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Purpose: We investigated changes in skeletal muscle mass and bone mineral density in degenerative lumbar scoliosis (DLS) patients during a 2-year follow-up following diagnosis., Method: This study included 418 Japanese women, identifying 50 patients for the DLS group (mean age 76.4 years) and 368 patients for the control group (mean age 73.4 years). Whole-body skeletal muscle mass was measured using a Bioelectrical Impedance Analyzer. Bone mineral density (BMD) was measured using DXA. Skin autofluorescence (SAF), a marker of advanced glycation end products in the skin, was measured using a spectroscope. Spinal alignment, skeletal muscle mass, BMD, grip strength, and SAF were examined and the amount of change 1 and 2 years from the initial examination for each item was compared between groups., Results: Height, body fat mass, grip strength, upper limb muscle mass, and trunk muscle mass in the DLS group were significantly lower, and lumbar spine BMD was significantly greater compared to controls at the first visit (p < 0.05). There was no significant difference in spinal alignment in the DLS group after 2 years compared with baseline. Trunk muscle mass also decreased significantly more in the DLS group (-2.7%) than in the control group (-1.1%) over the 2-year follow-up (p < 0.05)., Discussion: In this study, trunk muscle mass in the DLS group decreased about 2.4 times more in 2 years compared with the control group (p < 0.05). It may be possible to clarify the mechanism of kyphoscoliosis progression in the future with large-scale longitudinal studies., (© 2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Purpose: We investigated the involvement of sarcopenia in middle-aged and elderly women with degenerative lumbar scoliosis (DLS)., Methods: A total of 971 women (mean age 70.4 years) were included in our study. These included 87 cases of DLS (mean 73.8 years) and 884 controls (69.8). Lumbar and femur BMD was measured for all participants using dual-energy X-ray absorptiometry. We used a bioelectrical impedance analyzer to analyze body composition, including appendicular skeletal muscle mass index (SMI; appendicular lean mass (kg)/(height (m)) 2 . We determined bone density and skeletal muscle mass in both groups and determined the prevalence of sarcopenia. We examined the correlation between bone density and appendicular muscle mass in both groups. We also examined factors related to scoliosis using logistic regression analysis., Results: The DLS group showed significantly higher lumbar BMD, lower femur BMD, lower lean mass arm, and lower lean mass leg, and lower lean mass trunk (p < 0.05). Sarcopenia prevalence (SMI < 5.75) was 59.8% in DLS subjects and 42.8% in controls, revealing a high prevalence in DLS (p < 0.05). In both groups, lumbar and femur BMD were positively correlated with appendicular muscle mass. By logistic regression analysis, trunk muscle mass was detected as a risk factor for DLS independent of age (p < 0.05)., Conclusions: In middle-aged and elderly women, prevalence of sarcopenia was 59.8% in DLS cases and 42.8% in controls, which revealed a high prevalence in DLS. A decrease in trunk muscle was a significant risk factor for DLS that was independent of age. These slides can be retrieved under Electronic Supplementary Material.

Purpose: Advanced glycation end products (AGEs) have been implicated in the pathogenesis of sarcopenia. The objective of the study was to investigate the prevalence of sarcopenia in degenerative lumbar scoliosis (DLS), and the relationship between biochemical markers including major AGEs, pentosidine, and DLS in older women., Methods: Our study participants were 20 elderly women with idiopathic DLS (mean age 76.4 years, range 56-88). Nineteen age- and sex-matched volunteers (mean age 74.0 years, range 62-86) served as controls. Spinal and femoral BMD of all participants was measured using dual-energy X-ray absorptiometry. We used a bioelectrical impedance analyzer to analyze body composition, including appendicular skeletal muscle mass index [SMI; appendicular lean mass (kg)/(height (m)] 2 . SMI < 5.75 was considered diagnostic for sarcopenia. Coronal and sagittal spinal alignments were measured. The following biochemical markers were measured: serum and urinary pentosidine, serum homocysteine, 1,25(OA) 2 D, and 25(OH)D. The level of each variable was compared between DLS and controls. The relationship between biochemical markers including pentosidine and DLS was examined., Results: Sarcopenia was observed at a high prevalence in participants with DLS: 50% compared with 15.8% of healthy controls. Height, weight, femoral BMI, appendicular lean mass, total lean mass, and SMI all had significantly lower values in the DLS group. Serum pentosidine was significantly higher for the DLS group compared with controls. Correlations with serum pentosidine revealed a significant positive correlation between lumbar scoliosis, pelvic tilt, and pelvic incidence-lumbar lordosis mismatch, and a significantly negative correlation between thoracic kyphosis (P < 0.05)., Conclusions: We found that sarcopenia was involved in DLS, and high serum pentosidine levels are associated with severity of coronal and sagittal malalignment in older women, suggesting that high levels of AGEs are a potential biomarker for the progression of lumbar scoliosis and kyphotic deformity. Further studies are needed to clarify the pathogenesis of DLS.

In vitro synthesis of the first component of complement C1s was examined by using hamster epiphyseal chondrocytes (HAC) and human chondrosarcoma cell line HCS-2/8. Hamster and human C1s produced by the cells were quantified by immunoblotting and sandwich enzyme-linked immunosorbent assay (ELISA), respectively. It was possible to measure active and inactive C1s by sandwich ELISA, when we used anti-human C1s monoclonal antibodies, M241 recognizing only active C1s, and M365 and M81 recognizing both active and inactive C1s. Approximately 40% of C1s secreted from HCS-2/8 was found to be activated in the culture medium, whereas C1s from HAC was not. C1s production increased in accordance with chondrocyte differentiation induced by ascorbic acid. In contrast, transforming growth factor-beta1 and basic fibroblast growth factor, which inhibited differentiation, suppressed C1s production. These results confirmed our previous observation showing that C1s synthesis increased with differentiation into hypertrophic chondrocytes in vivo.

Expression of the first complement component (C1s) has been examined in chondrocytes of hamster epiphyseal cartilage during development and fracture healing. C1s is immunostained with anti-hamster C1s monoclonal antibody, PG11. The C1s staining increases in accordance with chondrocyte differentiation and reaches a maximal level in hypertrophic chondrocytes. This change is observed at both the tibia ossification center and at the callus in which the replacement of cartilage by bone marrow takes place. The concomitant increase of C1s and chondrocyte hypertrophy has been confirmed by RNA blot and by in situ hybridization. These results, in addition to previous findings on C1s collagenolytic and gelatinolytic activities, suggest C1s participation in cartilage remodeling.

The first component of complement C1s has been shown to degrade type I and type II collagens (Yamaguchi et al. 1990), the latter of which is a major constituent of the cartilage matrix. In order to understand the physiological roles of C1s in cartilage resorption, the expression of C1s was examined by immunohistochemistry in the primary ossification center where the matrix is removed and replaced by bone marrow. Hypertrophic chondrocytes, endothelium and hematogenous elements in the capillary buds were intensely stained by a monoclonal antibody against C1s. Matrix metalloproteinase 9 (MMP-9, 92kDa gelatinase/type IV collagenase) was also immunolocalized in hypertrophic chondrocytes, mesenchymal cells in the primitive bone marrow and the cartilage matrix adjacent to the marrow. In addition, C1s was found to activate the zymogen of MMP-9. These observations suggest that C1s and MMP-9 coordinately participate in matrix degradation in cartilage.