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].
Classifications of Fractures
Fracture classification systems have been developed in order to better direct treatment and prognostication and to provide information on biomechanical factors that promote fracture and therefore could be useful in prevention [170]. The topography, configuration and complexity of the fracture should be described in a thorough but concise manner. Fracture description should include the ‘what’, ‘where’ and ‘significance’ of the finding. For example, a typical fracture of the scapula in racehorses may be described as ‘a complete, displaced, closed, oblique fracture (what) at the level of the distal end of the spine (where), separating the bone into a large proximal fragment and a smaller distal fragment (significance)’ [170]. Features of fractures and qualifiers of features are provided in Table 3.2.
Fracture Topography
The bone involved and the location within the bone should be described as per Table 3.2. Fractures distal to the carpus/tarsus have a more favourable prognosis, primarily due to the capacity to supplement internal fixation with external coaptation [172], but are still associated with challenges including poor soft tissue coverage [173].
Physeal fractures generally occur in foals and yearlings, and may be classified according to the Salter–Harris type I–V scheme [174–176] (Figure 3.20). Physeal fractures are typically caused by a combination of compressive, shear and bending forces [176]. The proximal ulnar physis is not involved in the formation of a joint and is therefore termed an apophysis. The Salter–Harris classification system is therefore not completely applicable to fractures of the proximal ulnar physis, and a specific type 1–5 scheme is applied [178].
Table 3.1 Predictable sites of stress fractures and stress remodelling.
| Bone/joint | Anatomical region | References |
|---|---|---|
| Scapula | Distal aspect of the spine | [140] [145] |
| Humerus | Caudoproximal Craniodistal Medial diaphyseal Caudodistal | [146] [144, 147] [148, 149] |
| Carpus | Dorsomedial third carpal bone Radial carpal bone Intermediate carpal bone | [150] [151] [89] |
| Third metacarpal | Mid‐diaphyseal and supracondylar Parasagittal groove Proximal palmar Dorsal cortex Distal condyle | [152] [60] [153] [154] [69] [155] |