**2. Etiopathogenesis**

The causes of adult scoliosis are many. Aebi [1] classified adult scoliosis into four different groups, based on their etiologies. Type 1 refers to primary or de novo degenerative lumbar scoliosis. Type 2 refers to adult idiopathic scoliosis (ADIS), and type 3 refers to adult curves with other primary causes. The last type includes two subgroups. Type 3a refers to adult scoliosis caused by spinal or extra-spinal factors, while type 3b refers to those caused by metabolic bone diseases [1]. Thus adult scoliosis patients are not a homogeneous population group. Our present discussion would focus on DLS which is more prevalent than other types of adult scoliosis.

The pathomechanisms of DLS have not been entirely elucidated, though vertebral instability has been proposed to play a role in its pathogenesis [8, 9]. Kobayashi et al. [4], in a study of the prevalence of DLS, proposed that lateral osteophytes present at the endplate which are in excess of 5 mm together with an asymmetric tilt of disc space >3° are risk factors for the development of DLS [4].

The factors initiating the vertebral instability, however, are unknown. Lumbar paraspinal muscle atrophy; facet tropism, which is defined as the angular asymmetry between the left and right facet joint orientation; and osteoporosis have all been implicated in the pathogenesis of the condition [7, 10, 11].

Lumbar multifidus muscle atrophy (LMA) has also been postulated to contribute to vertebral instability [10]. The multifidus muscle is the deepest and most medial paraspinal muscle, adjacent to the facet joint. LMA is common in DLS, particularly on the concave side of the lumbar scoliosis (**Figure 1**) [12, 13]. Conversely, hyperplasia of the multifidus muscle is evident on the convex side of DLS [14]. Sun et al. [10] investigated the relationship between LMA and various coronal and sagittal radiographic parameters in 144 patients with DLS [10]. They showed that the LMA in the upper and lower vertebral levels adjacent to the apex on the concavity of the lumbar scoliosis correlated positively with the Cobb angle [10]. Conversely, the LMA on the convex side correlated negatively with the lumbar Cobb angle [10]. Sun et al. [10] postulated that LMA may cause vertebral instability and subsequent degenerative changes of lumbar facet joints. Remodeling of articular processes, which includes cartilage degeneration and bone erosion, generally lags behind LMA [10].

Facet tropism has also been postulated to increase the risk of vertebral rotatory olisthesis (VRO) and degenerative lumbar scoliosis [11, 15, 16]. Vertebral rotatory olisthesis refers to lateral and rotatory vertebral translation. Facet joints were found to be more angled in a coronal plane on the convex side of VRO than those of the control subjects without VRO [11]. More severe facet tropism is associated with a higher incidence of VRO [11]. The asymmetric facet orientation causes uneven stress distribution across the zygapophyseal tissues and brings about degenerative changes and segmental instabilities [11]. An intraoperative biomechanical study demonstrated that facet tropism contributed to lumbar vertebral instability [17].

The role of osteoporosis in DLS has been controversial, with some studies showing that osteoporosis contributed to DLS, a number showing that DLS caused the osteoporosis, with others showing no correlation between the two [7]. The lumbar scoliosis brought about by vertebral instability may stabilize or progress [8, 9]. In the presence of marked scoliotic wedging of one disc in the early phase of DLS, adjacent discs may compensate by wedging in the other direction to maintain balance, with resultant stabilization or even regression of the lumbar scoliosis (**Figure 2**) [8].

*Conservative Treatment of Degenerative Lumbar Scoliosis DOI: http://dx.doi.org/10.5772/intechopen.90052*

### **Figure 1.**

*Lumbar multifidus atrophy. From the MRI, it is evident that there was marked asymmetric lumbar multifidus atrophy at the level of L3/L4. The fatty infiltration area in the left multifidus was significantly larger than that in the right multifidus.*

In other cases, degenerative scoliosis may progress. The increased pressure and shear stress on the facet joints cause alterations within the synovial surfaces of the articular processes with subsequent facet hypertrophy, capsular degeneration, and ligamentous hypertrophy [18]. Also, asymmetric loading of the lumbar facet joints and intervertebral discs may result in spinal deformities occurring in three planes [19, 20], particularly in the presence of decreased bone density. Depending on the number of segments involved, this can also cause segmental or multi-segmental vertebral instabilities. Further instability in the sagittal and coronal planes may result in degenerative spondylolisthesis and rotatory olisthesis, respectively [21]. It has to be noted that rotatory olisthesis is present even in mild lumbar scoliosis of less than 20° [21].

Lumbar VRO is prevalent in L3–L4, followed by L2–L3 and L4–L5. Of all the VRO, L3–L4 laterolisthesis contributes around half of the prevalence [11, 22, 23]. Watanuki et al. [24] proposed that this was related to the mechanical stress at the L3–L4 levels, as the lower lumbar levels are more fixed and the upper lumbar

### **Figure 2.**

*Mild intervertebral disc wedging in one level is compensated by wedging in the opposite direction to maintain coronal balance. Mild disc wedging was evident in L4/L5 level. The wedging was compensated by disc wedging above (L3/L4) in the opposite direction, balancing the spine.*

segments are more mobile [24]. The smaller size of the L4 vertebral body may also contribute to the higher incidence of laterolisthesis at L3–L4, as a reduction of 25% of the vertebral cross-sectional area increases mechanical stress by 30% with an applied load, contributing to vertebral instability [25].

To reduce the instability, the body reacts by growing osteophytes (**Figure 3**). The spondylosis (osteophytes by the end plates) and the spondyloarthritis (degenerative changes of the facet joints) that result, together with the ligamentous hypertrophy, compromise the central spinal canal and the lateral recess and may bring about claudication and nerve root compression symptoms [1].

Apart from bone and articular involvement, paraspinal muscle atrophy is prevalent in DLS. Sarcopenia, which is a reduction in skeletal mass, is commonly seen in patients with DLS. Eguchi et al. [26], using DEXA scans to assess the appendicular and trunk skeletal muscle mass, showed that sarcopenia was present in 46.6% of the DLS patients [26]. Sarcopenia is defined as the appendicular skeletal mass index of less than 5.46 kg/m<sup>2</sup> [27]. The appendicular skeletal mass index (ASMI) is the sum of the arm and leg lean mass (kg) divided by square of the height (m<sup>2</sup> ) [27]. Studies have also shown that ASMI negatively correlated with pelvic tilt [26], whereas trunk skeletal mass index (Trunk SMI) which is defined as trunk lean mass

### **Figure 3.**

*The osteochondrosis at L4/L5 intervertebral level, together with the bridging osteophyte in the left of L3/L4, stabilized the mild scoliosis curve and maintained coronal balance in this man aged 63 years.*

divided by height<sup>2</sup> (m<sup>2</sup> ) significantly correlated with the sagittal vertical axis, pelvic tilt (PT), and lumbar scoliosis [26]. Moreover, trunk SMI correlated positively with bone mineral density (BMD), suggesting that reduction in trunk muscle mass was associated with osteoporosis and sagittal imbalance [26], which is prevalent in patients with DLS.
