Establishment of a risk prediction model for residual low back pain in thoracolumbar osteoporotic vertebral compression fractures after percutaneous kyphoplasty

Osteoporosis is a systemic metabolic bone disorder characterized by decreased bone mass and the destruction of trabecular bone structure, which often leads to fragility fractures [1]. Osteoporotic vertebral compression fractures (OVCFs), a prevalent complication of osteoporosis-related fragility fractures [2, 3], are frequently associated with chronic and persistent low back pain (LBP), progressive spinal deformity, and other issues, significantly impacting the patients' daily quality of life. In clinical practice, OVCFs can be managed through both conservative and surgical approaches. While conservative treatment of OVCFs has shown relatively high mortality rates, PKP has emerged as an effective treatment [4, 5], providing substantial relief from back pain, spinal stability restoration, early patient mobilization, and prevention of complications such as hypostatic pneumonia and pressure ulcers [6, 7]. However, our clinical observations have revealed that some patients continue to experience residual LBP after undergoing PKP. Previous research studies have reported various potential risk factors associated with the persistence of LBP following PKP [8], including factors such as non-healing bone cement interfaces, thoracolumbar fascia injury (TLFI), cement volume and distribution, and IVC. Some studies have developed risk prediction models for residual LBP after PKP. However, previous models had a limited set of potential independent risk factors. In our study, we conducted a comprehensive analysis of various baseline factors related to postoperative residual LBP in patients with OVCFs. We aimed to develop a predictive model that can be utilized by physicians to inform clinical decision-making for OVCFs patients.

In this study, we conducted postoperative follow-up for a total of 267 patients with OVCFs based on our inclusion and exclusion criteria. Among these patients, 46 (17.22%) experienced postoperative residual LBP, while the remaining 221 patients did not. As indicated in Table 1, the variances in preoperative VAS scores and Oswestry Disability Index (ODI) scores between the two groups did not demonstrate statistical significance (P > 0.05). In the postoperative assessments conducted at 1 day, 1 month, and 3 months, a significant difference in both VAS scores and ODI scores between the two groups was observed (P < 0.05).

PKP is a commonly used and effective treatment in clinical practice, surpassing conservative methods in significantly reducing long-term mortality. However, PKP treatment carries certain complications [ [17]], including postoperative adjacent vertebral fractures, pulmonary embolism, cement leakage, and postoperative residual LBP. Among these, the persistence of LBP post-surgery substantially diminishes patients' satisfaction and quality of life. The specific causes of this residual LBP after PKP treatment remain unclear. Our clinical observations have revealed a multitude of factors influencing postoperative LBP. In this study, we delved into the examination of factors impacting postoperative residual LBP, specifically in a total of 267 patients with thoracolumbar OVCFs. Through the development of a predictive model for residual LBP following PKP treatment in patients with thoracolumbar OVCFs, we identified five potential independent risk factors: posterior fascial oedema, IVC, time from fracture to surgery, sarcopenia, and degeneration of the interspinous ligament. Significantly, the ROC analysis demonstrated an AUC of 0.844 (95% CI 0.772–0.917), signifying the model's robust discrimination and calibration. Moreover, the DCA results in both the training and validation sets affirmed the model's substantial net clinical benefit. Moreover, a plausibility analysis of the predictive model again showed that the model was reasonable.

IVC is a condition typically associated with older individuals who have severe osteoporosis, and it is widely believed to be attributed to ischemic necrosis. Furthermore, as noted by Kim [18], the IVC sign was predominantly located at the thoracolumbar junction (81%). Considering the heightened activity and increased mechanical stress experienced by this region, biomechanics was also believed to have a notable impact on the formation of the IVC sign. Therefore, IVC is considered indicative of spinal instability. In the treatment of OVCFs accompanied by IVC, PVP or PKP is often the primary choice [19]. However, several studies have uncovered a strong association between IVC and long-term postoperative issues, such as residual low back pain, vertebral body collapse, and instability [20]. Li et al. [21] demonstrated that patients with OVCFs and IVC typically experience substantially higher VAS scores than those without IVCs. This could be attributed to the cement primarily filling the IVC, potentially leaving the rest of the vertebral body inadequately supported and treated. In alignment with these findings, our results also indicated that the preoperative presence of IVC was a significant risk factor for postoperative residual LBP following PKP.

Furthermore, despite posterior fascial oedema being categorized as a soft tissue injury, it remains a significant consideration in clinical practice. The majority of patients with OVCFs are caused by low-energy injury such as falls. Nevertheless, our study revealed that the presence of posterior fascial oedema in OVCFs patients is not uncommon (19.2%), consistent with previous research findings. Yang [22] and colleagues demonstrated that PKP effectively alleviated LBP in OVCFs patients, but the same relief was not observed in patients with posterior fascial oedema. Their conclusion pointed to a strong connection between posterior fascial oedema and residual LBP. The posterior spinal nerve roots' branches traverse through the thoracolumbar fascia (TLF). When fascial injury occurs, nerve compression, inflammatory factor stimulation, and soft tissue oedema emerge as potential culprits behind the associated pain. Additionally, research on models related to the induction of posterior fascial oedema had consistently shown that reducing oedema and inflammatory factors tended to correlate with gradual pain reduction [23]. Consistent with prior studies, multifactorial analysis underscores the status of posterior fascial oedema as an independent risk factor for post-PKP residual LBP.

Sarcopenia, an age-related condition, is both progressive and widespread [24]. It involves a reduction in muscle mass and function and is often closely linked to osteoporosis. Multiple studies have indicated that nutritional disorders can be the root cause of both sarcopenia and osteoporosis, leading to functional impairment. It is not uncommon for patients to grapple with both conditions [25]. Muscles play a pivotal role in maintaining spinal stability. Sho [26] and colleagues have illustrated how sarcopenia impacts LBP and daily life for osteoporosis patients. Additionally, Yu [27] and team have demonstrated that sarcopenia diminishes the clinical efficacy of PKP. Hence, it is reasonable to hypothesize that sarcopenia may influence the alleviation of LBP following PKP in patients with OVCFs. In this study, we assessed muscle mass using lumbar spine CT. The measurement of the total psoas major muscle area (TPA) at the level of the third lumbar vertebra's transverse process offers a simple and rapid method to evaluate sarcopenia [28, 29]. Our findings indicated a notably higher occurrence of sarcopenia in the residual LBP group when compared to the control group. Multifactorial regression analysis further confirmed that sarcopenia stands as an independent risk factor for post-PKP residual LBP. Consequently, for OVCFs patients with sarcopenia, the focus should extend beyond merely enhancing vertebral stiffness to also encompass muscle mass improvement. In clinical practice, the treatment of sarcopenia recommends a combination of exercise and multiple nutritional supplements, including protein and vitamin D supplementation [30, 31].

We have observed that some patients with OVCFs continue to experience persistent LBP even after a period of conservative treatment, significantly impacting their daily lives. In clinical practice, surgical intervention is often recommended. While numerous previous studies have compared the effectiveness of conservative treatment and vertebral augmentation, little attention has been given to the timing of vertebral augmentation. Akihito [32] and colleagues discovered that early surgical treatment in OVCFs patients reduced the incidence of postoperative LBP and re-fractures. However, for those OVCFs patients who still experience residual LBP after surgery, some studies have concluded that the timing of vertebral augmentation is not an independent risk factor [33]. In our study, we utilized a 4-week period from injury to surgery as a reference point and found that the proportion of patients with an injury-to-surgery interval exceeding 4 weeks was higher in the group with residual LBP compared to the control group. This led us to propose that the timing of vertebral augmentation may indeed be a significant factor influencing the development of residual LBP following surgery in OVCFs patients (OR 6.554, P = 0.00). This could be attributed to various factors: (1) It might be associated with the delayed formation of osseous junctions or pseudoarthrosis, often stemming from the delayed treatment of compression fractures. Such delays are known to contribute to chronic pain that ensues after an injury [34‐36]. (2) The formation of primitive callus typically takes place around four weeks post-fracture and undergoing vertebral kyphoplasty at a later date (more than 4 weeks) is not conducive to alignment improvement.

Degenerative changes in the lumbar spine rank among the primary causes of LBP and disability in the elderly [37]. Typically, we place our focus on alterations in intervertebral disks while overlooking the significance of non-disk structures within the spine, including the facet joints, paraspinal muscles, and spinal ligaments. Among these structures, the interspinous ligament holds a pivotal position within the posterior spinal ligament complex. It plays a crucial role in spinal flexion. When the body undergoes excessive forward bending or experiences an energetic impact, the posterior column structures of the lumbar spine come under increased tension and load, with the interspinous ligament often bearing the brunt of the injury. Multiple studies have assessed the interspinous ligament's role through biomechanical tests [38] and through the observation of anatomical, biochemical, and pathological changes in degenerative spines. Maes [39] and colleagues have concluded that the degeneration of posterior column ligaments is a significant contributor to LBP. In the investigation of changes within the interspinous ligament, MRI has established itself as the primary diagnostic method of choice. Keorochana et al. categorized ISLD into four types [40, 41]. However, our study encompassed cases beyond mild degeneration. In line with prior research, multifactorial analysis demonstrated that ISLD stands as a significant risk factor for persistent LBP following PKP (OR 5.061, P = 0.001). Consequently, we created a nomogram through the analysis of potential risk factors to predict the occurrence of residual LBP. This model proves to be a viable tool for risk assessment, enabling early identification of OVCFs patients with a high risk of residual LBP. With this knowledge, individualized strategies can be crafted for these patients during the perioperative period.

Our study has several limitations. First, it is important to acknowledge that our study is retrospective and has a restricted sample size. Second, our postoperative follow-up period is relatively short, and we acknowledge the importance of conducting studies with extended follow-up durations and multiple assessment time points. Third, it is essential to highlight that this study is conducted at a single center, and the validation of our findings would benefit from future multicenter studies conducted in different hospitals.

We have created a novel numerical model that can precisely forecast the potential risk factors associated with the onset of LBP following PKP in patients with thoracolumbar OVCFs. This model is poised to aid in the early identification of OVCFs patients at a heightened risk of enduring residual LBP, offering valuable insights to guide clinical decision-making.