Although PKP provides rapid pain relief, effectively restores the height of the injured vertebrae, and increases the mechanical stability of the injured vertebrae, it is associated with certain complications, such as infection, adjacent vertebral fractures, bone cement leakage, and postoperative RBP. Among these, RBP most significantly impacts patients’ quality of life and is also the most common adverse event. Recent studies show that the incidence of postoperative RBP in patients with OVCF ranges from 4.6 to 23.6% [3, 7, 14, 17]. In this study, the incidence of RBP was 19.5%, consistent with previous findings. In 1989, Hankin first described sarcopenia as a systemic degenerative disease characterized by progressive decrease in skeletal muscle mass [18]. While sarcopenia is known to impair the locomotor system, accelerate muscle atrophy and aging, and increase disability risk in elderly populations, limited research exists on its effects on RBP development after PKP. Therefore, we explored in depth the independent risk factors for the development of RBP in patients with OVCF after PKP. The results showed that patients’ BMD (OR = 0.743, 95% CI 0.557–0.990, P = 0.042) and sarcopenia (OR = 2.146, 95% CI 1.074–4.290, P = 0.031) were independent risk factors for the development of RBP after PKP. In the present study, we observed that the incidence of postoperative RBP in patients with sarcopenia was approximately twice as high as in patients with non-sarcopenia.

Indeed, sarcopenia may affect the development of RBP after PKP through multiple mechanisms. According to a systematic evaluation and meta-analysis by Lin et al., there is a strong positive correlation between sarcopenia and pain [19]. On the one hand, skeletal muscles are essential for maintaining normal spinal biomechanics, and in particular the erector spinae, multifidus, and abdominal muscle groups play a key role in spinal postural control and load distribution [20]. The loss of muscle mass and function in sarcopenia can lead to a biomechanical imbalance in the spine. If the spine’s equilibrium is disrupted, the body needs to exert more force to stay upright, which in turn increases fatigue and causes chronic pain [21]. Li et al. reported that spinal instability is an important cause of persistent postoperative low back pain in patients [9]. In patients with OVCF treated with PKP, although the bone cement restores the mechanical strength of the vertebral body, functional deficiencies in the muscular system may expose neighboring vertebrae to abnormal stresses and uneven distribution of vertebral loads. Kang et al. used finite element analysis to confirm that the load on the vertebral bones continued to decrease as the volume of the spinal muscles increased, which aided in the management of spinal pain [22]. In this study, we assessed sarcopenia by SMI and found that the SMI of patients in the RBP group was significantly lower than that of the control group (30.40 ± 5.66 vs. 32.76 ± 5.96, P = 0.017) and the proportion of sarcopenic patients was higher in the RBP group (48.89% vs. 27.42%, P = 0.005), suggesting that patients with sarcopenia showed poor improvement in postoperative back pain symptoms. Logistic regression analysis further confirmed that sarcopenia was an independent risk factor for postoperative RBP (P = 0.031). Wu et al. also demonstrated that sarcopenia was the main cause of negative clinical outcomes after PKP in patients with OVCF [12]. In another study, thoracolumbar fascia injury was found to be associated with RBP after PKP, and among the many risk factors, sarcopenia was the main factor contributing to thoracolumbar fascia injury [23], which is consistent with our findings. In addition, under conditions of skeletal discomfort loading and muscle degeneration, the vertebral body may become more susceptible to external forces, thereby increasing the risk of recompression fracture of the vertebrae [24]. Notably, sarcopenia is often accompanied by a chronic low-grade inflammatory state [25], and Bonanni et al. in their article on sarcopenia in relation to the development of pain concluded that the presence of chronic inflammation promotes injurious stimuli and pain sensitization in the skeletal system, a mechanism that is largely dependent on elevated levels of certain pro-inflammatory factors, such as prostaglandins, interleukin 6, and histamine [26]. These inflammatory factors not only accelerate muscle proteolysis, but also lower the pain threshold by activating nociceptor in the ganglia [27], which may explain why patients with sarcopenia report persistent low back pain even when vertebral stability is restored after PKP. In addition to sarcopenia, BMD was also found to be an independent risk factor for the development of RBP in the postoperative period in this study, and the results showed that the BMD of patients in the RBP group was significantly lower than that of the control group (-3.68 ± 1.25 vs. -3.17 ± 1.24, P = 0.013); therefore, an increase in BMD can be considered as a protective factor for RBP after PKP. Although low BMD is widely recognized as a risk factor for postoperative re-fracture in patients with OVCF [3, 28, 29], however, in recent years, several studies have found that BMD also influences the occurrence of postoperative RBP in patients. Shen et al. found that patients with higher BMD were relatively less likely to develop RBP after surgery [30]. Chen et al. confirmed in their study that BMD can be used as an aid in assessing the risk of a patient having or not having RBP after surgery [31], which is in agreement with our findings. Although all patients received anti-osteoporotic therapy, variations in individual response or adherence may affect fracture healing and pain relief. Future studies could explore the interaction between duration of drug therapy and incidence of RBP. In fact, in patients with osteoporosis, the trabecular structure of the vertebral body is more fragile with low BMD, and even if the height of the injured vertebra is restored after PKP, the mechanical properties of the bone cement within the vertebral body may still be insufficient due to the formation of a strength difference between the bone cement and the surrounding cancellous bone, resulting in residual pain [30]. Therefore, during PKP injection of bone cement, it should be ensured that the amount of bone cement injected is sufficient in order to achieve satisfactory filling and spreading, thus avoiding the occurrence of postoperative RBP.

This study also has some limitations. First, this study is only a retrospective study of short-term follow-up case data from a single center, and the results may be biased. Second, the occurrence of RBP after PKP is a multifactorial outcome, and although we analyzed some potential risk factors, the number was limited. Some risk factors were not included in this study, such as the thoracolumbar fascia injury status, the puncture method of surgery, and the wearing of postoperative patient assistive braces. In addition, patients were categorized into two groups based on their VAS scores at 1 month postoperatively, and long-term follow-up at multiple time points was more convincing. Nonetheless, some risk factors regarding the occurrence of RBP in patients after surgery have been demonstrated in this study.