The open section effect in a long bone with a longitudinal defect - a theoretical modeling study.
A longitudinal defect dramatically alters the stress distribution within a long bone. The altered stress distribution can influence the structural properties of the bone and the stimulus for repair and remodeling of the defect and the surrounding bone. For applied torsion, the defect interrupts the normal shear flow around the bone. Reversal of the shear flow along the inner cortex of the bone is the primary characteristic of the "open-section" effect. Stress concentration effects also produce large stresses at the defect corners. A finite element model of a femur mid-diaphysis with a rectangular defect in the posterior cortex was developed to quantify the femur stress distribution and torsional stiffness for defect widths ranging from one-tenth of the femur outer diameter (0.1 OD) to 0.3 OD, and defect lengths ranging from 0.5 to 5 OD. Defects with a length of 1 OD or shorter had little influence on the femur torsional stiffness or the femur shear-stress distribution. The torsional stiffness decreased most dramatically as the defect length increased from 2 to 3 OD, but began to approach an asymptote near 5 OD. Shear flow reversal peaked at the center of the defect for defects longer than 1 OD, and the magnitude of the reversal began to approach an asymptote near 5 OD. For each defect, the largest stresses within the bone, developed at the defect corners. The results indicate that the open-section effect decreases the torsional stiffness and stress concentration effects decrease the torsional strength of a long bone with a longitudinal defect.
Orthopaedic Biomechanics Laboratory, Johns Hopkins University School of Medicine, 235 Ross Research Building, 720 Rutland Ave, Baltimore, MD 21205, USA.
J J
JJ
Elias
F J
FJ
Frassica
E Y
EY
Chao
D001696:Biomechanical Phenomena; D001842:Bone and Bones / Q000503:physiopathology* / Q000601:surgery*; D005269:Femur / Q000503:physiopathology / Q000601:surgery; D006801:Humans; D008954:Models, Biological; D013314:Stress, Mechanical