Читать книгу Fractures in the Horse - Группа авторов - Страница 141

Bone has a well‐organized architecture of mineral, organic matrix and cells that has developed and adapted for mechanical efficiency and dynamic response to change in loading. The aim of ‘scarless healing’ is to restore this organizational paradigm in order to optimize use: fortunately, bone has the capacity to fulfil this goal. Nonetheless, optimizing fracture healing in the horse presents many challenges, including the size and behavioural nature of the animal, the location and configuration of the fracture, the amount of soft tissue damage and the ultimate stability of the fracture and/or its repair. These features, in turn, affect the mechanical and physiological environments of the injury, which are the two factors with the greatest influence on healing. This chapter discusses the interactions of physiological and mechanical factors in bone healing together with the influence of stability on cellular function and pain and the influence of pain on cellular events. It describes molecular, cellular, tissue‐ and organ‐based factors significant to fracture healing in order to identify those processes that can optimize repair and those that can lead to derangements in healing. Finally, current evidence for the use of exogenous physical, pharmacological and biological techniques is reviewed.

Fracture healing is principally influenced by its nature, i.e. location, configuration, etc., and by its stability. The classic fracture types are characterized in Chapter 3. From a perspective of stability, the fracture classification has significance. Fractures occur either in normal bone that fails due to a catastrophic force (monotonic fractures) or in pathologic bone that fails from sub‐catastrophic forces (fatigue fractures). Monotonic fractures are acute in nature and caused by a force that overloads the material properties of the bone. These fractures are often in multiple pieces (comminuted) and accompanied by significant soft tissue and vascular damage. The fracture configuration is usually unpredictable. Instability can be significant, often requiring invasive repair techniques to restore mechanical support. Fatigue (stress) fractures are consistent in location and configuration and result at the end of a cumulative pathologic process in which coalescence of osteoclastic resorption of bone remodelling and/or microdamage produce a clinical fracture [1]. These can be minor or catastrophic, depending on the amount of energy accumulated at the time of bone failure, and resulting fracture configurations can be consistent or variable respectively. Incomplete fractures are usually stable since the fracture does not break out from a secondary site [1]. However, they can become complete without immediate coaptation and attention. Complete fracture can be displaced or non‐displaced; the latter being more stable [1]. Comminuted fractures are complex and can be composed of multiple pieces often with significant soft tissue and vascular damage, compromising both mechanical and physiological factors that favour healing [1]. Fracture configuration greatly influences the mechanical and physiological environments, which is reflected by the variable prognosis given for each type of configuration. The quality of fracture healing depends on a sensitive balance of physiological and mechanical factors that function in parallel through the healing phases to regenerate tissue. The mechanical environment can have a significant effect on physiologic response and vice versa.

Primary or direct bone healing occurs in a stable environment in which the fracture ends are directly and completely opposed to promote early vascular bridging and direct bone remodelling [2]. Classically, there is no intermediate step and bone heals without a scar. The process requires rigid stability, usually with internal fixation. In this situation, the bone ends are not only put in close proximity (reduced), but are also frequently compressed to eliminate any fracture gap. 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.