Exploratory secondary analyses of a cognitive-behavioral intervention for knee osteoarthritis demonstrate reduction in biomarkers of adipocyte inflammation

Huebner, Janet L.; Landerman, Lawrence R.; Somers, Tamara J.; Keefe, Francis J.; Guilak, Farshid; Blumenthal, James A.; Caldwell, David S.; Kraus, Virginia B.

doi:10.1016/j.joca.2016.04.002

Cited by 16 publications

(13 citation statements)

References 53 publications

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“…Specifically, increased pro-inflammatory biomarkers—tumor necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1β), and IL-6—have been observed in obese children with no comorbidities [ 47 ] as well as in obese patients with OA [ 49 ]. However, diet and exercise can reduce these cytokine levels [ 49 , 50 ]. Such increased inflammatory cytokine activity can induce chondrocyte catabolism, resulting in degenerative changes such as decreased proteoglycan content [ 51 , 52 ].…”

Section: Discussionmentioning

confidence: 99%

Obesity alters the in vivo mechanical response and biochemical properties of cartilage as measured by MRI

et al. 2018

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BackgroundObesity is a primary risk factor for the development of knee osteoarthritis (OA). However, there remains a lack of in vivo data on the influence of obesity on knee cartilage mechanics and composition. The purpose of this study was to determine the relationship between obesity and tibiofemoral cartilage properties.MethodsMagnetic resonance images (3T) of cartilage geometry (double-echo steady-state) and T1rho relaxation of the knee were obtained in healthy subjects with a normal (n = 8) or high (n = 7) body mass index (BMI) before and immediately after treadmill walking. Subjects had no history of lower limb injury or surgery. Bone and cartilage surfaces were segmented and three-dimensional models were created to measure cartilage thickness and strain. T1rho relaxation times were measured before exercise in both the tibial and femoral cartilage in order to characterize biochemical composition. Body fat composition was also measured.ResultsSubjects with a high BMI exhibited significantly increased tibiofemoral cartilage strain and T1rho relaxation times (P <0.05). Tibial pre-exercise cartilage thickness was also affected by BMI (P <0.05). Correlational analyses revealed that pre-exercise tibial cartilage thickness decreased with increasing BMI (R2 = 0.43, P <0.01) and body fat percentage (R2 = 0.58, P <0.01). Tibial and femoral cartilage strain increased with increasing BMI (R2 = 0.45, P <0.01; R2 = 0.51, P <0.01, respectively) and increasing body fat percentage (R2 = 0.40, P <0.05; R2 = 0.38, P <0.05, respectively). Additionally, tibial T1rho was positively correlated with BMI (R2 = 0.39, P <0.05) and body fat percentage (R2 = 0.47, P <0.01).ConclusionsStrains and T1rho relaxation times in the tibiofemoral cartilage were increased in high BMI subjects compared with normal BMI subjects. Additionally, pre-exercise tibial cartilage thickness decreased with obesity. Reduced proteoglycan content may be indicative of pre-symptomatic osteoarthritic degeneration, resulting in reduced cartilage thickness and increased deformation of cartilage in response to loading.

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Section: Discussionmentioning

confidence: 99%

Obesity alters the in vivo mechanical response and biochemical properties of cartilage as measured by MRI

et al. 2018

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“…In addition, adiponectin levels detected in OA synovial fluid were almost 100 times lower than those in plasma and it correlated with OA severity and aggrecan degradation but not with type II collagen ( Figure 3(b) ) [ 154 , 160 ]. Remarkably, the adiponectin : leptin ratio in the synovial fluid has been proposed as a predictor of pain in knee OA [ 161 ]. A lower leptin : adiponectin ratio correlated with lower knee OA pain [ 143 ].…”

Section: Adipokines In the Pathobiology Of Osteoarthritic Cartilagmentioning

confidence: 99%

“…This decline was clearly mediated by weight change. However, the authors did not find differences regarding adiponectin [ 212 ]. Also, among a cohort of patients who underwent bariatric surgery and had symptomatic OA, leptin serum levels were elevated.…”

Section: Therapeutic Perspectivesmentioning

confidence: 99%

Adipokine Contribution to the Pathogenesis of Osteoarthritis

Azamar-Llamas

Hernández-Molina

Ramos-Ávalos

et al. 2017

Mediators of Inflammation

132

106

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Recent studies have shown that overweight and obesity play an important role in the development of osteoarthritis (OA). However, joint overload is not the only risk factor in this disease. For instance, the presence of OA in non-weight-bearing joints such as the hand suggests that metabolic factors may also contribute to its pathogenesis. Recently, white adipose tissue (WAT) has been recognized not only as an energy reservoir but also as an important secretory organ of adipokines. In this regard, adipokines have been closely associated with obesity and also play an important role in bone and cartilage homeostasis. Furthermore, drugs such as rosuvastatin or rosiglitazone have demonstrated chondroprotective and anti-inflammatory effects in cartilage explants from patients with OA. Thus, it seems that adipokines are important factors linking obesity, adiposity, and inflammation in OA. In this review, we are focused on establishing the physiological mechanisms of adipokines on cartilage homeostasis and evaluating their role in the pathophysiology of OA based on evidence derived from experimental research as well as from clinical-epidemiological studies.

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“…The progression of KOA is accompanied by injury of the entire joint structure and increased inflammation in the joint ( 20 , 21 ). Impaired muscle strength and dysfunction are common features in the affected legs and likely decrease the quality of life among patients with knee OA ( 22 , 23 ).…”

Section: Discussionmentioning

confidence: 99%

USF1 promotes the development of knee osteoarthritis by activating the NF‑κB signaling pathway

Song

Zhu

et al. 2018

Exp Ther Med

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The current study mainly aims to evaluate the expression pattern and underlying mechanism of upstream stimulating factor 1 (USF1) in the muscle tissues of knee osteoarthritis (KOA) patients. In accordance with previous findings, our data showed that muscle strength was significantly decreased in KOA patients compared with controls. Furthermore, several inflammatory factors, including tumor necrosis factor α (TNFα), IL-8, IL-6 and MCP-1, were associated with reduced muscle strength in KOA patients. Not surprisingly, NF-κB signaling was significantly activated in the muscle tissues of KOA patients compared with control individuals. Furthermore, we showed that USF1 was increased in the muscles of KOA patients compared with controls. More importantly, overexpression of USF1 in primary human skeletal muscle cells significantly increased the activation of NF-κB signaling as well as the levels of pro-inflammatory factors. In summary, we showed novel data that the upregulation of USF1 promoted NF-κB activation-induced inflammatory responses in muscle tissues of KOA patients.

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Exploratory secondary analyses of a cognitive-behavioral intervention for knee osteoarthritis demonstrate reduction in biomarkers of adipocyte inflammation

Cited by 16 publications

References 53 publications

Obesity alters the in vivo mechanical response and biochemical properties of cartilage as measured by MRI

Obesity alters the in vivo mechanical response and biochemical properties of cartilage as measured by MRI

Adipokine Contribution to the Pathogenesis of Osteoarthritis

USF1 promotes the development of knee osteoarthritis by activating the NF‑κB signaling pathway

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