title: Cybernetic aspects of bone modeling and remodeling, with special reference to osteoporosis and whole-bone strength.
abstract: Assume mythical physiologists were taught that renal physiology and its disorders depend on "kidney cells" and their regulation by nonmechanical factors, but were taught nothing about nephrons. For decades they "knew" that idea was correct, just as Ptolemy "knew" the universe centers on our planet. But then others began to describe nephrons, their roles in renal physiology and disorders, and problems they revealed in former views, so doubts and controversies began. Today real physiologists encounter a similar situation for bone health and its disorders. A 1960 paradigm attributed such things to bone's effector cells (osteoblasts and osteoclasts) and their regulation by nonmechanical factors, without "nephron-equivalent" or biomechanical input. But both mechanical and nonmechanical factors regulate bone's nephron equivalents. Adding features of those equivalents to the 1960 views led to the Utah paradigm, which suggests problems in former views and better explanations for "osteoporosis," whole-bone strength, and other bone disorders. Such things incited controversies among current skeletal physiologists. Cybernetics concerns the relationships, mechanisms, signals, and message traffic that help to control the behavior and other features of dynamic systems. A cybernetic analysis of the bone physiology in the Utah paradigm can add many features to the 1960 paradigm that help to understand osteoporoses, other bone disorders, and whole-bone strength (and bone mass). The added features also show new and pertinent targets for the related research.
authors.affiliation: Department of Orthopaedic Surgery, Southern Colorado Clinic, Pueblo 81008-9000, USA.
authors.forename: H M
authors.initials: HM
authors.lastname: Frost
mesh_terms: D001846:Bone Development / Q000502:physiology*; D016723:Bone Remodeling / Q000502:physiology*; D003491:Cybernetics; D005246:Feedback; D006801:Humans; D010024:Osteoporosis / Q000209:etiology / Q000503:physiopathology*