Lumbar intervertebral disc degeneration (IVDD) is a complex process involving many factors. At present, the mechanism of lumbar IVDD is still not fully understood [10]. Youn et al. [12] found that factors such as biomechanics, nutritional status, apoptosis, cytokines and degrading enzymes have a great influence on IVDD. The latest research reports: In the population coding, a certain genetic mutation of aggrecan was found, and the aggrecan can shorten the length of the proteoglycan core protein chain [13]. Interestingly, through further investigation, it was found that these certain populations are more prone to multi-segment degenerative disc changes clinically, which may indicate that the IVDD is related to human genetic factors [14]. In addition, according to related studies, the combined use of in vitro insulin-like growth factor and platelet-derived growth factor can delay the rate of apoptosis in IVDD [15]. The main biomechanical feature of the IVD is to maintain the height of the intervertebral space, resist the compressive force from the longitudinal direction and limit the relative motion of the two adjacent vertebral bodies to a small painless range [16]. Therefore, abnormal or uncoordinated mechanical loading can lead to the formation of intervertebral disc degeneration. In particular, axial-related force factors and trauma (mechanical violence) have been regarded as the main pathogenic factors of intervertebral disc degeneration [17]. Some studies have found that the sagittal changes of facet joints are related to the IVDD [5, 18].
According to previous studies, the changes in the shape and position of the facet joints of the lumbar spine are caused by many factors, such as facet joint osteoarthritis, IVDD and other factors [19]. The exact cause of the shift has not yet formed a unified view in the academic world. Some people think that it is caused by acquired facet joint remodeling, while some scholars believe that it is caused by congenital [10, 20]. There are many studies on the relationship between the lumbar facet joints and the IVDD, but the relationship between the sagittalization of the lumbar facet joints and the degree of IVDD has always been controversial [21, 22]. Therefore, this study takes the LFJA as the starting point, and focuses on the relationship between LFJA and IVDD.
In terms of biomechanics and anatomy, the IVD and the facet joint behind it together form a "three-joint complex", which is the functional unit of the spinal movement system [23]. The IVD has the functions of buffering pressure, bearing load, and maintaining the stability of the spine. When the mechanical balance is destroyed, the stability and motor function of the spine will inevitably be affected [24]. It may affect the adjacent functional units of the spine and even affect the overall stability and motor function of the spine. Previous studies have established that facet sagittalization is associated with vertebral advancement in degenerative lumbar spine, and that increasing the location and direction of vertebral advancement greatly increases the risk of facet instability [25, 26]. Regarding the relationship between lumbar IVD and facet joints, Huang et al. [27] believed that lumbar facet joints and IVDD are interrelated and causal in the whole process of lumbar degeneration. The main causes of lumbar IVDD and facet joint degeneration are natural aging and abnormal stress. Wang et al. [28] believed that lumbar vertebral degeneration begins with facet joint degeneration, and lumbar IVDD and facet joint degeneration affect each other. With the increase of age, lumbar IVDD accelerates and gradually surpasses the speed of lumbar facet joint degeneration. Some foreign scholars believe that lumbar spine degeneration begins with IVDD [25, 29, 30]. Due to the dehydration of the IVD and the loss of the height of the intervertebral space, the stress of the facet joints changes, which in turn leads to degeneration of the facet joints.
In 2001, Pfirrmann et al. [31] proposed their own grading method for IVDD based on the signal intensity of the IVD on MRI, the structure of the IVD, the demarcation between the nucleus pulposus and the annulus fibrosus, and the height of the IVD, and confirmed that it has high reliability. (kappa = 0.69–0.90). This study reclassified IVDD according to the modified Pfifirrmann score [31]: grade I, Pfifirrmann 1; grade II, Pfifirrmann 2, 3, based on signal from nucleus pulposus and inner annulus; grade III, Pfifirrmann 4, 5, based on external Signal of annulus fibrosus; grade IV, Pfifirrmann 6–8, based on loss of disc height. This is mainly to reduce subjective evaluation errors, but also to highlight differences in classification.
The results of this study showed that the LFJA of each segment in the patient group were significantly smaller than those in the control group (P < 0.01). In the patient group, as the lumbar vertebral segment were lower, the LFJA gradually decreased, which was statistically significant (P < 0.01). In addition, according to the Pfifirrmann classification, it was showed that there was no significant difference in the LFJA between grades I and II (P > 0.05). Further, we analyzed the relationship between the LFJA and the Pfirrmann score by using Pearson correlation. It was found that with the increase of the Pfirrmann grade of the IVD, the LFJA gradually decreased, and the degree of sagittalization of the facet joint became more significant. There was a strong negative correlation (ρ = − 0.736, P < 0.001). These results fully indicate that there is a close relationship between the sagittalization of the facet joints and the degree of IVDD, and the sagittalization of the facet joints is likely to be the main pathogenic factor of IVDD.
According to the results obtained in this study, we analyzed its main mechanism in two points: First, the "three-joint complex" formed by the IVD and the facet joints on both sides—This special structure plays a very important role in maintaining and stabilizing the balance and coordination of lumbar spine activities [23, 26]. Abnormalities in any one part will affect the other two parts and thus the whole. The lumbar IVD of the patients in this study group all have different degrees of degeneration. The earliest due to the IVDD changes, the intervertebral space is narrowed, the height of the IVD is lost, and the lumbar vertebral is unstable, which further causes local load bearing on the facet joints [32]. As a result, the stress-increasing site are more prone to bone hyperplasia, and the stress-reduced site is more prone to osteoporosis, accompanied by the existence of corresponding soft tissue repair and reconstruction, and finally the sagittal change of the facet joints. Second, there are different biomechanical factors in L4/5 and L5/S1 IVDD. The degeneration of the L4/5 IVD is mainly related to the way of rotational movement, and the morphological basis of the L4/5 facet joint is the curved articular surface [32] The degeneration of the L5/S1 IVD is mainly related to the stability of the spine and the gravitational load. The morphological basis of the L5/S1 facet joint is a straight articular surface [25, 26]. This causes the lower the lumbar vertebrae segment, the more sagittal the LFJA. This change in the LFJA causes stress concentration in the force transmitted from top to bottom, so the gravitational load on the L5/S1 facet joint will increase, which will seriously affect the function of this joint, further causing instability of the spine and in turn promoting the IVDD [33] .
This study has certain limitations: First, this is a retrospective study; Second, factors such as occupation, smoking, age, and body mass index were not included in the analysis of the relationship between the LFJA and IVDD, which may lead to differences in the observed IVDD and LFJA [28–31]; Finally, this study provides only key insights into the association of facet joint parameters with L3/4, L4/5, and L5/S1 IVDD. The more vertebral segments and influencing factors need to be included for in-depth research.