J. Shiozawa

Osteoarthritis as a Cause of Locomotive Syndrome: Its Influence on Functional Mobility and Activities of Daily Living

Abstract“Locomotive syndrome” is defined as a condition associated with restriction in one’s ability to walk or lead a normal life due to a dysfunction in one or more of the parts of the locomotion system, including the muscles, bones, joints, cartilage or intervertebral discs. This syndrome especially refers to individuals who have come to need nursing care services because of problems with the locomotive organs, or those who have conditions which may require them to need such services in the near future. Recent epidemiological studies revealed that the one-fourth of elderly individuals who require special assistance or nursing care have locomotive disorders in Japan. Osteoarthritis of the knee (knee OA) and hip (hip OA), and osteoporosis and spinal canal stenosis due to spondylosis are three major locomotive disorders that cause elderly individuals require special assistance or nursing care. In this review, we focus on the effects of knee and hip OA on the lives of elderly individuals and the recent advantages in clinical research on the pathophysiology and management of these diseases.

The MRI-detected osteophyte score is a predictor for undergoing joint replacement in patients with end-stage knee osteoarthritis

Abstract Objectives: The aim of this prospective cohort study was to examine whether MRI-detected osteoarthritis (OA)-structural changes at baseline could predict knee OA patients who would undergo total knee arthroplasty (TKA). Methods: In total, 128 end-stage medial-type knee OA patients were enrolled and followed up for 6 months. MRI using the whole-organ MRI scoring (WORMS) method, radiographic findings, visual analog scale (VAS) for pain and a patient-oriented outcome measure, and the Japanese Knee Osteoarthritis Measure (JKOM) were recorded at baseline. The area under the curve (AUC) was estimated to determine the discriminative value of the prediction models. Results: While 74 patients (57.8%) did not undergo TKA, the remaining 54 patients (42.2%) underwent TKA during this period. The AUCs of the receiver operating characteristic (ROC) curve for the activities of daily living (ADL) score evaluated by the JKOM ADL score [0.70 (95% CI: 0.60–0.79)] and osteophyte score [0.72 (0.64–0.81)] were 0.70 or greater. The JKOM ADL score (17/40) and the osteophyte score (30/98) showed relative risks (RR) of 2.61 (1.32–5.15) and 3.01 (1.39–6.52) for undergoing TKA, respectively. Conclusion: The osteophyte score detected by MRI, in addition to ADL score, was found to be an important factor in determining whether the patient should undergo TKA.

Hyaluronan-Binding Protein Involved in Hyaluronan Depolymerization Is Up-Regulated and Involved in Hyaluronan Degradation in Human Osteoarthritic Cartilage

Hyaluronan (HA)-binding protein involved in HA depolymerization (HYBID), also called cell migration-inducing protein (CEMIP; alias KIAA1199), plays a key role in the degradation of HA in skin and arthritic synovial fibroblasts, but its functions in osteoarthritic (OA) cartilage remain elusive. Here, we investigated the expression and roles of HYBID in human OA cartilage. HYBID was highly expressed by chondrocytes in the HA-depleted area of OA cartilage, and HYBID immunoreactivity was correlated with Mankin score, the histopathologic severity of OA lesions of cartilage. Real-time quantitative PCR indicated that HYBID expression was significantly higher in OA cartilage than in control cartilage. In addition, OA chondrocytes exhibited HA-degrading activity, which was abolished by knock-down of HYBID by siRNAs. Although OA chondrocytes also expressed certain levels of hyaluronidases 1 and 2 and CD44, knock-down of these molecules exhibited negligible effects on HA degradation. Double immunostaining of HYBID and clathrin heavy chain revealed that HYBID was localized in the clathrin-coated vesicles, and HA was endocytosed within the vesicles of OA chondrocytes. Among eight factors including cytokines and growth factors examined, only tumor necrosis factor α stimulated OA chondrocytes to overexpress HYBID. These data are the first to demonstrate that HYBID is up-regulated in OA cartilage, and suggest that tumor necrosis factor α-stimulated HYBID plays a role in HA degradation in OA cartilage.