This Article Figures Only Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Add to Saved Citations Download to citation manager Request Permissions Request Reprints Add to My Marked Citations Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Citing Articles via Scopus Google Scholar Articles by Lerner, U. H. Search for Related Content PubMed PubMed Citation Social Bookmarking                         What's this?

NEW MOLECULES IN THE TUMOR NECROSIS FACTOR LIGAND AND RECEPTOR SUPERFAMILIES WITH IMPORTANCE FOR PHYSIOLOGICAL AND PATHOLOGICAL BONE RESORPTION

Department of Oral Cell Biology, Umeå University, 901 87 Umeå, Sweden; ulf.lerner{at}odont.umu.se

Osteoclasts are tissue-specific polykaryon bone-resorbing cells derived from the monocyte/macrophage hematopoietic lineage with specialized functions required for the adhesion of the cells to bone and the subsequent polarization of the cell membrane, secretion of acid to dissolve mineral crystals, and release of proteolytic enzymes to degrade the extracellular matrix proteins. Most pathological conditions in the skeleton lead to loss of bone due to excess osteoclastic bone resorption, including periodontal disease, rheumatoid arthritis, and osteoporosis. In rare cases, most of them genetic, patients with osteopetrosis exhibit sclerotic bone due either to a lack of osteoclasts or to non-functional osteoclasts. Mainly because of phenotypic findings in genetically manipulated mice or due to spontaneous mutations in humans, mice, and rats, several genes have been discovered as being crucial for osteoclast formation and activation. Recent breakthroughs in our understanding of osteoclast biology have revealed the critical roles in osteoclast differentiation played by RANKL, RANK, and OPG, three novel members of the tumor necrosis factor ligand and receptor superfamilies. The further study of these molecules and downstream signaling events are likely to provide a molecular basis for the development of new drugs for the treatment of diseases with excess or deficient osteoclastic bone resorption.

Key Words: RANKL • OPG • osteoclasts • periodontal disease • osteopetrosis • osteoporosis

Critical Reviews in Oral Biology & Medicine, Vol. 15, No. 2, 64-81 (2004)
DOI: 10.1177/154411130401500202


CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter    What's this?

This article has been cited by other articles:

				H. H. Conaway, E. Persson, M. Halen, S. Granholm, O. Svensson, U. Pettersson, A. Lie, and U. H. Lerner Retinoids inhibit differentiation of hematopoetic osteoclast progenitors FASEB J, October 1, 2009; 23(10): 3526 - 3538. [Abstract] [Full Text] [PDF]

				J. C. Earp, D. C. DuBois, D. S. Molano, N. A. Pyszczynski, C. E. Keller, R. R. Almon, and W. J. Jusko Modeling Corticosteroid Effects in a Rat Model of Rheumatoid Arthritis I: Mechanistic Disease Progression Model for the Time Course of Collagen-Induced Arthritis in Lewis Rats J. Pharmacol. Exp. Ther., August 1, 2008; 326(2): 532 - 545. [Abstract] [Full Text] [PDF]

				U.H. Lerner Bone Remodeling in Post-menopausal Osteoporosis Journal of Dental Research, July 1, 2006; 85(7): 584 - 595. [Abstract] [Full Text] [PDF]

				U.H. Lerner Inflammation-induced Bone Remodeling in Periodontal Disease and the Influence of Post-menopausal Osteoporosis Journal of Dental Research, July 1, 2006; 85(7): 596 - 607. [Abstract] [Full Text] [PDF]

				C. Swanson, M. Lorentzon, H. H. Conaway, and U. H. Lerner Glucocorticoid Regulation of Osteoclast Differentiation and Expression of Receptor Activator of Nuclear Factor-{kappa}B (NF-{kappa}B) Ligand, Osteoprotegerin, and Receptor Activator of NF-{kappa}B in Mouse Calvarial Bones Endocrinology, July 1, 2006; 147(7): 3613 - 3622. [Abstract] [Full Text] [PDF]

				H. Zheng, X. Yu, P. Collin-Osdoby, and P. Osdoby RANKL Stimulates Inducible Nitric-oxide Synthase Expression and Nitric Oxide Production in Developing Osteoclasts: AN AUTOCRINE NEGATIVE FEEDBACK MECHANISM TRIGGERED BY RANKL-INDUCED INTERFERON-beta VIA NF-{kappa}B THAT RESTRAINS OSTEOCLASTOGENESIS AND BONE RESORPTION J. Biol. Chem., June 9, 2006; 281(23): 15809 - 15820. [Abstract] [Full Text] [PDF]

				P. Palmqvist, P. Lundberg, E. Persson, A. Johansson, I. Lundgren, A. Lie, H. H. Conaway, and U. H. Lerner Inhibition of Hormone and Cytokine-stimulated Osteoclastogenesis and Bone Resorption by Interleukin-4 and Interleukin-13 Is Associated with Increased Osteoprotegerin and Decreased RANKL and RANK in a STAT6-dependent Pathway J. Biol. Chem., February 3, 2006; 281(5): 2414 - 2429. [Abstract] [Full Text] [PDF]

				G. N. Belibasakis, A. Johansson, Y. Wang, C. Chen, S. Kalfas, and U. H. Lerner The Cytolethal Distending Toxin Induces Receptor Activator of NF-{kappa}B Ligand Expression in Human Gingival Fibroblasts and Periodontal Ligament Cells Infect. Immun., January 1, 2005; 73(1): 342 - 351. [Abstract] [Full Text] [PDF]

				P. Kelk, R. Claesson, L. Hanstrom, U. H. Lerner, S. Kalfas, and A. Johansson Abundant Secretion of Bioactive Interleukin-1{beta} by Human Macrophages Induced by Actinobacillus actinomycetemcomitans Leukotoxin Infect. Immun., January 1, 2005; 73(1): 453 - 458. [Abstract] [Full Text] [PDF]