Stability also provides pain relief that in turn creates a favourable environment for the horse's other limbs. Although direct healing is typically described for cortical bone, the same principles apply to subchondral compacta with the goal of precise articular reconstruction and normalization of joint homeostasis. Primary bone healing is the ultimate goal for the surgeon. Primary or direct bone healing is further classified by fracture gap size and interfragmentary strain. Contact healing occurs when the fracture gap is less than 0.01 mm and the interfragmentary strain is less than 2% [3]. In this situation, osteoclasts at the ends of the osteons closest to the fracture ends establish cutting cones that cross the fracture, creating continuous cavities that residing osteoblasts fill with osteoid. This simultaneously re‐establishes bone union and an intact Haversian system without callus formation [4]. Gap healing is similar but lacks simultaneous establishment of healing and Haversian system reformation. Gap healing occurs in defects less than 1 mm in size. Lamellar bone is initially deposited perpendicular to the long axis of the bone by vascularized osteons over three to eight weeks, creating matrix in which secondary remodelling can occur [3].

      Secondary or indirect healing occurs in an environment in which there is micromotion (from instability) or a gap between the bone ends [2]. It results when precise apposition and/or rigid fixation are not completely achieved. The classic phases of fracture healing, including progression from haematoma to creation of soft callus, formation of hard callus and ultimately bone remodelling, follow in sequential order as mechanical stability increases. Further in the chapter, secondary healing is used as a model to explain the physiologic progression of bone healing.

      In reality, many fractures have a combination of primary and secondary healing [2]. Although most fracture repairs appear clinically stable, they are all likely to have some areas of imperfect apposition in which secondary healing occurs. In equine fracture repair, gap healing can occur either throughout an entire fracture or within parts of the repair as precise anatomic alignment and absolute mechanical stability are often impossible. This is an important principle as micromotion can produce significant stress on, and ultimately result in, failure of implants.

      Appropriately stabilized fractures heal with primary, a combination of primary and secondary or secondary healing. However, over‐stabilized (which almost never happens in horses) and under‐stabilized repairs (which is more common in horses) can lead to derangements in healing [5]. Over‐stabilized repairs, which can occur in man and small animals, remove mechanical strain that is needed to stimulate a healing cascade in the fracture environment. Reduced strain leads to a poor physiologic response and tissue atrophy.

      Derangements in fracture healing may be produced by all and any influencing factors. These are broadly classified as delayed, non‐ and mal‐unions. Delayed union occurs when the repair process is slower than normal. Non‐union occurs when the fracture fails to heal radiographically [6]. There are several types of non‐union fracture characteristics that reflect the individual processes that negatively affect healing. Mal‐union occurs when the fracture heals with abnormal fragment orientation.

Phases of Bone Healing

      The classic stages of bone healing have been known for decades and provided the guiding principles for fracture repair. However, it has become apparent that these are not finite and that individual fractures are likely to exhibit variations in the intensity and duration of each stage. For any type of tissue to heal, there are several basic requirements. Progenitor cells must migrate into the damaged area either from local or systemic sources [7, 8]. Extracellular matrix needs to be produced by local clotting factors, clotting cascades and progenitor cell production [2]. Growth factors are necessary to induce differentiation of progenitor cells into the desired cell type that may be vascular, chondrocytic, osteoclastic or osteoblastic [2]. Adequate blood supply is also necessary to provide appropriate oxygen tension, nutrients and, specifically for bone, minerals [2]. The coordination of these events impacts the quality of healing and resulting function.

In the haematoma/inflammatory phase (Figure 6.1a), a clotting cascade and inflammatory/immune factors are released to stimulate fibrin formation and cell signalling of progenitor cells [9]. In the soft callus phase (Figure 6.1b), chondrocyte proliferation and intramembranous woven bone formation occur due, at least in part, to relative local hypoxia and/or continued motion [10]. Once vascularity to the area is restored, ossification will follow, resulting in hard callus formation by both intramembranous bone production and endochondral ossification [11, 12] (Figure 6.1c). As these phases progress, mineralization and expansion of the callus produce more rigid stability and pain is likely to be reduced. Bone remodelling (Figure 6.1d) follows the hard callus phase and completes healing [10]. The stages are interdependent and overlap throughout. The classic staging of bone healing provides a guide and working template for consideration of potentially beneficial interventions. For the equine surgeon, establishing stability and comfort are key to success.

Information, principally from other species, has demonstrated that the molecular, cellular and tissue‐based mechanisms involved in fracture repair are not only complex, but also well synchronized in order to optimize the tissue environment for bone healing. Equine surgeons have become better at fracture repair (mostly through improved stabilization techniques), recognizing factors that influence healing and identifying problems early. Not all common practices favour fracture healing. As new medications become available, surgeons and researchers can better predict their influence on fracture healing and can use this information to develop strategies to enhance primary repair and to manage complex or failed repairs.

      

Figure 6.1 The process of secondary bone healing is a coordinated cascade of biological and mechanical influences leading to progression of bone union. (a) Haematoma/inflammatory phase.

      Source: Modified from Walters et al. [9].

      (b) Soft callus phase.

      Source: Based on Sathyendra and Darowish [10].

      (c) Hard callus phase.

      Source: Based on Aro and Chao [11]; Kwong and Harris [12].

      (d) Remodelling phase.

      Source: Based on Sathyendra and Darowish [10].

      In considering the physiological environment of fracture healing, both the condition of the bone and the surrounding soft tissues must be taken into account. In the majority of animals, the most common cause of fracture is an acute traumatic episode in which either external or internal forces lead to bone failure. However, in the equine athlete, there is strong evidence to show that many fractures occur within pathologic bone [13, 14], and its influence on bone healing must be taken into consideration. It is expected that healing of compromised bone is not the same as normal bone. The influence of the individual problem (vitality, remodelling, demineralization, hypermineralization, osteopenia, etc.) and treatment on prognosis requires consideration.

Cellular and Humeral Influences on Bone Healing

      The goal of this section is to introduce the basic building blocks for understanding the processes of bone healing. This includes an understanding of the importance of vascularity, the role of inflammatory cells and the immune complex within the healing