Correlation of synovial fluid leptin concentrations with the severity of osteoarthritis

Department of Orthopedic Surgery, Good Samsun Hospital, 193-5, Jurye-dong, Sasang-gu, Busan, South Korea.
Clinical Rheumatology (Impact Factor: 1.77). 08/2009; 28(12):1431-5. DOI: 10.1007/s10067-009-1242-8
Source: PubMed


Leptin is known to play an important role in the pathophysiology of osteoarthritis (OA). This study investigated whether synovial fluid (SF) leptin level is related to the radiographic severity of OA and its role as a quantitative marker for the detection of OA. SF was obtained from 42 OA patients who underwent knee surgery and 10 who had no abnormality of articular cartilage during arthroscopic examination. The progression of OA was classified by Kellgren-Lawrence grading scale. The concentrations of leptin were measured with commercial enzyme-linked-immunosorbent serologic assay kits. Median leptin concentrations in SF were significantly higher in OA patients (median 4.40 ng/ml; range 0.5-15.8) compared to controls (median 2.05 ng/ml; range 1.0-4.6; P = 0.006). SF leptin levels showed significant difference according to the severity of OA (P = 0.0125). Median SF leptin level was highest in stage IV patients (11.1 ng/ml), which was significantly higher compared to all other groups including controls (P < 0.05). Age showed a significant positive correlation with leptin concentrations in OA patients (P < 0.05), but not in controls. These results demonstrate that SF leptin concentrations were closely related to the radiographic severity of OA, suggesting that SF leptin levels could be used as an effective marker for quantitative detection of OA.

37 Reads
  • Source
    • "Strikingly, obese mice with impairment in leptin signaling, due to deletion of leptin or leptin receptor, do not exhibit differences in terms of severity of OA in comparison to mice with normal body weight (Griffin et al., 2009). In fact, synovial fluid of OA patients was characterized to have elevated levels of leptin (Dumond et al., 2003; Ku et al., 2009). Increased levels of leptin in synovial fluid and cartilage promote cartilage catabolism by upregulating MMP13 and NOS2 expression (Iliopoulos et al., 2007; Otero et al., 2005). "
    [Show abstract] [Hide abstract]
    ABSTRACT: Osteoarthritis (OA) is one of the most prevalent forms of joint disorder, associated with a tremendous socioeconomic burden worldwide. Various non-genetic and lifestyle-related factors such as aging and obesity have been recognized as major risk factors for OA, underscoring the potential role for epigenetic regulation in the pathogenesis of the disease. OA-associated epigenetic aberrations have been noted at the level of DNA methylation and histone modification in chondrocytes. These epigenetic regulations are implicated in driving an imbalance between the expression of catabolic and anabolic factors, leading eventually to osteoarthritic cartilage destruction. Cellular senescence and metabolic abnormalities driven by OAassociated risk factors appear to accompany epigenetic drifts in chondrocytes. Notably, molecular events associated with metabolic disorders influence epigenetic regulation in chondrocytes, supporting the notion that OA is a metabolic disease. Here, we review accumulating evidence supporting a role for epigenetics in the regulation of cartilage homeostasis and OA pathogenesis.
    Moleculer Cells 08/2015; 38(8). DOI:10.14348/molcells.2015.0200 · 2.09 Impact Factor
  • Source
    • "Furthermore, chondrocytes from human OA cartilage produce much more leptin than those from normal cartilage [64]. In fact, the expression pattern of leptin was related to the grade of cartilage destruction [64], with the highest levels of leptin in the advanced stages of the disease [72, 73]. Leptin could perpetuate cartilage-degrading processes by inducing VCAM-1 expression, adhesion molecule responsible for leukocyte and monocyte infiltration at inflamed joints [74]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: The metabolic syndrome (MetS) is a cluster of cardiometabolic disorders that result from the increasing prevalence of obesity. The major components of MetS include insulin resistance, central obesity, dyslipidemia, and hypertension. MetS identifies the central obesity with increased risk for cardiovascular diseases (CVDs) and type-2 diabetes mellitus (T2DM). Patients with rheumatic diseases, such as rheumatoid arthritis, osteoarthritis, systemic lupus erythematosus, and ankylosing spondylitis, have increased prevalence of CVDs. Moreover, CVD risk is increased when obesity is present in these patients. However, traditional cardiovascular risk factors do not completely explain the enhanced cardiovascular risk in this population. Thus, MetS and the altered secretion patterns of proinflammatory adipokines present in obesity could be the link between CVDs and rheumatic diseases. Furthermore, adipokines have been linked to the pathogenesis of MetS and its comorbidities through their effects on vascular function and inflammation. In the present paper, we review recent evidence of the role played by adipokines in the modulation of MetS in the general population, and in patients with rheumatic diseases.
    Journal of Immunology Research 02/2014; 2014(25):343746. DOI:10.1155/2014/343746 · 2.93 Impact Factor
  • Source
    • "In addition, leptin seems to be locally involved in joint erosion in OA since SF concentrations were significantly higher in OA patients compared to controls. Importantly, leptin levels were highest in patients with more severe disease [120], suggesting that SF levels could be used as an effective biomarker for quantitative detection of OA. Recent findings showed the association of higher serum leptin levels with increased odds of both prevalent and incident knee OA in a cohort of mid-life women [121]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Inflammation has been recognized as a common trait in the pathogenesis of multifactorial diseases including obesity, where a low-grade inflammation has been established and may be responsible for the cardiovascular risk related to the disease. Obesity has also been associated with the increased incidence and a worse outcome of rheumatoid arthritis (RA) and osteoarthritis (OA). RA is characterized by systemic inflammation, which is thought to play a key role in accelerated atherosclerosis and in the increased incidence of cardiovascular disease, an important comorbidity in patients with RA. The inflammatory process underlying the cardiovascular risk both in obesity and RA may be mediated by adipocytokines, a heterogeneous group of soluble proteins mainly secreted by the adipocytes. Many adipocytokines are mainly produced by white adipose tissue. Adipocytokines may also be involved in the pathogenesis of OA since a positive association with obesity has been found for weight-bearing and nonweight-bearing joints, suggesting that, in addition to local overload, systemic factors may contribute to joint damage. In this review we summarize the current knowledge on experimental models and clinical studies in which adipocytokines were examined in obesity, RA, and OA and discuss the potential of adipocytokines as comorbidity biomarkers for cardiovascular risk.
    Mediators of Inflammation 11/2013; 2013(5):808125. DOI:10.1155/2013/808125 · 3.24 Impact Factor
Show more

Similar Publications