2 Lucas A. Smolders and Franck Forterre From a biomechanical viewpoint, the intervertebral disc (IVD) can be regarded as a water-filled cushion that mediates and transmits compressive forces between vertebral bodies and provides mobility as well as stability to the spinal segment [1–4]. The IVD functions in relation to the ligamentous apparatus of the spine, which consists of the interspinal, interarcuate, dorsal longitudinal, and ventral longitudinal ligaments and the annulus fibrosus of the IVD. The healthy IVD exerts a high swelling pressure, which accounts for the separation of contiguous vertebrae. The separation of adjacent vertebrae creates constant tension on the spinal ligaments, preventing uncontrolled displacements that would cause stress peaks of the vertebrae. Therefore, the IVD creates the necessary tension for optimal functionality and stability of the ligamentous apparatus of the spine [4]. The healthy IVD is composed of three distinct components: the nucleus pulposus (NP), annulus fibrosus (AF), and cartilaginous end plates (EPs). Each component exhibits specialized physical–mechanical properties and specific biomechanical functions. The collaboration of these individual structures results in optimal biomechanical function of the IVD. The healthy NP is composed of approximately 80% water. This high water content results in a high intradiscal swelling pressure that allows the NP to serve as a hydraulic cushion transmitting compressive forces while providing spinal mobility and stability [1–3, 5–9]. The NP is surrounded ventrally, dorsally, and laterally by the AF, with the ventral part of the AF being 2–3 times thicker than the dorsal part [10–12]. The fibers of the AF provide reinforcement when the IVD is twisted (axial rotation), bent (flexion/extension), and/or compressed (axial compression), with the inner and outer AF mainly resisting compressive and tensile forces, respectively [5, 6, 8]. The AF contains the NP, preserving its internal swelling pressure and protecting it against shearing [5, 6, 8, 13]. The cranial and caudal borders of the IVD are formed by the cartilaginous EPs, situated between the disc and the epiphyses of the respective cranial and caudal vertebral bodies [5, 11, 14]. The EPs are partially deformable due to their high water content (50–80%) and serve to contain the NP during loading of the spine [15]. All in all, this IVD can be viewed as an inflated tire, with the NP providing intradiscal pressure and resistance to compressive loads, the AF coping with tensile forces, and the partially deformable EP containing the NP. Owing to the specialized conformation of these structurally and functionally divergent entities, the IVD concurrently provides mobility and stability to compressive, tensile, and shear stresses applied to the spine [2, 5, 6, 8]. Degeneration of the IVD is the fundamental process that lies at the root of most IVD displacements. Due to this degeneration, the NP loses the ability to absorb and maintain water and thereby to function as a hydraulic cushion [16–20]. Consequently, more of the compressive load bearing, which is normally resisted by the hydrated NP, is transmitted to the AF [21–23]. This results in a compensatory increase in functional size of the AF [21, 24–26]. However, the AF is not built to resist compressive forces, and the increase in functional size consists of biomechanically inferior matrix [17–19, 25]. As a result, the AF becomes stiffer and weaker leading to structural failure that impedes the ability of the AF to resist tensile forces and to contain the NP. Eventually, these degenerative changes result in outward bulging of the IVD when subjected to physiological loading [16]. In addition, structural failure of the AF can result in annular defects or tears, through which degenerated NP material can extrude and which further compromise the function of the IVD [12, 16]. In essence, the degenerated IVD functions as a flat tire, being unable to cope with physiological loading, with consequent displacement of the IVD. Since the dorsal AF is 2–3 times thinner than the ventral AF, the dorsal side is usually where the AF shows structural failure and IVD displacement. In addition to structural failure of the NP and AF with consequent disc displacement, degeneration of the NP and AF results in an uneven distribution of load onto the EP, making the EP more susceptible to damage [27]. Although the EPs are deformable when axially loaded, they are a weak link within the IVD [13]. Degeneration of the IVD can cause cracks in the EP [28–30]. The degenerated NP can displace through these EP defects, which is referred to as a Schmorl’s node [31]. Although displacement of the IVD is commonly the result of IVD degeneration, displacement can also occur as a result of strenuous exercise or trauma. This type of IVD displacement involves abrupt extrusion of nondegenerated NP material through the dorsal or dorsolateral AF and is referred to as acute noncompressive nucleus pulposus extrusion [12, 32–34] (see Chapter 13). The biomechanical alterations involved in degeneration of the IVD can occur in any dog. However, when speaking of actual herniation of the IVD, a clear distinction can be made between chondrodystrophoid (CD) and nonchondrodystrophoid (NCD) dogs. Chondrodystrophoid and NCD dogs display significant differences in the character, age of onset, prevalence, and spinal location of IVD displacement. Due to these distinct differences, it is conceivable that the etiological factors for IVD displacement are different between these two groups of dogs. Chondrodystrophoid dog breeds are characterized by an accelerated form of IVD degeneration [12]. Consequently, the NP abruptly loses its hydraulic function, with consequent degenerative changes in the AF [12]. This predisposes to explosive herniations of the IVD, with complete rupture of the AF and dorsal longitudinal ligament, and extrusion of the NP into the vertebral canal [12]. These disc displacements are referred to as Hansen type I IVD herniations [12, 35–37]. Another remarkable feature of CD dogs is that IVD degeneration occurs throughout the entire vertebral column [12, 38, 39]. Therefore, biomechanical factors inherent to individual spinal levels seem to be of less importance to IVD degeneration in CD dogs. At first impression, a logical biomechanical factor in CD dogs may be the disproportion between the length of the spine and the length of the legs. However, there is no correlation between a relatively long spine and IVD degeneration in these dogs [12, 28]. Moreover, CD dogs with a relatively shorter spine, a larger height at the withers, and a large pelvic circumference are at higher risk for IVD herniation [29]. In CD dogs, all IVDs show signs of degeneration at an early age; therefore, a genetic component linked to the CD trait causing aberrant synthesis of the NP extracellular matrix appears to be the main etiological factor [12, 30, 38, 40]. However, causative factors for the high susceptibility of IVD herniation at certain spinal levels (cervical and thoracolumbar spine) in CD dogs are still unclear. It has been proposed that the transition from the rigid, thoracic spine to the more flexible, lumbar spine is a causative biomechanical factor for herniation of thoracolumbar IVDs in CD dogs; however, definitive evidence to support this theory is still lacking [41]. In contrast, it is well known that IVD displacement is seldom seen in the midthoracic spine (T1–T9). This may be because of the intercapital ligaments present ventral to the dorsal longitudinal ligament at each level from T1–T2 to T9–T10 [12, 42, 43]. These ligaments may prevent dorsal and dorsolateral displacement of the IVD at these levels [12, 36].
Biomechanics of the Intervertebral Disc and Why Do Discs Displace?
Biomechanical function of the healthy intervertebral disc
Biomechanical failure of the IVD
Displacement of the IVD in CD dogs
Displacement of the IVD in NCD dogs
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