CORTICAL BONE FRACTURE R. O. RITCHIE University of California Berkeley, California J. H. KINNEY Lawrence Livermore National Laboratory Livermore, California J. J. KRUZIC Oregon State University Corvallis, Oregon R. K. NALLA Intel Corporation Chandler, Arizona 1. INTRODUCTION The structural integrity of ‘‘hard’’ mineralized tissues such as bone is of great importance, especially because bone is the primary structural component of the body, serving as a protective load-bearing skeletal framework. As a structural material, bone is unique when compared with other engineering materials because of its well- known capacity for self-repair and adaptation to changes in mechanical usage patterns (e.g., see Refs. 1–5). Unfor- tunately, bone mass decreases with aging; furthermore, elevation in bone turnover, concurrent with menopause in aging women, can lead to osteoporosis, a condition of low bone mass associated with an increased risk of fracture. However, low bone mass is not the sole reason why bone becomes more prone to fracture with age; indeed, the re- cent realization that bone mineral density alone cannot explain the therapeutic benefits of antiresorptive agents in treating osteoporosis (6,7) has re-emphasized the ne- cessity for understanding how other factors control bone fracture. Much of this renewed emphasis is currently be- ing focused on ‘‘bone quality,’’ where quality is a term used to describe some, as yet not clearly known, characteristics of the tissue that influence a broad spectrum of mechan- ical properties such as elastic modulus, strength, and toughness. Although there have been many studies on how such mechanical properties vary with age, disease, and changes in microstructure (8–30), there still remains much to be determined about how variations within the hierarchical microstructure of bone alter the fracture properties. The underlying microstructure of cortical bone is quite complex. The basic building blocks, namely an organic matrix (90% type-I collagen, 10% amorphous ground sub- stance) and mineral phase (calcium phosphate-based hydroxyapatite), are similar for all collagen-based miner- alized tissues, although the ratio of these components and the complexity of the structures they form varies with the function of the particular tissue and the organ it forms. The composition and the structure of bone are not invari- ant; they vary with factors such as skeletal site, age, sex, physiological function, and mechanical loading, making bone a very heterogeneous structure. On average, how- ever, the organic/mineral ratio in human cortical bone is roughly 1:1 by volume and 1:3 by weight. The hierarchical structure of bone (14,16,31) can be considered at several dimensional scales (14). At nano- scale dimensions, bone is composed of type-I mineralized collagen fibers (up to 15 mm in length and 50–70 nm in di- ameter) bound and impregnated with carbonated apatite nanocrystals (tens of nm in length and width, 2–3 nm in thickness) (14). These fibers are further organized at mi- crostructural length-scales into a lamellar structure with adjacent lamellae being 3–7 mm thick (16). Threaded throughout this lamellar structure are the secondary ost- eons (31) (up to 200–300 mm diameter), large vascular channels (up to 50–90 mm diameter) oriented roughly along the longitudinal direction of the bone and sur- rounded by circumferential lamellar rings, with so-called ‘‘cement lines’’ at the outer boundary. Critical for developing a realistic framework for frac- ture risk assessment is an understanding of the impor- tance of bone’s microstructural hierarchies on its mechanical properties. Indeed, the difficulty in under- standing the mechanisms of fracture in bone clearly lies in determining the role that the underlying microstruc- tural constituents and morphology play in crack initiation, subsequent crack propagation and final unstable fracture, and in separating their effects on the critical fracture events. It is the intent of this chapter to describe how fracture mechanics, along with various characterization techniques, have been used to begin developing such a mechanistic framework for the fracture behavior of corti- cal bone, and, where possible, to relate the specific tough- ening mechanisms to the underlying nature of the microstructure. The initial focus will be directed to the large body of early literature that addressed these issues by measuring ‘‘single-value’’ fracture toughness behavior, using such parameters as the work of fracture, W f , the critical stress-intensity factor, K c , or the critical strain-en- ergy release rate, G c . Secondly, more recent results that address the fact that cracking in bone involves rising frac- ture resistance with crack extension will be discussed, in light of the salient mechanisms involved. Finally, the topic of time-dependent damage and fracture is described in terms of the specific mechanisms involved. 2. SINGLE-VALUE TOUGHNESS MEASUREMENTS 2.1. Fracture Mechanics One method that is used to characterize the toughness of materials uses the work of fracture, W f , which is obtained by dividing the area under the load-displacement curve measured during the toughness test by twice the nominal crack-surface area. This approach has been used for cor- tical bone to quantify the toughness of nominally ‘‘flaw- free’’ specimens (8,11,17,25,26,32) but suffers because re- sults can be both specimen size- and geometry-dependent. Consequently, work of fracture results generally are not useful for comparing values determined in different stud- ies that used different sample geometries, but may be used successfully to assess trends when the nominal sample size and geometry are held constant. 1 Wiley Encyclopedia of Biomedical Engineering, Copyright & 2006 John Wiley & Sons, Inc.