No abstract

Repeat courses of HA injections reduced the degree of articular degeneration in a rabbit ACLT model of OA. Sequential courses of HA therapy may be advantageous in the long-term management of OA.

Objective-The first complement component C1s was reported to have novel functions to degrade matrix components, besides its activities in the classic complement pathway. This study explores participation of C1s in articular cartilage degradation in rheumatoid arthritis (RA). Methods-Normal articular cartilage (n=6) and cartilage obtained from joints with RA (n=15) and osteoarthritis (OA, n=10) were immunostained using antiC1s monoclonal antibodies PG11, which recognises both active and inactive C1s, and M241, which is specifically reactive to activated C1s. The eVects of inflammatory cytokines on C1s production by human articular chondrocytes were also examined by sandwich ELISA. Results-In normal articular cartilage, C1s was negative in staining with both PG11 and M241. In contrast, degenerating cartilage of RA was stained with PG11 (14 of 15 cases), and in most of the cases (13 of 15 cases) C1s was activated as revealed by M241 staining. In OA, C1s staining was restricted in severely degrading part of cartilage (5 of 10 cases), and even in that part C1s was not activated. In addition, C1s production by chondrocytes in vitro was increased by an inflammatory cytokine, tumour necrosis factor . Conclusion-These results suggest that C1s activated in degenerative cartilage matrix of RA but not in that of OA. C1s is thought to participate in the pathogenesis of RA through its collagenolytic activity in addition to the role in the classic cascade.

No abstract

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.

BackgroundAge-related sarcopenia may cause physical dysfunction. We investigated the involvement of sarcopenia in dropped head syndrome (DHS).MethodsOur study subjects were ten elderly women with idiopathic DHS (mean age 75.1 years, range 55–89). Twenty age- and sex-matched volunteers (mean age 73.0, range 58–83) served as controls. We used a bioelectrical impedance analyzer (BIA) 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. Cervical sagittal plane alignment: C2–7 sagittal vertical axis (SVA), C2–7 angle (C2–C7 A), and C2 slope (C2S) were also measured. We investigated sarcopenia prevalence in both groups, height, weight, BMI, lean mass arm, lean mass leg, lean mass trunk, appendicular lean mass, total lean mass, and SMI. In addition, we also examined the correlation between cervical spine alignment and SMI in DHS.ResultsSarcopenia was observed at a high rate in DHS subjects: 70% compared to 25% of healthy controls. Height, weight, BMI, lean mass arm, lean mass leg, axial lean mass, appendicular lean mass, total lean mass, and SMI all had significantly lower values in the DHS group. In particular, total lean mass, lean mass arm, and lean mass trunk were considerably lower in the DHS group. There was no correlation noted between cervical spine alignment and SMI.ConclusionsSarcopenia prevalence was high in the DHS group—70 versus 25% in the control group, suggesting the involvement of sarcopenia in DHS. In particular, axial lean mass and lean mass arm were markedly reduced in the DHS group. DHS is due to significant weakness of the neck extensor group, and chin-on-chest deformity occurs. Until the present, evaluation of DHS has been done using only MRI; no studies have systematically examined skeletal muscle mass. In the present study, muscle mass decrease was noted not only in the neck muscles but also throughout the entire body. Involvement of trunk and upper limb muscles in particular suggests a disuse atrophy of the upper body and spinal muscles. BIA can easily and systemically evaluate skeletal muscle mass. We expect it to contribute to further elucidating the pathogenesis of DHS.

Study DesignCross-sectional observational study.PurposeTo compare measurements of appendicular skeletal muscle mass (ASMM) and whole fat mass (WFM) obtained using dualenergy X-ray absorptiometry (DXA) and bioelectrical impedance analysis (BIA) among patients with low back pain (LBP). Moreover, the study investigated the correlation between BIA-based ASMM and DXA-based bone mineral density (BMD).Overview of the LiteratureIf reliable, BIA may be a useful alternative to DXA as a screening tool for sarcopenia and osteoporosis among patients with LBP.MethodsMeasurements were performed in 130 patients, including BMD of the lumbar spine and femoral neck. The correlation between DXA and BIA as well as between BIA-ASMM and BMD were evaluated.ResultsBIA and DXA were highly correlated in both male and female patients (r =0.73–0.90, p <0.0001). However, BIA consistently overestimated ASMM by 1.5–2.5 kg on an average (p <0.0001) and underestimated WFM (−4.0 to −2.7 kg) on an average (p <0.0001). BIA-based ASMM correlated with BMD of the lumbar spine in both male and female patients (r =0.28–0.37, p ≤0.02) and that of the femoral neck (r =0.34–0.51, p ≤0.005). Regarding the calculated skeletal muscle index (SMI: ASMM/height [m2]) used as a criterion for sarcopenia, BIA-based SMI correlated with BMD of the lumbar spine in male patients (r =0.44, p =0.0004) and that of the femoral neck in female patients (r =0.33, p =0.009).ConclusionsBIA may be a favorable alternative to DXA as a screening tool for sarcopenia and osteoporosis among patients with LBP. Considering the overestimation of BIA-based ASMM and SMI, we recommend using the cutoff values for sarcopenia of 7.9 kg/m2 for males and 6.1 kg/m2 for females.

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.