Читать книгу Fractures in the Horse - Группа авторов - Страница 142

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.