One of the most frequently asked questions I hear about vertebral fractures is this. Does placement of bone cement via vertebroplasty or kyphoplasty make the adjacent level more likely to fracture? This is a medical 'old wives tale' that is generally propagated by people who aren't familiar with these procedures.
Those who think bone cement causes adjacent level fractures usually suggest that it makes the fixed vertebral body harder that the adjacent level vertebrae. What people fail to consider is that the intervertebral disc acts as a cushion, dampening forces as the spine is loaded.
Theorhetically, if a disc is severely degenerated (end-stage intervertebral osteochondrosis), we might be transmitting forces directly across to the next vertebral endplate. However, I rarely see that severe of disc disease in osteoporotic patients.
I have seen several well-funded studies that have tried to prove the old 'adjacent level fracture' myth. All have tried and failed. A couple in particular have compared traditional vertebral augmentation using PMMA with that done using 'softer' material such as morselized (ground up) bone graft or osteoconductive material. None has shown an increased rate of adjacent level fractures with PMMA.
Still, when a patient comes in with a fracture and they get PMMA, then next time they have a fracture, they often fracture at an adjacent level. The reason is simple--biomechanics.
Biomechanical Causes Of Adjacent Level Fractures
The first reason that patients tend to fracture at an adjacent level is because most vertebral fractures due to osteoporosis occur between the T11 and L2 levels, most at T12 and L1. Hence, when a patient has a T12 or L1 fracture (the most common areas), the next fracture they have tends to be at an adjacent level because that's where they usually happen anyway.
Second, for someone who has a significant compression fracture, particularly an anterior wedge fracture, there is generally anterior shift of the center of gravity due to increased kyphosis. This results in redistribution of weight anteriorly (relative to before) along the anterior column.
Similar to the femur, when load-bearing stresses change in location, bony remodeling occurs to better allow the bone to bear that load. In patients with metabolic bone disease, such as osteoporosis, the speed of remodeling is impaired. As a result, the weight is shifted anteriorly, where the supporting vertical trabeculae are weaker. Thus, a fracture is more likely to occur here. This partly explains why most osteoporotic VCFs are anterior wedge in morphology.
Third, when there is an increase in kyphosis, the gravity creates a vector force due to the weight of the entire upper body being shifted anterior relative to the spine below the fracture. This increase in angular momentum and force meet at the fractured vertebral body (which serves as a fulcrum). This is the reason fractures tend to continue to collapse with time. The immediately adjacent vertebral bodies are also closer to the fulcrum and recieve a higher force/stress than vertebral bodies further away.
The result of all of this is that when a patient gets one VCF, they tend to get additional VCFs. These new VCFs tend to be next to the affected vertebral body for a variety of reasons--and this happens whether the initial fracture has been fixed or not.
The picture above is a great, practicle example. This patient developed a T12 fracture that was not treated. She now has presented with an adjacent level endplate compression at L1--note that it is at the superior endplate and closest to the fulcrum of T12.
So the next time someone suggests that vertebral augmentation causes adjacent level fractures, you now know why that is a myth. You also have a great example of the real underlying cause.