Bone is a dynamic tissue which, through the process of bone remodeling in the mature skeleton, renews itself during normal function and adapts to mechanical loads. It is, therefore, important to understand the effect of remodeling on the mechanical function of bone, as well as the effect of the inherent time lag in the remodeling process. In this study, we develop a constitutive model for bone remodeling which includes a number of relevant mechanical and biological processes and use this model to address differences in the remodeling behavior as a volume element of bone is placed in disuse or overload. The remodeling parameters exhibited damped oscillatory behavior as the element was placed in disuse, with the amplitude of the oscillations increasing as the severity of disuse increased. In overload situations, the remodeling parameters exhibited critically sensitive behavior for loads beyond a threshold value. These results bear some correspondence to experimental findings, suggesting that the model may be useful when examining the importance of transient responses for bone in disuse, and for investigating the role fatigue damage removal plays in preventing or causing stress fractures. In addition, the constitutive algorithm is currently being employed in finite element simulations of bone adaptation to predict important features of the internal structure of the normal femur, as well as to study bone diseases and their treatment.
Although most fractures heal, some fail to heal and become nonunions. Many animal models have been developed to study problems of fracture healing. The majority of nonunion models have involved segmental bone defects, but this may not adequately represent the biologic condition in which nonunions clinically develop. The objective of the present study is to develop a nonunion model that better simulates the clinical situation in which there is soft tissue damage including periosteal disruption and to compare this model to a standard closed fracture model utilizing identical fracture stabilization, providing a similar mechanical environment. A total of 96 three month old Long Evans rats were utilized. A 1.25 mm diameter K-wire was inserted into the femur in a retrograde fashion, and a mid-diaphyseal closed transverse fracture was created using a standard three-point bending device. To create a nonunion, 48 of the rats received additional surgery to the fractured femur. The fracture site was exposed and 2 mm of the periosteum was cauterized on each side of the fracture. Fracture healing was evaluated with serial radiographs every two weeks. Animals were maintained for intervals of two, four, six or eight weeks after surgery. Specimens from each time interval were subjected to bioniechanical and histological evaluation. None of the cauterized fractures healed throughout the eight weeks experimental duration. The radiographical appearance of nonunion models was atrophic. This investigation showed pronounced differences between the experimental nonunions and standard closed fractures both histologically and biomechanically. In conclusion, we have developed a reproducible atrophic nonunion model in the rat femur that simulates the clinical condition in which there is periosteal disruption but no bone defect.
An important concept in bone mechanics is that osteons influence mechanical properties in several ways, including contributing to toughness and fatigue strength by debonding from the interstitial matrix so as to "bridge" developing cracks. Observations of "pulled out" osteons on fracture surfaces are thought to be indicative of such behavior. We tested the hypothesis that osteon pullout varies with mode of loading (fatigue vs. monotonic), cortical region, elastic modulus, and fatigue life. Mid-diaphseal beams from the dorsal, medial, and lateral regions of the equine third metacarpal bone were fractured in four point bending by monotonic loading to failure under deflection control, with or without lo5 cycles of previous fatigue loading producing 5000 microstrain (15-20'%) of the expected failure strain) on the first cycle; or sinusoidal fatigue loading to failure, under load or deflection control, with the initial cycle producing 10,000 microstrain (3040% of the expected failure strain). Using scanning electron microscopy, percent fracture surface area exhibiting osteon pullout (%OP.Ar) was measured. Monotonically loaded specimens and the compression side of fatigue fracture surfaces exhibited no osteon pullout. In load-controlled fatigue, pullout was present on the tension side of fracture surfaces, was regionally dependent (occurring to a greater amount dorsally), and was correlated negatively with elastic modulus and positively with fatigue life. Regional variation in '%OP.Ar was also significant for the pooled (load and deflection controlled) fatigue specimens. '%)OP.Ar was nearly significantly greater in deflection controlled fatigue specimens than in load-controlled specimens (p = 0.059). The data suggest that tensile fatigue loading of cortical bone eventually introduces damage that results in osteonal debonding and pullout, which is also associated with increased fatigue life via mechanisms that are not yet clear.
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