Background This study was conducted to analyze the effects of low skeletal muscle mass index (SMI) and obesity on aging-related osteoarthritis (OA) in the Korean population.
Methods A total of 16,601 participants who underwent a dual-energy X-ray absorptiometry and 3,976 subjects with knee X-rays according to the modified Kellgren-Lawrence (KL) system were enrolled. Knees of ≥KL grade 2 were classified as radiologic OA. The severity of joint space narrowing (JSN) was classified by X-rays as normal, mild-to-moderate, and severe JSN in radiologic OA. The subjects were grouped as normal SMI (SMI of ≥–1 standard deviation [SD] of the mean), low SMI class I (SMI of ≥–2 SDs and <–1 SD), and low SMI class II (SMI of <–2 SDs). Obesity was defined as a body mass index (BMI) of ≥27.5 kg/m2.
Results The modified KL grade and JSN severity were negatively correlated with the SMI and positively correlated with BMI and age. The SMI was negatively correlated with age. JSN severity was significantly associated with a low SMI class compared to a normal SMI, which was more prominent in low SMI class II than class I. Obesity was significantly associated with more severe JSN, only for obesity with a low SMI class. Furthermore, patients with a low SMI class, regardless of obesity, were prone to having more severe JSN.
Conclusion This study suggested that a low SMI class was associated with aging and that an age-related low SMI was more critically related to the severity of JSN in OA.
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Osteoarthritis (OA) is the most prevalent form of arthritis and a major cause of disability in people aged 65 and older. OA is not a single disease; rather, it is a group of overlapping yet distinct diseases with different etiologies but similar pathologic, morphologic, and clinical outcomes. OA occurs when the dynammic equilibrium between the breakdown and reapir of joint tissues is overwhelmed. Systemic and local biomechanical factors contribute to the development of the disease, with systemic factors also making the joint vulnerable and resulting in a greater impact of local joint factors. Systemic risk factors include ethnicity, gender, age, genetic factors, hormonal status, bone density, and nutritional factors. Local biomechanical factors include altered joint biomechanics, prior injuries, the effects of physical activities, sports participation, occupation, developmental abnormalities, and obesity. The normal joint is protected by biomechanical factors such as alignment and muscle strength, the lubrication provided by the synovial fluid, and the shock-absorbing function of bone and cartilage. When these functions are altered, changes occur at both the macroscopic and cellular levels, with derangements in any structure contributing to further joint destruction. 1) Further studies of both risk factor modification and cellular changes in OA will hopefully continue to enhance our understanding of this complex disease and lead to improved outcomes.
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BACKGROUND Accumulating evidence shows that interleukin(IL)-1 plays a critical role in inflammation and connective tissue destruction observed in both osteoarthritis and rheumatoid arthritis. IL-1 induces gene expression related to cytokines, chemokines and matrix metalloproteinases by activation of many different transcription factors. MATERIALS AND METHODS: The chondrosarcoma cell line, SW1353, is known to be a valuable in vitro system for investigating catabolic gene regulation by IL-1beta in chondrocytic cells. To explore and analyze the changes in gene expression by IL-1 responsible for arthritis, SW1353 was treated with IL-1 for 1, 6 and 24 h and then total RNAs were purified for each time. The changes in gene expression were analyzed with 17k human cDNA microarrays and validated by semi-quantitative RT-PCR. RESULTS: Greater than a two-fold change was observed in 1,200 genes including metallothioneins, matrix metalloproteinases, extracellular matrix proteins, antioxidant proteins, cytoskeleton proteins, cell cycle regulatory proteins, proteins for cell growth and apoptosis, signaling proteins and transcription factors. These changes appeared to be correlate with the pathophysiological changes observed in early osteoarthritis. CONCLUSION: cDNA microarray analysis revealed a marked variability in gene expression, and provided insight into the overall molecular changes. The result of this study provide initial information for further studies to identify therapeutic targets in osteoarthritis pathogenesis.