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Fractures can occur as a result of a single extreme load or smaller repeated loads. A monotonic fracture occurs when a single extreme load deforms the bone beyond its ultimate limit, resulting in complete and sudden failure [85]. Examples include a fall over a fence during jump racing or cross country, or an accident during recovery from general anaesthesia [85, 86]. Stress fractures are the result of repetitive loads, caused by a few repetitions of a high load or by multiple repetitions of lower loads. The vast majority of bone injuries in racehorses are due to repeated high‐intensity loading, which results in weakening of the bone and subsequent failure [85,87–89].

Experimentally, loading conditions are simulated by monotonic (single cycle to failure or quasi‐static tests) and cyclic loading. Materials that fail from repeated cyclic loading are typically viewed as failing secondary to fatigue [90]. The ‘fatigue life’ refers to the number of load cycles that can be sustained at a given load before catastrophic failure occurs [87]. The in vitro fatigue life of bone is related to the magnitude of the applied load as well as the geometry and material properties of the loaded structure [85, 87]. The fatigue life can be deduced from the S–N curve that depicts the relationship between the applied stress (S) and the number of loading cycles before failure (N) (Figure 3.17). At high loads, a relatively low number of cycles will induce failure, whereas at lower loads the bone endures a greater number of cycles before failure. The fatigue limit of a material is the stress level at which the material can endure an infinite number of loading cycles without failure. The fatigue limit can be determined from the stress plateau in the S–N curve. When loaded below the stress plateau, the material has infinite fatigue life. Bone does not exhibit a fatigue limit [10,91–93]; however, an endurance limit has been characterized for bone, which is defined as the stress amplitude at which the material can sustain a defined number of cycles [94, 95].

Figure 3.17 An idealized S–N curve for cortical bone illustrates the relationship between load magnitude (stress) and cycles to failure. Larger loads have a disproportionately larger effect on reducing fatigue life than smaller loads.

Source: Modified from Kawcak et al. [89].

Cyclic loading of bone results in formation of cracks at micro‐ and ultrastructural levels [96]. Most cracks stop enlarging after reaching a certain length because cracks interact with microstructural features that retard their propagation [97]. This observation is supported by studies that have demonstrated an increase in crack density but not length, with continued loading [2, 98, 99]. However, excessive accumulation of microdamage reduces bone stiffness and ultimate strength, increasing the risk of catastrophic fracture [85, 92, 100].

Paradoxically, the process of microcrack formation can also increase resistance to crack propagation (toughness) and catastrophic failure [85]. Energy is released when the bone material yields, marking the onset of plastic deformation. If the amount of energy released is less than the energy required to form the initial crack, the damage will arrest. Otherwise, the crack will continue to spread, and more cracks will form [99, 101]. The stable (subcritical) cracking that precedes outright fracture is best characterized by the rising resistance curve (R‐curve), where fracture resistance actually increases with crack extension [28, 102, 103]. Rising R‐curve behaviour has been reported in equine bone under static and dynamic loading conditions [26, 104] (Figure 3.18).

Figure 3.18 Example of a rising R‐curve (K_R vs. crack length) for transverse crack growth in a third metacarpal specimen from a horse. K_R: crack growth resistance; K₀: crack growth initiation toughness; K_peak: peak stress intensity factor; and a₀: initial crack length.

Source: Based on Yeni and Norman [105].

Rising R‐curve behaviour is predominantly the result of extrinsic toughening mechanisms including crack bridging by uncracked ligaments and intact collagen fibrils, crack deflection along the cement lines and microcracking in the crack wake, which redistributes stress from the tip [105–110] (Figure 3.19). These mechanisms depend on specific microstructural features, which in turn vary with orientation [113]. The marked anisotropy in fracture toughness, in that bone is easier to split than break, can be related to the relative contributions of these mechanisms [114]. Lower toughness is observed in the longitudinal orientation where cracks can propagate along cement lines, which provide a path of relatively low resistance. Crack bridging appears to be the prominent source of toughening in the longitudinal orientation [114]. Crack bridging refers to unbroken regions that span the crack in the wake of the crack tip and act to resist crack opening [109]. The highest toughness is observed in the transverse orientation, where cracks encounter osteonal boundaries. Crack deflection around cement lines is the extrinsic mechanism that increases toughness most substantially in the transverse orientation [113]. The degree to which bone can employ microcracking and other extrinsic toughening mechanisms to disperse energy ultimately determines the brittleness or toughness of the specimen [115].

Pre‐existing fatigue damage reduces the capacity of compact bone to exploit microcracking to reduce stress intensity at the crack tip [116]. This is because a significant proportion of available microcrack ‘sites’ are used up [117]. There is also the risk that beyond a certain density of microcracks, the risk of catastrophic fracture increases [118]. Reduced stiffness of bone secondary to fatigue damage exacerbates the risk of fracture because there is increased deformation of the bone in response to a given load [91, 100, 118, 119]. in vitro, multiplication and coalescence of microcracks under continued stress results in the eventual formation of a macroscopic fissure and potentially catastrophic failure [120].

Figure 3.19 Schematic illustrations of some toughening mechanisms possible in cortical bone. (a) Crack deflection by osteons, (b) crack bridging by collagen fibres, (c) uncracked ligament bridging and (d) diffuse microcracking.

Source: Ritchie [102]; Ager et al. [111]; Launey et al. [112].

The bones of racehorses in training are subjected to high loads, resulting in a relatively high risk of damage until bone stiffness is increased through adaptive mechanisms [85]. Adaptive modelling refers to changes in bone shape and internal structure in response to mechanical forces placed on the bone, according to Wolff’s law [121]. New bone formation in response to repeated loading improves biomechanical properties and increases fatigue life [122–126]. An excellent example of adaptation to load is the increase in cortical thickness and bone volume fraction in the metacarpal bones of Thoroughbred racehorses in response to training [127–129].

The acquisition of damage with cyclic loading alone may not be sufficient to result in complete fracture in living horses [130]. Living bone not only has the ability to change its shape and volume to reflect the mechanical loads it must support (modelling) but can also replace damaged or fatigued bone with new bone (remodelling). Remodelling involves resorption of bone by osteoclasts and replacement by osteoblasts in a highly orchestrated and controlled series of events. Remodelling has an important role in enhancing the fatigue life of bone by replacing material that has accumulated microdamage with new, healthy tissue [131]. The extent of fatigue damage at any one time is a balance between the rate of accumulation of microdamage and the rate of repair [85, 132].

Microcrack formation plays a role in initiating the remodelling process [133, 134]. Damaged bone can be resorbed rapidly; however, bone deposition takes longer. Remodelling to remove fatigued bone increases porosity during the initial phase of bone resorption, and this decreases stiffness [135]. A focus of damage that initiates intense remodelling can induce transient focal osteopenia and predispose to the development of a clinical fracture [135]. Sites of transient osteopenia include stress fractures and subchondral stress remodelling. The majority of catastrophic fractures in racehorses are secondary to pre‐existing stress fractures or subchondral bone stress remodelling [136–140].

Criteria for the identification of stress fractures in Thoroughbred racehorses have been determined from epidemiological and histopathological studies. As previously summarized [85] these include:

1 Absence of specific trauma, but association with repetitive, high strain loading (e.g. intense race training) [69, 141].

2 A high degree of morphologic consistency and tendency to occur in certain predilection sites [142–144]. Common sites for stress remodelling and stress fractures in Thoroughbred racehorses are presented in Table 3.1.

3 Microdamage is chronic and occurs on a progressive scale. There is often long‐standing pathology at the fracture margins, and incomplete fractures are regularly identified at the same locations where complete fractures commonly occur [19, 143,167–169].