Perforation of cancellous bone trabeculae by damage-stimulated remodelling at resorption pits: a computational analysis.
Loss of trabeculae in cancellous bone is often attributed to a general decline in the bone mass leading to fracture of the thin trabeculae. It has never been investigated whether trabecular perforation may have any other biomechanical mechanism. In this paper, an alternative hypothesis is proposed and tested using a computational model. Taking it as given that osteoclastic resorption is targeted to microdamage, it is hypothesised that the creation of a resorption cavity during normal bone remodelling could cause a stress-concentration in the bone tissue. If the resorption cavities were excessively deep, as is seen during osteoporosis, then this stress concentration may be sufficient to generate more microdamage so that osteoclasts "chase" newly formed damage leading to perforation. If this were true then we should find that, for a given trabecular thickness, there is a critical depth of resorption cavity such that smaller cavities refill whereas deeper cavities cause microdamage accumulation, continued osteoclast activity, and eventual trabecular perforation. Computer simulation is used to test this hypothesis. Using a remodelling stimulus calculated from both strain and damage and a simplified finite element model of a trabeculum with cavities of different sizes, it is predicted that such a critical depth of resorption cavity does indeed exist. Therefore we suggest that an increase in resorption depth relative to the thickness of trabeculae may be responsible for trabecular perforation during osteoporosis, rather than simply trabecular fracture due to insufficient strength.
McNamara
Laoise M
LM
Center for Bioengineeing, Deparment of Mechanical Engineering, Trinity College, Dublin, Ireland.
Prendergast
Patrick J
PJ
D000465:Algorithms; D001696:Biomechanical Phenomena; D015519:Bone Density; D001854:Bone Marrow Cells / Q000166:cytology; D016723:Bone Remodeling; D001862:Bone Resorption; D001842:Bone and Bones / Q000033:anatomy & histology / Q000378:metabolism / Q000473:pathology*; D019295:Computational Biology; D003198:Computer Simulation; D020342:Finite Element Analysis; D017102:Fracture Healing; D015775:Fractures, Stress; D006801:Humans; D015233:Models, Statistical; D010010:Osteoclasts / Q000166:cytology; D010024:Osteoporosis / Q000473:pathology; D012984:Software; D013696:Temperature