title: Trabecular architecture can remain intact for both disuse and overload enhanced resorption characteristics.
abstract: The paradigm that bone metabolic processes are controlled by osteocyte signals have been the subject of investigation in many recent studies. One hypothesis is that osteoblast formation is enhanced by these signals, and that osteoclast resorption is enhanced by the lack of them. Reduced, or absent, osteocyte signaling can be an effect of reduced mechanical loading (disuse) or of defects in the canalicular network, due to microcracks. This would mean that bone is resorbed precisely there where it is mostly needed. In our study, we addressed this apparent contradiction. The purpose was to investigate how alternative strain-based local stimuli for osteoclasts to resorb bone would affect remodeling and adaptation of the trabecular architecture. For this purpose, a computer-simulation model was used, which couples morphological and mechanical effects of local bone metabolism to changes in trabecular architecture and density at large. Six resorption characteristics were studied in the model: (I) resorption occurs spatially random, (II) resorption is enhanced or (III) strongly enhanced where there is disuse, (IV) resorption is enhanced or (V) strongly enhanced where there are high strains, i.e. overload, and (VI) resorption is enhanced where there is disuse and where there are high strains. Results showed that the rates of structural adaptation to alternative loading were higher for disuse-controlled resorption than for overload-controlled resorption. Architecture and mass remained stable for all cases except (V) in which the structure deteriorated as in osteoporotic bone. We conclude that, given the potential of osteoblasts to form bone in highly strained areas, based on signals from osteocytes, osteoclast resorption can normally be compensated for.
authors.affiliation: Orthopaedic Research Laboratory, Radboud University Nijmegen Medical Center, P.O. Box 9101, 6500 HB Nijmegen, The Netherlands. e.tanck@orthop.umcn.nl
authors.forename: E
authors.initials: E
authors.lastname: Tanck
authors.forename: R
authors.initials: R
authors.lastname: Ruimerman
authors.forename: R
authors.initials: R
authors.lastname: Huiskes
mesh_terms: D000222:Adaptation, Physiological / Q000502:physiology; D000465:Algorithms; D000818:Animals; D015519:Bone Density / Q000502:physiology; D001857:Bone Matrix / Q000033:anatomy & histology / Q000378:metabolism*; D016723:Bone Remodeling / Q000502:physiology*; D001862:Bone Resorption / Q000378:metabolism*; D003198:Computer Simulation; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D040542:Mechanotransduction, Cellular / Q000502:physiology; D008954:Models, Biological; D010006:Osteoblasts / Q000502:physiology; D010010:Osteoclasts / Q000502:physiology; D010011:Osteocytes / Q000502:physiology; D016474:Weight-Bearing / Q000502:physiology*