Kümmell disease was first described in 1891 as an uncommon complication of osteoporotic vertebral fracture, more frequently encountered in patients with severe osteoporosis that have taken long-term courses of corticosteroids or sustained a spinal injury. Kümmell disease is different from fresh vertebral fracture, and intra-bone clefting is the most important characteristic used to diagnose Kümmell disease. Kümmell disease mostly occurs in women. The thoracolumbar junction, particularly the T12 vertebra, is the most commonly affected vertebral segment. In our study, 76% of injured vertebra were in the thoracolumbar segment.
Different stages of Kümmell disease have unique pathological features. The early stages include avascular necrosis characterized by an accumulation of fluid and inflammatory exudate components. During stage Ⅲ, the compressed, fractured vertebral body compresses the posterior spinal cord, leading to continuous back pain and other neurological symptoms. Stage III Kümmell disease is characterized by the collapse of the posterior vertebral body wall, the formation of spinal canal stenosis, and dural sac compression. Most stage Ⅲ patients, including 84% of the patients in our study, have preoperative neurological symptoms.
The treatment of the Kümmell disease remains controversial. Most spinal surgeons suggest that Kümmell disease should be treated by operative interventions because conservative treatments are less effective and are associated with a high risk of complications and delayed neurological deficits. For early stages patients without neurological symptoms, the aim of treatment is to preserve movement in the diseased vertebrae, and maintain the sagittal balance of the spine. PKP and PVP restore the height of the vertebral body and correct any deformities, which can help achieve satisfactory pain relief. However, PVP and PKP are less suitable for stage III patients because the surrounding vertebral cortex has already been compromised, as well as a higher risk of severe nerve damage caused by bone cement leakage. In our study, the bone cement leakage rate was 25.28%, but there were no serious complications, suggesting that short-term leakage is not damaging. Delayed cement displacement and further collapse have been reported in cases of Kümmell disease treated by cement augmentation alone, with poor bone incorporation of cement noted after a long-term follow-up[22, 23]. Therefore, displacement of bone cement and further vertebral collapse may occur after PKP or PVP.
There are alternative treatment strategies for stage III Kümmell disease, but consensus regarding which is most feasible and effective is lacking. For stage III patients with severe stenosis of the spinal canal and neurological symptoms, the objective of surgery is to relieve cord compression, eliminate spinal instability, and restore the sagittal balance of the spine[12, 19] Many studies have suggested that the main factor contributing to delayed neurological deficits following vertebral collapse in the osteoporotic spine is instability at the fracture site, rather than mechanical compression of the spinal cord by bone fragments[25, 26]. Therefore, maintaining spinal stability is important for treating stage III patients. Other studies suggested that modified posterior vertebral column resection surgery was an effective and safe surgical method to treat stage III Kümmell disease, especially for patients with kyphosis and obvious symptoms of nerve compression; however, the long-term clinical effects require additional evaluation8. Anterior reconstruction and posterior osteotomy have also been proposed for the management of stage III Kümmell disease with neurological deficits. Anterior reconstruction permits direct resection of bony fragments and provides anterior column support. Posterior osteotomy is a common treatment; the advantages include dissection of the posterior cortex by posterior spinal shortening osteotomy and correction of kyphosis[28, 29]. Moreover, these major surgical interventions can be challenging in patients of advanced age, and confer numerous morbid complications and frequent instrumentation failure secondary to severe osteoporosis. Traditional posterior long-segment fixation was not appropriate for stage III Kümmell disease because the procedure was associated with significant trauma and multiple complications, which are worrisome in elderly patients with comorbidities.
There is high risk of pedicle screw loosening because of the osteoporotic vertebra in stage III Kümmell disease. Considering the unsatisfactory performance of traditional pedicle screws in damaged spines, bone cement-augmented pedicle screw fixation strengthens the anti-pullout capability by injecting cement carefully through the screws into the vertebral body. Moreover, it can effectively improve the sagittal balance and stability of the spine.
Bone cement-augmented pedicle screw fixation maintained the stability of the spine and pelvis of the stage III Kümmell disease patients. Posterior screw stress was markedly reduced because of the anterior support provided by the intravertebral cement, which can decrease the risk of internal fixation failure.
There are some limitations to our study. First, it was a retrospective study at a single center with a small sample size. Thus, further studies with larger samples are needed to confirm our findings. Secondly, we observed long segmental fixation and short segmental fixation together; however, these two fixation methods may have different therapeutic effects.