Microdamage and osteocyte-lacuna strain in bone: a microstructural finite element analysis.
Damage accumulation in living tissues occurs when the rate of damage formation is greater than the rate of damage repair. For very large increases in the loading rate of bones, this can result in "stress fractures" due to the growth and coalescence of fatigue related microdamage. At lower increases of loading rates, the damage accumulation process is halted because there is time for adaptive bone-remodeling to occur in response to the new load. However, it is not known if there is a relationship between microdamage and bone remodeling per se. One hypothesis for the control of bone remodeling is that osteocytes sense strains and mediate osteoblastic and osteoclastic activity. The purpose of this study was to investigate whether damage generates strains which may trigger bone remodeling. If this were true, then accumulative damage would cause adaptive bone remodeling. This study applies the methods of finite element analysis to determine the effect of observed damage mechanisms on the proposed sensors of remodeling in Haversian bone. Individual lamellae are modeled and osteocyte-lacunae are included in a generalized plane strain geometric representation. It is predicted that microdamage alters the local deformation behavior around lacunae, and that the changes increase as microdamage accumulates. Hence, if damage accumulates in a bone, it could be sensed as a change in strain at a microstructural level. The results give theoretical support to the experimental studies that have shown a correlation between microdamage and the initiation of resorption as a first step in bone remodeling.
Prendergast
P J
PJ
Institute of Orthopaedics, University of Nijmegen, The Netherlands.
Huiskes
R
R
D016723:Bone Remodeling / Q000502:physiology*; D003094:Collagen / Q000032:analysis; D004548:Elasticity; D006253:Haversian System / Q000473:pathology* / Q000503:physiopathology; D006801:Humans; D008954:Models, Biological; D010011:Osteocytes / Q000473:pathology*; D013314:Stress, Mechanical; D013312:Stress, Physiological / Q000473:pathology* / Q000503:physiopathology; D016474:Weight-Bearing / Q000502:physiology
D003094:Collagen