Degenerative Disc Disease and Spondylosis

Degenerative disc disease (with its characteristic clinical syndromes of disc herniation, spondylosis, and radiculopathy) is associated with vascular, biochemical, and anatomic changes in the disc. There is a consistent anatomic pattern of disc degeneration in the spine, with most changes occurring in the midcervical and lower lumbar regions. This pattern is thought to reflect the distribution of the mechanical stresses caused by spine movement and loading, as well as those due to erect posture. There is an inconsistent correlation between the extent and distribution of degenerative spondylotic changes seen radiographically and the reported symptoms from patient to patient.

The intervertebral disc consists of three components: (1) the nucleus pulposus; (2) the annulus fibrosus, which surrounds the nucleus pulposus; and (3) the cartilaginous end plates, which attach these structures to the rostral and caudal vertebrae of the motion segment. The annulus is formed by a series of lamellae that have high collagen content and thereby provide significant resistance to tensile forces. The ventral annulus is usually wider and more organized than the dorsal annulus, within which discontinuous lamellae may be present. The nucleus pulposus, derived embryologically from the primitive notochord, has a much higher proteoglycan and water content than the annulus fibrosus. The hyaline cartilage end plates are similar in collagen type to the inner annulus fibrosus and the nucleus pulposus.

Proteoglycans contribute to osmotic pressure elevation and increased turgidity of the nucleus pulposus, which generates an internal hydrostatic pressure that exerts radial stress during axial loading. Circumferential annular fibers are pushed outward and the end plates separate when intradiscal pressure increases. Stress in the end plates is greatest over the nucleus pulposus and diminishes toward the outer annulus. The nucleus of the disc acts as a deformable, fluid-like material, whose tendency to bulge is resisted by the tensile stress in the annular lamellae and the end plates. Therefore, a substantial intradiscal pressure is required to resist a high circumferential annular stress and thus prevent excessive disc deformation (bulging). Hyperflexion and torsional loading increase axial disc load-bearing and can lead to progressive degenerative changes, including disc desiccation and annular stiffening, as well as to catastrophic failure and disc herniation. A reduction in intradiscal pressure and volume leads to thinning of the intervertebral space and increased annular bulging.

The disc initially receives its nutrients through small vessels in the cartilage end plates and from the periphery of the annulus. Once skeletal maturity occurs, the vessels have disappeared and the disc receives its nutrition and metabolic exchange through diffusion, making discs the largest nonvascularized structures in the body. The loss of vasculature promotes increased anaerobic metabolism, increasing lactic acid production, and cellular necrosis. The water content of the annulus fibrosus decreases from 78% at birth to 70% by the fourth decade, and the nucleus pulposus water content decreases from 90% to less than 70% with maturation. Along with this change in vascularity, and water loss in the region of the inner annulus and nucleus pulposus, there is a relative increase in fibrocytes and chondrocytes, which are more tolerant of the low-pH environment.

By 2 years of age the nucleus pulposus is translucent and anatomically distinct from the annulus fibrosus. The next three decades bring a cascade of increasing fibrosis, diminished height, and proteoglycan loss; the annulus weakens with the development of a series of fissures, and the nucleus continues to dehydrate and fragment. Magnetic resonance imaging (MRI) grading systems for this pattern of disc degeneration have been published. Plain films detail a spectrum of normal disc height and end plates (grade I) through severe end plate sclerosis, disc space narrowing, and osteophyte formation (grade IV).

Nucleus pulposus herniation through a disrupted annulus is a frequent cause of radiculopathy ( Fig. 15-1 ). The biomechanical mechanism of disc herniation is related to a combination of complex movements involving compression, lateral flexion, or rotation. Flexion forces migration of the nucleus pulposus dorsally and increases hydrostatic forces adjacent to the posterior annulus, a region that has fewer and more disorganized lamellae and is inherently weaker than the thicker ventral annulus. Annular degeneration leads to radial tears and progressive disc herniation. The typical dorsolateral herniation pattern affects the traversing nerve root passing to the next lower foramen, whereas a more laterally placed foraminal or extraforaminal disc protrusion will compress the exiting nerve root. Far lateral disc herniations constitute 7% to 12% of all disc herniations. They are often extruded or sequestrated fragments and occur predominantly at the L4-5 and L3-4 levels. Because the ganglion, in addition to the root, is compressed or stretched there may be considerable and unrelenting radiculopathic pain.

Disc desiccation and herniation in the lumbar spine. A, Sagittal T2-weighted MRI of the lumbar spine demonstrating multiple discs with varying degrees of hydration, degeneration, and herniation (white arrows heads point to three disc spaces in descending order that are represented by their corresponding axial images in B, C, D). B, Axial T2-weighted MRI of a healthy lumbar disc with good hydration and no evidence of disc bulging or herniation. C, Axial T2-weighted MRI of a mildly degenerated lumbar disc with poor hydration and early evidence of disc bulging. D, Axial T2-weighted MRI of a degenerated lumbar disc with complete loss of hydration and reduction in height with extensive disc herniation and thecal sac effacement.

Bulging discs are identified by asymmetry at the vertebral margins, whereas a prolapse (protrusion) has breached the annular fibers and may remain contiguous with the central nucleus by a broad-based pedicle that is bright on T2-weighted MRI. An extruded disc has a narrower neck than dome and may migrate above or below the level of the disc. A sequestered or free fragment is no longer in continuity with the disc. These may migrate in a rostral or caudal direction. Far-lateral herniated discs are more likely to migrate in a rostral direction, thus affecting the exiting nerve root above the disc space.

Disc degeneration leads to changes affecting the biomechanical function and stability of both the intervertebral and articular facet joints. Although opinions differ regarding whether facet or disc degeneration is the initial event that causes spondylosis, stress shielding ensures that loads are transferred from incompetent to more functional segmental units. Such load sharing invariably leads to insidious reciprocal joint degeneration, including cartilaginous erosion, osteophyte growth and facet hypertrophy at sites of excessive motion, and further decline in the integrity of the disc with hypertrophy of the ligamentous facet capsule. These changes contribute to lumbar stenosis ( Fig. 15-2 ) and lateral recess syndromes.

T2-weighted MRI of the lumbar spine demonstrating lumbar spinal canal stenosis, particularly at L2-3. Osteophytic spurs are evident ventrally with some mild disc bulging and hypertrophied ligamentum flavum dorsally leading to an area of considerable focal stenosis. A, Sagittal T2-weighted MRI of lumbar spine (white arrowhead pointing to area of focal stenosis). B, Axial T2-weighted MRI demonstrating hypertrophied ligamentum flavum dorsally (white arrowheads pointing to hypertrophied ligamentum flavum).

Patients with significant lumbar spinal canal narrowing resulting in stenosis may complain primarily of pain, weakness, and leg numbness with upright posture often aggravated by ambulation. This pain can be relieved when the patient flexes the lumbar spine by sitting or by leaning forward while standing or during ambulation (shopping cart sign). The symptomatic improvement associated with these maneuvers is related to an increase in lateral recess, neural foramen, and spinal canal dimensions. Flexion results in stretching of the protruding ligamentum flavum and posterior longitudinal ligament, as well as reduction of overriding laminae and facets, whereas extension may aggravate these alterations. This small amount of change in the circumferential spinal canal, lateral recess, and foraminal diameters alleviates pressure on the nerve roots. Returning to the erect posture leads to repeated compression and a recurrent exacerbation of symptoms. During ambulation, some patients experience symptoms because of an increased metabolic demand in nerve roots that have become ischemic as a result of stenotic compression. Such “neurogenic claudication” is relieved when the subject sits. Often, bicycling or uphill ambulation (which are associated with flexion of the lumbar spine) are well tolerated.

Cervical disc senescence causes characteristic spine alterations that can result in progressive kyphotic deformity, mechanical neck pain, radiculopathy or myelopathy. Physiologic cervical lordosis aligns and balances the head mass over T1 and yields highly efficient load carrying by the active (muscles) and passive (ligaments, discs, facets) support systems. With aging, however, intradiscal water loss and disc narrowing occur, leading to progressive spine straightening. The greatest range of intervertebral motion is at C5-6 and C6-7, and spondylosis characterized by foraminal narrowing and joint degeneration is most marked at these levels as the spine attempts to stabilize through autofusion ( Fig. 15-3 ). Altered local dynamics lead to increased motion and anterolisthesis at C3-4 and C4-5 where disc height is typically maintained. In this scenario, the spinal cord of the patient with cervical spondylotic myelopathy may not only be compressed by osteophytes, but may also suffer repeated injuries secondary to intervertebral hypermobility or instability. Dynamic flexion-extension radiographs can evaluate degenerative spondylolisthesis to determine the extent of subluxation with physiologic motion.

Cervical spine degeneration with disc height reduction and progression to disc herniation and spinal cord compression in a patient over a 4-year period of surveillance imaging (C5-6 and C6-7 levels). A, Sagittal T2-weighted MRI of cervical spine on initial presentation. B, Sagittal T2-weighted MRI of cervical spine 2 years lateral in the same patient. C, Sagittal T2-weighted MRI of cervical spine with significant progression of disc herniation at C5-6 and spinal cord compression.

Rheumatoid Arthritis

Rheumatoid arthritis (RA) is a disease of the synovium and therefore affects both the spine and peripheral joints. It has a prevalence of approximately 1%, with the greatest incidence in the fourth through sixth decades. Early joint synovitis is accompanied by an acute inflammatory response as a result of antibody-antigen complex formation. These processes activate the complement cascade and generate biologically active substances that can lead to complete joint destruction. This acute process is followed by a chronic granulomatous process, or pannus formation, which produces collagenase and other enzymes that destroy surrounding cartilage and bone. Ligamentous incompetence often leads to spinal instability.

The prevalence of RA associated cervical spine disease varies widely depending on study populations, ranging from 16% to 70%. Risk factors for cervical instability include peripheral joint erosion, cervical cartilaginous and osseous destructive changes, corticosteroid therapy, disease modifying antirheumatic drugs (DMARD) failure, age < 45 years, younger age at onset, and disease duration. There is controversy regarding whether the pathogenesis of cervical spine rheumatoid joint disease revolves around (1) the apophyseal joint, with resultant facet destruction and progressive secondary instability of the intervertebral disc, or (2) inflammation in the uncovertebral joint, which leads to primary disc destruction with secondary degenerative involvement of the apophyseal joints. Cervical disease manifestations include atlantoaxial instability (AAI), occipitocervical instability (OCI, with or without basilar invagination due to vertical displacement of the dens), subaxial subluxation (SAS), C1-2 pannus, and inflammatory discitis. AAI is the most common form of cervical rheumatoid involvement, followed by OCI and then SAS. Progressive destructive inflammation of the synovial joint between the atlas and dens leads to transverse ligament laxity. The loss of ligamentous integrity allows C1 to move ventrally on C2. If there is further significant disruption and osteomalacia of the dens itself, then dorsal C1-2 subluxation can also occur. Atlantoaxial synovial apophyseal joint involvement leads to unstable lateral rotation.

OCI results from involvement of the atlanto-occipital articulations. Articular facet destruction leads to progressive collapse of the occiput and vertical displacement of the dens ( Fig. 15-4 ), a process called atlantoaxial impaction, vertical subluxation, cranial settling , and basilar invagination. Vertical displacement of the dens occurs in 5% to 32% of RA patients, and it is believed to represent a more advanced stage of systemic disease burden. A 10-year retrospective review of patients with RA cervical instability treated with OC fusion noted significantly worse long-term outcomes in the subset of patients with vertical displacement of the dens.

Pannus formation and basilar invagination in the context of various acquired and congenital pathologies of the craniovertebral junction. Sagittal T2-weighted MRIs of the cervical spine ( A, C, E, G, ) with corresponding sagittal CT scans ( B, D, F, H ).

In the subaxial region, the levels most commonly involved with rheumatoid synovitis are C2-3 and C3-4. Subluxation occurs in 7% to 29% of the patients and is most likely in patients who have undergone previous rostral surgical fusion. These “staircase” subluxations are caused by the significant ligamentous laxity and facet degeneration. At any of the various sites of rheumatoid involvement, osseous erosion caused by osteoclastic resorption occurs frequently.

Joint destruction and ligamentous laxity result in cervical instability, leading to mechanical neck pain and risk of radiculopathy or myelopathy. Headaches of occipital neuralgia can occur from encroachment on upper cervical roots, and cranial settling can lead to cranial neuropathy, bulbar findings, and even sudden death from cervicomedullary compression. Pannus formation further encroaches on neural elements. Early and periodic dynamic radiographic examination is important to stratify progression risk as well as to gauge the degree of pannus formation resulting in neural compression. MRI has the greatest sensitivity to cervical joint disease involvement, and computed tomography (CT) is the best modality to document bone erosion, whereas dynamic anteroposterior (AP) and lateral plain films provide an excellent method to assess instability.

The incidence of cervical rheumatoid lesions has decreased in the setting of aggressive polytherapy with disease-modifying antirheumatic drugs (DMARDs) and newer biologic agents, even though the protective mechanism is not clear. There is some suggestion that intensive nonoperative management of known instability can arrest symptoms, although biologic agent therapy has little effect on existing destructive pathology. Demographic data suggest a declining rate for atlantoaxial or posterior cervical fusion in RA patients, even though prevalence rates among the general population have increased. Surgical intervention is indicated for progressive symptomatic and radiographic instability, as well as for neural decompression in the setting of symptomatic pannus. The optimal time to proceed with operative intervention has yet to be determined, though there is consensus that surgery should occur before neurologic deterioration (i.e., myelopathy) due to the relatively poor surgical and conservative therapy outcomes with advanced disease. Patients operated on earlier in their disease course and with a better functional preoperative score have a more pronounced overall improvement than those undergoing delayed surgical management.

Surgical fusion yields multiple benefits, including a reduction of both pain and neurologic sequelae; retrospective analysis of long-construct dorsal fusion demonstrates significant recovery of these two complications, with improvement of an average of one to two grades on the Ranawat scales for pain and neurologic symptoms ( Boxes 15-1 and 15-2 ). These improvements were persistent, even in the setting of failure to accomplish permanent postoperative reduction of deformity and imbalance. The chronic granulomatous pannus often decreases in size with the elimination of abnormal movement after successful arthrodesis. The techniques for cervical fusion and decompression vary, but one must keep in mind the inherent poor quality of RA bone, the laxity of ligaments, the insidious inflammatory nature of RA itself, and the destructive effects of the myriad pharmacologic interventions, especially with respect to osteoporosis due to treatment with corticosteroids and DMARDs.

Scheuermann Disease (Juvenile Kyphosis)

Scheuermann first described the progressive dorsal kyphosis of adolescent children in 1920. The deformity is usually evident as a fixed thoracic kyphosis that does not correct with hyperextension, thereby differentiating it from a postural kyphosis. Compensatory hyperlordosis of the lumbar and cervical spine may also be present. A mild scoliosis is noted in up to 30% of patients. Sørensen described the characteristic feature of ventral wedging of 5 degrees or more in at least three adjacent vertebrae. Other characteristics include kyphosis of greater than 40 degrees, vertebral end plate irregularity, and disc space narrowing. The prevalence of the disease ranges from 0.4% to 8%, and is the most common cause of pediatric kyphosis. Though historically thought to occur predominantly in males, more recent studies indicate that male-female ratio is closer to 2 : 1, with a strong genetic component for disease transmission.

Basic biomechanical factors and forces may play a role in this disorder. The thoracic spine has a natural kyphosis determined primarily by the shape of the vertebrae; in the adolescent thoracic spine, 20 to 40 degrees of kyphosis is normal. The dorsal elements, including the ligamentum flavum and the laminae, resist forward flexion of the spine in tension, whereas the ventral bony elements (vertebral bodies) and discs resist compression. The facet joint capsules in the thoracic region are biomechanically “weaker” than those in the lumbar region, so that any factor that increases the torque of the spine can result in greater deformity. The more marked the initial angulation of the spine, the larger the load (subject’s weight), and the longer the duration of load application, the greater the likelihood of deformity progression.

Scheuermann disease must be differentiated from juvenile postural kyphosis, which, as the name attests, is a kyphosis seen during flexion that will correct with improved posture and extension. The apex of the curve is smooth. The condition will improve with therapy that targets improved posture and core strengthening.

The pathogenesis of the disease remains unclear. Scheuermann believed that aseptic necrosis of the ring apophyses interrupted growth and resulted in ventral vertebral body wedging. Subsequent work refuted this theory by demonstrating that the apophyses do not contribute to longitudinal growth. Such growth is now known to result from endochondral ossification of the end plates. Schmorl felt that damage to the end plate by herniated disc material was of importance. Schmorl nodes are, however, not limited to the kyphotic region of the spine and are common in otherwise normal patients. It has been postulated that osteoporosis is involved, but investigations have found no differences in the trabecular bone density between patients with Scheuermann disease and controls matched for age, gender, and race. Other factors such as inflammation, hormonal influences, genetic factors, altered calcium metabolism, hypovitaminosis, neuromuscular disorders, extradural cyst formation, defective collagen formation of the end plate, and a decrease in the collagen-proteoglycan ratio of the end plate have been implicated, but their roles in the development of the disease have not been substantiated.

There is a high association (> 90%) between ventral osseous extensions from the anterior margin of the vertebral body and the diseased vertebrae, a feature that is absent in normal specimens. Histologic examination reveals disorganized endochondral ossification, which may be a result of abnormal stress. Traumatic features of vascular and fibrocartilage proliferation are evident in the ventral end plates in Scheuermann disease. The dorsal vertebral height in cases of Scheuermann disease is not significantly different from that of controls, implying that either the ventral and dorsal stresses are different or that the kyphotic changes occur after dorsal growth is complete (the normal pattern of ring apophysis, closure starts dorsolaterally).

A dull nonradiating pain with localized tenderness is a common presenting symptom. Other complaints include tightness of the hamstrings and iliopsoas as well as stiffness of the shoulder girdle. Patient examination can reveal a hyperpigmented lesion at the apex of the thoracic curve—a result of friction injury from the abnormally protruded spinous process. Patients often have a compensatory lumbar and cervical hyperlordosis that leads to negative sagittal balance and a forward-protruding head. One third of patients have a coronal deformity. Neurologic complications, which are rare, are due to thoracic disc herniation, dural tenting, extradural cysts, or vascular compromise.

The natural history is not well described for either treated or untreated patients. Kyphotic progression is relatively uncommon after skeletal maturity. Progressive spondylosis and disc degeneration can lead to deteriorating deformity, back pain, and neurologic function as an adult. One study found that patients with untreated Scheuermann disease had minor functional limitations, without a major influence on quality of life.

Surgical treatment should be considered to correct the deformity, prevent progression, and alleviate pain. The extent of the kyphosis and the age of the patient are important criteria for intervention. The nonoperative forms of treatment, such as bracing (Milwaukee brace) or casting, are the first line of treatment for most cases in which kyphosis is nonrigid and < 65 degrees. These cases have a high success rate in correcting the deformity, especially if treatment begins before closure of the iliac apophyses (i.e., skeletal maturation). Operative treatment with fusion is reserved for cases of progressive deformity, pain not responsive to an adequate trial of casting or bracing, degenerative changes in adults associated with the kyphosis, cardiopulmonary compromise, fixed deformity, and for curves greater than 65 degrees. Correction is lost in 30% of patients after brace removal.

Dorsal long-construct instrumentation that extends rostrally and caudally well above the thoracic apex is often adequate for stabilization and deformity correction. Both an anterior and posterior surgical approach may be necessary in the event of extreme kyphosis or ankylosis. With the advent of pedicle screw fixation and posterior column shortening with segmental osteotomies, posterior-alone approaches can achieve equivalent deformity correction without loss of correction on long-term follow-up. Several large retrospective reviews comparing posterior only or combined anterior-posterior release and instrumentation showed a comparable degree of deformity correction, although rates of junctional kyphosis and operative morbidity were higher in the combined approach. The authors conclude that dorsal release and fixation alone should be the favored procedure whenever possible due to the associated morbidities of a ventral approach, as well as decreased operative time and blood loss compared to a combined approach.

Regardless of the surgical intervention, the entire length of the kyphosis should be included in the fusion. The most distal level should be the first lordotic segment so as to decrease the incidence of junctional kyphosis; however, there is evidence that including the distal vertebral body that is bisected by a line drawn from the posterior superior corner of the sacrum (the sagittal stable vertebra) further prevents development of junction kyphosis. Deformity correction should not exceed 50% of the original curve, as doing so will increase the rate of junctional kyphosis without the benefit of a further decrease in pain.

Paget Disease

Paget disease is a metabolic bone disorder thought to be of possible viral origin. Prevalence has a marked geographic variation. In the United States, Paget disease is found radiographically in 3% to 4% of patients older than age 40. It is characterized histologically by areas of bone resorption and deposition resulting from focal increases in osteoclast levels. Individual osteoclasts are larger than normal and contain inclusion bodies similar to paramyxovirus capsids, suggesting viral induction of osteoclastic activity. There is no disturbance of reactive bone formation; increased osteoblastic activity compensates for bone resorption and, in fact, produces a net-positive balance of bone. The bone is usually lamellar and normally mineralized. Woven and osteoid bone are also present and result in reduced quality with disruption of the lamellar structure of both cortical and trabecular bone.

The pelvic bones and spine are the most commonly affected. Approximately 70% of patients have lumbar spine involvement, 45% have thoracic lesions, and the cervical spine is involved in 15% of cases. The frequent involvement of the lumbar spine is thought to be potentiated by increased loading. The lesions are primarily in cancellous bone. Approximately two thirds of the radiographically evident lesions are asymptomatic. Back pain in Paget disease is related to the combination of bone deformity and subchondral bone enlargement that alters the contours of the joint surfaces and leads to joint degeneration. The subchondral changes include increased bone deposition and subchondral infarcts from abnormal pressure on expanded bone, each of which causes the bone to lose its normal flexibility and usual biomechanical properties. The involved vertebral body can interfere with nutrition of the intervertebral disc, leading to early degenerative sclerotic changes.

Radiographically, the majority of patients with Paget disease have involvement of both the vertebral body and the dorsal osseous element; involvement of only ventral or dorsal structures is rare. Consistent with histologic analysis supporting periosteal bone formation and endosteal absorption, early radiographs show increased density in the osseous periphery contrasted with a central lucency. Commonly, sclerotic areas are present as well as localized osteolytic lesions, which may coalesce with time. As a result of the disorganized pattern of bone deposition, biomechanical efficiency is reduced and the risk of fracturing increases. Healing of fractures is usually efficient, and the histologic features of Paget disease are observed in the fracture line.

Back pain is the most frequent presenting symptom; possible etiologies include periosteal stretch, deranged vascularity with resulting zones of ischemia, stenosis, nerve root compression, facet arthropathy, and osseous microfracture. Neurologic sequelae have been reported in 25% to 30% of cases. These deficits are most often caused by bony compression of the spinal canal or foramina, with the neural arch and the facet joints most commonly affected by the proliferative bone deposition. Some advocate that a component of epidural fat ossification is a factor, though this may be simply a component of advancing periosteal bone formation that projects into the canal. Fractures and subluxations can also compromise the spinal canal, and progressive platybasia can result in compression of the medulla. Vascular “steal,” due to increased vascularity of the pathologic bone, has also been implicated in the development of neurologic deficits.

Treatment focuses on reducing the burden of hypertrophied and abnormal bone. Despite the prevalence of stenosis with resultant neural element compression, surgery is rarely indicated due to the success of medical therapy (bisphosphonates, calcitonin, etc). If surgery is considered, an aggressive preoperative medical treatment course should be undertaken to reduce the volume of abnormal and highly vascularized tissue, which can lead to voluminous blood loss. Pagetic lesions rarely degenerate to either benign or malignant neoplasms that require more aggressive surgical management, with osteosarcomas predominating in the latter category.

Ankylosing Spondylitis

Ankylosing spondylitis (AS) is a heritable rheumatic condition in a group of inflammatory joint disorders that share a predilection for the spine and sacroiliac (SI) joints, called spondyloarthropathies. Distinguished by its genetic association with the antigen presenting major histocompatibility complex (MHC) HLA-B27, AS shares many similarities to rheumatoid arthritis but uniquely lacks the seropositivity for rheumatoid factor. The most notable pathologic findings include inflammation of ligament, tendon and capsule attachments to bone (enthesopathy), discovertebral erosion, and new bone formation that results in the ankylosis or autofusion of intervertebral joints (syndesmophyte). Patients describe an inflammatory type of axial spine pain that is often relieved with nonsteroidal anti-inflammatory drug (NSAID) therapy. The spine demonstrates erosive changes at the corners of vertebral bodies and bony spur formation, giving it the characteristic “bamboo-spine” appearance on x-rays.

The pathophysiologic mechanism of AS remains elusive, but the strong genetic association with HLA-B27 has cued scientists to explore autoimmune versus autoinflammatory dysregulation as potential etiologies. Several lines of research have converged to implicate specific immune pathways including the interleukin (IL)-17/IL-23 pathway, control of nuclear factor kappa B (NF-kB) activation, MHC antigen presentation, and genetic control of CD8 and CD4 T-cell subsets in the pathophysiology of AS. Prevalence ranges from 0.1% to 1.4% depending on the population studied with a predisposition among Caucasians. There is a male predominance, varying from 3 : 1 to 8 : 1. Peak age of onset is between 15 and 29 years, with less than 5% beginning after age 50.

The earliest signs of AS occur in the region of ligamentous attachment to bone (the enthesis), which shows multiple, focal, microscopic inflammatory lesions that eventually destroy the ligament and erode the adjacent cortical bone. This process leads to an osteitis, primarily at the ventral and ventrolateral aspects of the attachment of the annulus fibrosus to the vertebral bone. This is the anterior spondylitis, or Romanus lesion, that is observed radiographically. As the reparative process occurs, woven bone replaces the cortical erosion (ossification in fibrous tissue without preceding cartilage formation). Ultimately, this is replaced by lamellar bone. Syndesmophytes form on the ventrolateral aspects of the vertebrae adjacent to each disc. This results in new enthesis formation above the original level of cortical bone. Further thickening and growth of the syndesmophyte may be caused by inflammatory lesions in this new bone or chondroid metaplasia with ossification.

In the apophyseal joint, osteitis and enthesopathy occur at the junction of capsule and bone and result in reactive bone formation and ossification of the capsule, usually in the presence of well-preserved articular cartilage, implying that the capsule-ligamentous attachment is of primary importance in the apophyseal joint pathology. Ultimately the joint may become ankylosed by endochondral ossification. This may be the result of capsular ossification or the general immobility of the spine as a result of discovertebral syndesmophyte formation as described previously. However, the observation that apophyseal joint ankylosis may occur in the absence of vertebral ankylosis at the same level makes the former more likely.

A nonspecific inflammatory process of the supraspinous and interspinous ligaments leading to ossification also occurs simultaneously. The anterior longitudinal ligament, however, does not usually become ossified, except at its deep fibers adjacent to the annulus fibrosus. Bone resorption (resulting in squaring of the vertebrae), syndesmophyte formation, bony ankylosis of the intervertebral discs, and apophyseal joint and ligament ossification complete the classic radiographic “bamboo-spine” appearance. Although bone formation at the attachments of the ligaments and at the apophyseal joints is increased, the vertebrae in ankylosing spondylitis are generally osteoporotic. This may be a result of the systemic effects of the disease, immobilization of the vertebrae, the inflammatory process, or drug treatment.

As the bony ankylosis in the discovertebral region and the apophyseal joints progresses, the normal flexibility of the spine is lost. The spine is much stiffer than normal and is unable to absorb and dissipate loading energy in an efficient manner. Indeed, the ankylosing process itself may introduce a “lever-arm” quality to regions of the affected neuraxis, increasing the magnitude of injury that may be focused at specific spinal levels. Because of these factors and osteoporosis, the bone is much more prone to fracture and subluxation after trivial trauma ( Fig. 15-5 ). Due to the long lever-arm effect of inflexible segments adjacent to the fracture, the spinal cord is significantly vulnerable when dislocation occurs in these fractures. The cervical spine appears to be particularly susceptible; approximately 75% of the spinal fractures occur in this region, primarily in the lower cervical spine. These fractures tend to pass through the ventrodorsal width of the vertebra and may involve the calcified ligaments in the spinous processes. This process may occur either at the level of the disc space or through the vertebral body. A cervical kyphosis is often present, and the neck is especially vulnerable to hyperextension injuries. Some authors have tried to predict the mechanism of injury based on the fracture location, associating extension with transdiscal fractures and flexion with transvertebral fractures, whereas others have not been able to confirm this relationship.

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