TY - JOUR
T1 - The role of osteogenic index octahedral shear stress and dilational stress in the ossification of a fracture callus
AU - Gardner, Trevor
AU - Mishra, S
AU - Marks, L
PY - 2004/1/1
Y1 - 2004/1/1
N2 - The exact mechanism by which mechanical stimulus regulates the healing process of a bone fracture is not understood. This has led to the development of several hypotheses that predict the pattern of differentiation of tissue during healing that may arise from characteristic fields of stress or strain at the fracture. These have so far remained unproved because data on stress fields in actual fracture tissue have been unavailable until recently. Thus the present study examines the predictive performance of the hypothesis proposed in J Orthop Res 6 (1988) 736, against measured and calculated data reported in J Biomech 33 (2000) 415, using a 2D FEM of a clinical fracture. The hypothesis was used to predict the influence of stress fields present in the Gardner et al. tissues at four temporal stages during healing. These predictions were then correlated with callus-size, rate of endochondral ossification and ossification pattern subsequently observed by Gardner et al. in the clinical fracture. Results corroborate the hypothesis that high octahedral shear stresses may increase the size of the callus during the initial phase of healing, and they also suggest that this may be true during the later stages of the fracture fixation period. However, compressive dilatational stresses were not found to inhibit endochondral ossification, as suggested by the hypothesis. Although high shear stresses were found in regions indicative of fibrous tissue as postulated by the hypothesis, this was not found to be the case for high tensile dilatational stresses. Also, contour diagrams of Osteogenic index (I) indicated only limited correlation with callus maturation and the pattern of healing. Therefore, the hypothesis was not wholly successful in predicting healing pattern. (C) 2004 IPEM. Published by Elsevier Ltd. All right reserved.
AB - The exact mechanism by which mechanical stimulus regulates the healing process of a bone fracture is not understood. This has led to the development of several hypotheses that predict the pattern of differentiation of tissue during healing that may arise from characteristic fields of stress or strain at the fracture. These have so far remained unproved because data on stress fields in actual fracture tissue have been unavailable until recently. Thus the present study examines the predictive performance of the hypothesis proposed in J Orthop Res 6 (1988) 736, against measured and calculated data reported in J Biomech 33 (2000) 415, using a 2D FEM of a clinical fracture. The hypothesis was used to predict the influence of stress fields present in the Gardner et al. tissues at four temporal stages during healing. These predictions were then correlated with callus-size, rate of endochondral ossification and ossification pattern subsequently observed by Gardner et al. in the clinical fracture. Results corroborate the hypothesis that high octahedral shear stresses may increase the size of the callus during the initial phase of healing, and they also suggest that this may be true during the later stages of the fracture fixation period. However, compressive dilatational stresses were not found to inhibit endochondral ossification, as suggested by the hypothesis. Although high shear stresses were found in regions indicative of fibrous tissue as postulated by the hypothesis, this was not found to be the case for high tensile dilatational stresses. Also, contour diagrams of Osteogenic index (I) indicated only limited correlation with callus maturation and the pattern of healing. Therefore, the hypothesis was not wholly successful in predicting healing pattern. (C) 2004 IPEM. Published by Elsevier Ltd. All right reserved.
UR - http://www.scopus.com/inward/record.url?scp=3242660119&partnerID=8YFLogxK
U2 - 10.1016/j.medengphy.2004.03.009
DO - 10.1016/j.medengphy.2004.03.009
M3 - Article
C2 - 15234685
VL - 26
SP - 493
EP - 501
JO - Medical Engineering & Physics
JF - Medical Engineering & Physics
IS - 6
ER -