Vertebral Compression Fracture

This article is still missing information.

The compressive force on the thoracolumbar spine is the force that acts along the long axis of the spine as arises from tension in the paraspinal muscles and gravity. The compressive force is resisted mainly by the anterior column (vertebral bodies and discs), plus a variable amount of around ~15% from the posterior column (zygapophysial joints). Narrowing of the intervertebral discs leads to an increase of force taken up by the posterior column. It can also lead to the inferior articular process tip to impinge on the caudal lamina. With severe reduction of disc height, up to 90% of the compressive force is resisted by the posterior column.

The endplate is the weakest part of the vertebral body of the lumbar spine. Initial damage from compressive forces usually occurs in the endplate or in the trabeculae that support the endplate. It is thought that the endplate needs to be thin to allow nutrient diffusion into the intervertebral disc. The superior endplate of the vertebral body is thinner and weaker than the inferior endplate and has less trabecular support from the pedicles in the parasagittal plane. Please note that the superior endplate of the vertebral body is the same thing as the inferior endplate of the intervertebral disc. Failure occurs with the endplate bulging into the vertebra due to pressure from the nucleus pulposus.

Normal and Young Vertebra

Figure 1. Types of vertebral compression fractures in the non-osteoporotic lumbar spine. © 1989 Elsevier

Various types of macroscopic endplate fracture have been found to occur in the lumbar spine (figure 1). In some instances there can be intrusion of disc material into the trabecular bone called intraosseous herniation. This defect can become calcified in what is called a Schmorl's node. In adolescents, endplate failure may occur differently with fracture of the posterior edge that runs from the endplate down to the cartilage growth plate. Endplate fractures are not always seen on plain films. MRI is more accurate and this modality can also show Modic changes which are reactions to the endplate fracture.

Burst fractures are comminuted vertebral body fractures where the anterior and posterior walls of the vertebral body are disrupted. They are characterised by an increased interpedicular distance. Bone can retropulse into the spinal canal causing neurological signs and symptoms. The adjacent intervertebral discs are also damaged with this injury and disc material is forced into the vertebral bodies. They are more common in the thoracic spine but resemble the transverse fracture type in figure 1. They are less likely to occur with intervertebral disc degeneration.

At the microscopic level, it is thought that compressive fatigue damage is a common event throughout life because microfractures and healing trabeculae are found in most cadavers.

Fracture Morphology

Figure 2. Types of osteoporotic vertebral body compression fractures and respective Genant classifications

Osteoporotic fractures are fragility or low-trauma fractures. Vertebral compression fractures are the most common type of osteoporotic fracture. They often occur at the midthoracic region (T7-8) and at the thoracolumbar junction (T12-L1). They can result in significant back pain and loss of function however those that occur slowly over time are often asymptomatic. They also lead to height loss and kyphosis.

Types

Osteoporotic vertebra display different patterns of failure: anterior wedge fractures, biconcave fractures, and crush fractures (figure 2).

Anterior wedge fractures are where there is collapse of the cortex of the vertebral body plus collapse of the underlying trabecular bone leading to a wedge shape. It is thought that with osteoporosis there is relative loss of thickness of the anterior trabeculae compared to the posterior trabeculae. There is also relative loss of the horizontal compared to the vertebral trabeculae, which reduces resistance to tension. Furthermore, the endplate is weaker anteriorly than posteriorly.

With intervertebral height reduction, more of the compressive load is taken up by the posterior column, and the anterior column is "stress-shielded" in the neutral and extended positions. However in the flexed position the anterior vertebral body is severely loaded in the degenerative disc. The elderly may spend less time in flexion leading to a reduced mechanical stimulus for hypertrophic adaptation. This combined with a reduced ability for the endplate to adapt (e.g. due to menopause), may explain why fractures occur in the anterior vertebral body and why flexion movements often precipitate it.

Posterior wedging is uncommon and may suggest an underlying destructive lesion.

Biconcave fractures involves compression of the central portion of the vertebral body, resulting in depression of both the superior and inferior endplates (the central aspects are weaker), while the anterior and posterior walls maintain their height. They are also common in the elderly and in this setting the endplates are often smooth which suggests repeated microfractures having occurred. In younger spines compression failure usually leads to more discontinuous endplate damage.

In the elderly the discs may not have an overall reduced height even though degeneration has occurred due to the nucleus pushing into the weakened vertebra. The annulus fibrosus may be reduced in thickness, however, and this may be a better sign of intervertebral disc integrity than overall height or nucleus height.

Burst/Crush fractures are terms describe more severe fractures involving significant, often more uniform, height loss across the entire vertebral body. Burst fractures, specifically, imply failure of both the anterior and middle columns under high axial load, often with retropulsion of bone fragments from the posterior vertebral wall into the spinal canal. This poses a risk of neurological compromise. They are thought to be due to a sudden compressive force acting on the anterior and posterior vertebral cortices at the same time. In younger spines this type of trauma can cause burst fractures which have a similar appearance to crush fractures.

Grading

Osteoporotic spinal fractures are graded with the Genant classification based on vertebral height loss on lateral radiographs (figure 2):

• Grade 0: normal
• Grade1 : mild, up to 20-25% reduction in anterior, middle, and/or posterior height
• Grade 2: moderate, up to 25-40% reduction in any height
• Grade 3: severe, >40% reduction in any height

Additionally, a modifier of 0.5 can be added for borderline deformed vertebrae.

Schmorl's Nodes and Modic Changes

As described, endplate fracture can lead to vertical herniation of the nucleus pulposus into the vertebral body. Calcification around this herniated tissue are called Schmorl's nodes when see on radiographs. Approximately 1/3 of endplate fractures as seen on MRI can be seen on plain radiographs. Yet smaller vertical herniations are seen in approximately 3/4 of spines in dissection.

Schmorl's nodes are most common near the thoracolumbar junction. They are rare below L2. They most commonly affect the central part of the endplate, and are more common on the inferior vertebral endplate than the superior endplate. Remember it is actually the superior endplate that is stronger, so one thought is that the endplates haven't formed properly in some people. Genetics play an important role with a heritability of 70%. There are also mechanical risk factors, namely: increased height, increased weight, and male gender. The prevalence increases with age up to 30, and then plateaus. Schmorl's nodes are also associated with disc degeneration. They are twice as common in patients with back pain, and are common in young sportsmen. (See also Scheuermann's Disease).

Modic changes are endplate patterns seen on MRI. Modic type 1 change is decreased signal intensity on T1, and increased signal intensity on T2, and reflects inflammatory change. Modic type 2 change is increased signal intensity on both T1 and T2 (or isointense on T2), and reflects fatty change. Type 1 can convert to type 2 after a few years. Inflammatory changes are thought to be more closely associated with pain than endplate injury itself. Modic changes are associated with confirmed discogenic pain by discography.

Internal Disc Disruption

Main article: Internal Disc Disruption

Figure 3. Compression of an intervertebral disc may result in vertebral endplate fracture. This may heal or it may trigger nuclear degradation. Degradation may lead to isolated disc resorption or extend to the anulus and cause internal disc disruption (grade III shown). Internal disc disruption may lead to disc herniation

Endplate fractures can heal or it can trigger events leading to nuclear degradation (figure 3). Nuclear degradation in turn can lead to isolated disc resorption or internal disc disruption, the latter being an important cause of chronic low back pain. Internal disc disruption is the presence of isolated, radial fissures that penetrate from the nucleus pulposus through to the anulus fibrosus, however the outer anulus is not breached. It is a common

Endplate fracture is an important initial event in the pathogenesis of internal disc disruption. With compressive damage to the vertebra, the endplate bulges into the vertebral body. The volume of the nucleus pulposus increases, and therefore the pressure within the nucleus drops. This reduced pressure means it is less able to resist the applied compression loads, and so more of the load is placed on the annulus fibrosus, with peak loads on the posterior annulus. Inner lamellae can even collapse inwards.

With endplate fracture, disc cell metabolism becomes impaired with very high and very low matrix compressive stresses. This leads to reduced proteoglycan synthesis in the nucleus, which further reduces the nucleus volume and pressure, and a vicious cycle emerges. With very high loads degradative pathways can also be stimulated.

Young spines are better able to adapt because the inner annulus is more fluid-like and can accommodate the altered shape of the endplates better and so the pressure within the nucleus doesn't fall, and therefore there is less or no change in the stress on the annulus.

At the other end of the spectrum of the age, old and severely degenerative discs may also be less affected by endplate damage. In this case the reason is due to stress shielding where the posterior column takes up more of the load. Any decompression of the nucleus therefore leads to extra compressive loading on the posterior column rather than the anulus.

Biomechanical Impact

Regardless of the specific morphology, VCFs invariably alter spinal biomechanics, potentially initiating a cascade of deleterious effects.

• Altered Spinal Alignment: Wedge fractures, by definition, induce a focal kyphosis at the fracture level or reduce segmental lordosis. This anterior angulation shifts the center of gravity of the trunk anteriorly relative to the spinal column below the fracture, increasing the lever arm for flexion moments during upright posture and activities. Multiple VCFs can lead to progressive global kyphosis, significantly impacting posture and potentially pulmonary and gastrointestinal function.
• Shifted Load Pathways: The spine functions as a three-column structure (anterior, middle, posterior). The anterior column (vertebral body and disc) normally bears the majority of axial compressive loads. VCF compromises the load-bearing capacity of the anterior column. This forces a redistribution of loads, increasing the stress on adjacent structures. The anterior shift in the center of gravity associated with kyphotic deformity necessitates increased compensatory activity from the posterior spinal muscles (e.g., erector spinae) to maintain posture, which in turn increases compressive forces on the spine. Finite element models demonstrate that wedge fractures can substantially increase intradiscal pressure in adjacent segments. Furthermore, the failure of the anterior vertebral body leads to increased load transmission through the posterior elements, namely the facet joints. Facet joints, which normally bear a smaller proportion of the axial load (estimated 3-25%), may experience significantly higher forces, particularly in extension or when adjacent disc height is reduced.
• Segmental Instability: When vertebral body collapse is severe (e.g., >50% height loss), it can lead to segmental instability. An unstable segment exhibits abnormal motion under physiological loads, further increasing stress on adjacent intact segments as they compensate for the lack of support.

These biomechanical alterations create a precarious situation. The initial fracture not only causes local damage but also changes the loading environment for the rest of the spine. This altered loading, combined with potential progression of underlying osteoporosis and the stiffening effect of treatments like vertebroplasty or kyphoplasty, can increase the risk of subsequent fractures at adjacent or remote levels, a phenomenon sometimes termed a "vertebral fracture cascade". Studies show that having one VCF increases the risk of a subsequent fracture fivefold, and two or more VCFs increase the risk twelvefold. This highlights the importance of understanding and managing the biomechanical consequences of the initial injury.

Fracture Type	Primary Mechanism (Typical)	Key Morphological Feature	Primary Biomechanical Consequence
Wedge	Flexion-compression	Disproportionate anterior height loss; posterior wall intact	Induces kyphosis; shifts center of gravity anteriorly; increases flexion moment; increases load on posterior elements and adjacent discs
Biconcave	Compression (often osteoporotic)	Central vertebral body/endplate depression; anterior/posterior walls intact	Reduced overall vertebral height; altered endplate loading
Burst/Crush/"Pancake"	High axial load (+/- flexion)	Significant global height loss; often involves posterior wall disruption; potential retropulsion	Major loss of anterior/middle column support; significant load shift to posterior elements; potential for direct neural compression; potential for instability

Associated Facet Joint Pain

Several mechanisms can lead to the facet joints becoming painful following a VCF:

Altered Loading and Biomechanics: As discussed, VCF disrupts normal load distribution, shifting forces posteriorly onto the facet joints. This increased compressive and shear stress can directly irritate joint tissues or accelerate degenerative processes. The kyphotic deformity resulting from wedge fractures increases the flexion moment arm, requiring compensatory muscle action and potentially altered joint kinematics that further stress the facets.

Capsular Strain and Stretch: Abnormal spinal motion or sustained compensatory postures (e.g., excessive extension to counteract kyphosis) can lead to stretching or impingement of the facet joint capsule. Studies, including those by Bogduk on whiplash mechanisms, demonstrate that capsular stretch can activate mechanoreceptors and nociceptors, leading to pain.

Inflammation and Osteoarthritis: Chronic overloading and altered joint mechanics can trigger inflammatory responses within the synovial joint or exacerbate pre-existing degenerative changes (osteoarthritis). Inflammatory mediators released during tissue injury or degeneration can sensitize nerve endings, lowering the threshold for pain perception. Studies show a correlation between prevalent VFs and subsequent progression of facet joint osteoarthritis.

Posterior Element Subluxation: When a vertebral body loses height due to a fracture, it creates a length discrepancy between the anterior and posterior columns of the spine. Because the posterior elements maintain their height, the spine must adjust to accommodate this difference. This necessary adjustment leads to the subluxation (partial dislocation) of the posterior elements, either upwards (cephalad) or downwards (caudad), depending on the nature of the fracture.

The specific way the posterior elements adjust, and the potential source of pain, varies with the fracture type. In an anterior wedge fracture, the vertebra above the fractured one tilts forward, causing its inferior articular processes to slide upwards and forwards. This can strain the capsule of the zygapophysial joint above the fracture or lead to irritating point contact between the articular processes. Conversely, in vertical compression fractures, the loss of height forces the posterior elements of the fractured vertebra to subluxate downwards, potentially straining the zygapophysial joint below or causing irritation where the lamina contacts the process below. Thus, the model proposes that persistent pain after such fractures may originate from these affected posterior structures rather than the fractured bone itself

In this model, an anterior wedge fracture affects the joint above the fractured vertebra; while in a vertical compression fracture it is the joint below.

Resources

Vertebral Compression Fracture - Members Subpage