Osteocytes, strain detection, bone modeling and remodeling.

Abstract

One of the characteristic features of mammalian and avian bone is a population of live cells of the osteoblast lineage distributed both on the surface and throughout the matrix. These cells communicate with one another via gap junctions. A number of roles have been proposed for both osteocytes and the lacunar/canalicular labyrinth they occupy. These include arrest of fatigue cracks, mineral exchange, osteocytic osteolysis, renewed remodeling activity after release by resorption, stimulation, and guidance of osteoclastic cutting cones involved in mineral exchange and the repair of microdamage, strain detection, and the control of mechanically related bone modeling/remodeling. The question of whether osteocytes control or influence modeling and remodeling is of major importance. Such influence could be crucial in relation to three importance consequences of remodeling activity: calcium regulation, microdamage repair, and mechanically adaptive control of bone architecture. Mechanically adaptive control of bone architecture requires feedback concerning the relationship between current loading and existing architecture. This feedback is most probably derived from the strain in the matrix. The arrangement of the osteocyte network seems ideally suited to both perceive strain throughout the matrix and to influence adaptive modeling and remodeling in a strain-related manner. The hypothesis that osteocytes perform this role has growing experimental support.