journal of cell science.

[15]  D. Hewett‐Emmett,et al.  Carbonic anhydrase II deficiency identified as the primary defect in the autosomal recessive syndrome of osteopetrosis with renal tubular acidosis and cerebral calcification. , 1983, Proceedings of the National Academy of Sciences of the United States of America.

[16]  M. Holtrop,et al.  The Ultrastructure of the Osteoclast and its Functional Implications , 1977, Clinical orthopaedics and related research.

[17]  S. Q. Cohlan,et al.  Growth Inhibition of Prematures Receiving Tetracycline: A Clinical and Laboratory Investigation of Tetracycline-Induced Bone Fluorescence , 1963 .

[18]  H. Frost POSTMENOPAUSAL OSTEOPOROSIS: A DISTURBANCE IN OSTEOCLASIA * , 1961, Journal of the American Geriatrics Society.