To our knowledge, this is the first prospective cohort study of segmental artery occlusion in KD. Our results suggest that the degree of occlusion of KD segmental arteries was significantly higher than that of non-KD segmental arteries. Fractured segments with a high degree of artery occlusion had a significantly higher probability of recollapsing after vertebroplasty. There was no significant difference in postoperative VAS and ODI scores between KD and non-KD patients.
There are many hypotheses about the pathogenesis of KD formation[4, 11, 12], among which ischemic osteonecrosis is the most widely supported and studied hypothesis. Avascular osteonecrosis after VCFs has its own anatomical theory. Ratcliffe used microangiography to study the arterial anatomy of the adult lumbar vertebral body and proposed that the upper and lower anterior segments of the vertebral body are the watershed areas of the vertebral body. These areas are susceptible to ischemia. Prakash also reported that the central anterior branch of the pair of segmental arteries supplies the ventral side of one vertebral body, while the central posterior branch supplies the dorsal side of two adjacent vertebral bodies. Therefore, the dorsal side of the vertebral body receives collateral blood flow, but the ventral side does not; this will theoretically make the ventral part of the vertebral body have a higher risk of blood supply destruction.
Lin et al. reported that in patients with osteoporotic VCFs before vertebroplasty, decreased bone marrow perfusion, as measured by DCE-MRI, was associated with IVC formation. Kim et al. found that most patients with IVC have unilateral or bilateral segmental artery occlusion through MRA. In our study, compared with normal vertebral bodies and simple VCFs, we found that the degree of KD segmental artery occlusion was significantly increased. All these results suggest that the destruction of blood supply may be an important reason for the formation of IVC, indicative of KD.
In many research reports, IVC has been suggest to be an important high-risk factor for recollapse after vertebroplasty[9, 19, 22]. Our results suggest that the recollapse rate of KD segments was significantly higher than that of non-KD segments. At the same time, the recollapse rate of VCFs with a high degree of artery occlusion in non-KD segments was also significantly increased. Therefore, we believe that in addition to IVC being a high-risk factor for recollapse, segmental artery occlusion is also an important high-risk factor for recollapse after vertebroplasty.
At present, the main treatment for KD is vertebroplasty[23–25]. Complications such as recollapse after vertebroplasty are relatively high in patients with KD, and therefore, some clinicians have tried to use short-segment vertebral fixation to treat KD[26–28]. Our research suggests that there was no significant difference in VAS and ODI scores between KD and non-KD patients. This is also consistent with the results of many clinical reports that vertebroplasty is an effective treatment for KD[23–25]. There are also studies comparing the prognosis of vertebroplasty and short-segment vertebral fixation, and the results showed no significant differences in VAS and ODI scores[26–28]. We found that no non-KD segments progressed to KD after surgery, regardless of the degree of segmental artery occlusion. This may be because vertebroplasty restores the stability of the vertebral body, disrupts the vicious cycle mechanism leading to KD formation, and avoids the further blood supply damage.
It takes an amount of time for VCF to progress to KD, and the time duration is currently inconclusive. Our findings suggest that the average course of disease in KD patients was significantly higher than that in non-KD patients. We also had a pretty interesting finding. The average LSOR of KD patients within 1 week, 1 month, 3 months, and over 3 months were 2.71, 1.00, 0.60, and 1.67, respectively. The average LSORs within 1 week and more than 3 months were significantly higher than those in the other two stages. For the short course within 1 week, we believe that it is precisely because of the high occlusion rate that VCF rapidly progresses to KD. Regarding the long course of more than 3 months, due to the long course of the disease, the degree of compression of the vertebral body increased, destroyed the blood supply and resulted in aggravation of segmental artery occlusion. Therefore, the destruction of blood supply and vertebral compression fracture are mutually promoting and vicious cycle processes that ultimately produce KD.