title: Osteoclast-derived activity in the coupling of bone formation to resorption.
abstract: The cells of bone and the immune system communicate by means of soluble and membrane-bound cytokines and growth factors. Through local signalling mechanisms, cells of the osteoblast lineage control the formation and activity of osteoclasts and, therefore, the resorption of bone. Both T and B lymphocytes produce activators and inhibitors of osteoclast formation. A local 'coupling factor' linking bone resorption to subsequent formation in the bone multicellular unit (BMU) has long been proposed as the key regulator of the bone remodelling process, but never identified. There is evidence in support of the view that the coupling mechanism is dependent on growth factors released from the bone matrix during resorption, or is generated from maturing osteoblasts. We argue that osteoclasts contribute in important ways to the transiently activated osteoclast, and stimulate osteoblast lineage cells to begin replacing the resorbed bone in each BMU.
authors.affiliation: St. Vincent's Institute of Medical Research, 9 Princes Street, Fitzroy, Victoria 3065, Australia. jmartin@sci.edu.au
authors.forename: T John
authors.initials: TJ
authors.lastname: Martin
authors.forename: Natalie A
authors.initials: NA
authors.lastname: Sims
mesh_terms: D000818:Animals; D016723:Bone Remodeling / Q000502:physiology*; D001862:Bone Resorption / Q000378:metabolism* / Q000628:therapy; D002450:Cell Communication; D006801:Humans; D051379:Mice; D010010:Osteoclasts / Q000502:physiology*; D010012:Osteogenesis / Q000502:physiology*; D010281:Parathyroid Hormone / Q000494:pharmacology / Q000502:physiology; D018003:Receptors, Calcitonin / Q000235:genetics / Q000502:physiology
chemical_list: D010281:Parathyroid Hormone; D018003:Receptors, Calcitonin