Does a high-fat diet affect the development and progression of osteoarthritis in mice? A systematic review

Sansone, Valerio; Applefield, Rachel C.; Luca, Paola De; Pecoraro, Valentina; Gianola, Silvia; Pascale, Walter; Pascale, Valerio

doi:10.1302/2046-3758.812.bjr-2019-0038.r1

Cited by 28 publications

(33 citation statements)

References 39 publications

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“…Data showed that the BMD of rats with intermittent unloading was comparable with that of normal controls, while being significantly greater than that of rats with full-time suspension (Supplementary Figure c). In addition, weight and obesity are important risk factors during the development of OA, 34 and our data reveal that the weight of rats was comparable among the three groups at the endpoint of the experiment (Supplementary Figure d).…”

Section: Discussionsupporting

confidence: 51%

“…On the other hand, inflammatory cytokines brought about by diet or injuries are also intensively involved in joint destruction in OA. 14 , 34 Among them, IL-1β is an important cytokine participant in catabolism and degeneration of cartilage during OA development. 13 , 35 IL-1β can not only increase the expression and activation of MMPs, 36 but also accelerate the breakdown of collagen II and proteoglycans.…”

Section: Discussionmentioning

confidence: 99%

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Less mechanical loading attenuates osteoarthritis by reducing cartilage degeneration, subchondral bone remodelling, secondary inflammation, and activation of NLRP3 inflammasome

Nie

et al. 2020

Bone & Joint Research

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Aims Osteoarthritis (OA) is a disabling joint disorder and mechanical loading is an important pathogenesis. This study aims to investigate the benefits of less mechanical loading created by intermittent tail suspension for knee OA. Methods A post-traumatic OA model was established in 20 rats (12 weeks old, male). Ten rats were treated with less mechanical loading through intermittent tail suspension, while another ten rats were treated with normal mechanical loading. Cartilage damage was determined by gross appearance, Safranin O/Fast Green staining, and immunohistochemistry examinations. Subchondral bone changes were analyzed by micro-CT and tartrate-resistant acid phosphatase (TRAP) staining, and serum inflammatory cytokines were evaluated by enzyme-linked immunosorbent assay (ELISA). Results Our radiographs showed that joint space was significantly enlarged in rats with less mechanical loading. Moreover, cartilage destruction was attenuated in the less mechanical loading group with lower histological damage scores, and lower expression of a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS)-5, matrix metalloproteinase (MMP)-3, and MMP-13. In addition, subchondral bone abnormal changes were ameliorated in OA rats with less mechanical loading, as reduced bone mineral density (BMD), bone volume/tissue volume (BV/TV), and number of osteophytes and osteoclasts in the subchondral bone were observed. Finally, the level of serum inflammatory cytokines was significantly downregulated in the less mechanical loading group compared with the normal mechanical loading group, as well as the expression of NACHT, LRR, and PYD domains-containing protein 3 (NLRP3), caspase-1, and interleukin 1β (IL-1β) in the cartilage. Conclusion Less mechanical loading alleviates cartilage destruction, subchondral bone changes, and secondary inflammation in OA joints. This study provides fundamental insights into the benefit of non-weight loading rest for patients with OA. Cite this article: Bone Joint Res 2020;9(10):731–741.

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Section: Discussionsupporting

confidence: 51%

Section: Discussionmentioning

confidence: 99%

Less mechanical loading attenuates osteoarthritis by reducing cartilage degeneration, subchondral bone remodelling, secondary inflammation, and activation of NLRP3 inflammasome

Nie

et al. 2020

Bone & Joint Research

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“…It should be noted that while previous studies revealed unequivocally that HFD caused exacerbation of PTOA, inconsistent results have been observed in regard to the ability of HFD in OA induction in mouse models [195].…”

Section: Obesity-induced Oa Modelsmentioning

confidence: 91%

“…Higher OA incidence in obese people is attributed to not only excessive joint loading caused by increased body weight, but also the associated systemic inflammation, dysregulated lipid metabolism, and altered adipokine profile [193,194]. Mice fed with a high-fat diet (HFD) exhibit higher levels of proinflammatory cytokines, including IL-1β, IL-6, IL-8, IL-13, leptin, and TNF-α; also present at higher levels in these mice are proteins involved in cartilage metabolism, such as TGF-β1, MMP-13, and vascular endothelial growth factor-α (VEGF-α) [195].…”

Section: Obesity-induced Oa Modelsmentioning

confidence: 99%

“…Schott et al created a PTOA model in C57BL/6J mice with HFD-induced obesity, and found that the gut microbiome can be targeted to curb systemic inflammation and thus treat OA in obese mice [ 198 ]. It should be noted that while previous studies revealed unequivocally that HFD caused exacerbation of PTOA, inconsistent results have been observed in regard to the ability of HFD in OA induction in mouse models [ 195 ].…”

Section: Experimental Modelsmentioning

confidence: 99%

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Pathogenesis of Osteoarthritis: Risk Factors, Regulatory Pathways in Chondrocytes, and Experimental Models

Alexander

et al. 2020

Biology

185

115

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As the most common chronic degenerative joint disease, osteoarthritis (OA) is the leading cause of pain and physical disability, affecting millions of people worldwide. Mainly characterized by articular cartilage degradation, osteophyte formation, subchondral bone remodeling, and synovial inflammation, OA is a heterogeneous disease that impacts all component tissues of the articular joint organ. Pathological changes, and thus symptoms, vary from person to person, underscoring the critical need of personalized therapies. However, there has only been limited progress towards the prevention and treatment of OA, and there are no approved effective disease-modifying osteoarthritis drugs (DMOADs). Conventional treatments, including non-steroidal anti-inflammatory drugs (NSAIDs) and physical therapy, are still the major remedies to manage the symptoms until the need for total joint replacement. In this review, we provide an update of the known OA risk factors and relevant mechanisms of action. In addition, given that the lack of biologically relevant models to recapitulate human OA pathogenesis represents one of the major roadblocks in developing DMOADs, we discuss current in vivo and in vitro experimental OA models, with special emphasis on recent development and application potential of human cell-derived microphysiological tissue chip platforms.

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Lipopolysaccharide Binding Protein and CD14, Cofactors of Toll‐like Receptors, Are Essential for Low‐Grade Inflammation–Induced Exacerbation of Cartilage Damage in Mouse Models of Posttraumatic Osteoarthritis

Yang

Park

Chun

2021

Arthritis & Rheumatology

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Objective. Osteoarthritis (OA) is initiated by pathogenic factors produced by multiple stimuli, including mechanical stress, metabolic stress, and/or inflammaging. This study was undertaken to identify novel low-grade inflammationassociated pathogenic mediators of OA.Methods. Candidate pathogenic molecules were screened using microarray data obtained from chondrocytes exposed to OA-associated catabolic factors. In mice with OA generated by destabilization of the medial meniscus (DMM), low-grade inflammation was induced by a high-fat diet or endotoxemia. Functions of candidate molecules in OA pathogenesis were examined using primary-culture chondrocytes from mice with DMM-induced OA, following intraarticular injection of adenovirus expressing the candidate gene. Specific functions of candidate genes were evaluated using whole-body gene-knockout mice.Results. Bioinformatics analysis identified multiple candidate pathogenic factors that were associated with lowgrade inflammation, including components of the Toll-like receptor (TLR) signaling pathways (e.g., TLR-2, TLR-4, lipopolysaccharide binding protein [LBP], and CD14). Overexpression of the individual TLR signaling components in mouse joint tissue did not alter cartilage homeostasis. However, the low-grade inflammation induced by a high-fat diet or endotoxemia markedly enhanced posttraumatic OA cartilage destruction in mice, and this exacerbation of cartilage destruction was significantly abrogated in LBP −/− and CD14 −/− mice. Additionally, LBP and CD14 were found to be necessary for the expression of matrix-degrading enzymes in mouse chondrocytes treated with proinflammatory cytokines.Conclusion. LBP and CD14, which are accessory molecules of TLRs, are necessary for the exacerbation of posttraumatic OA cartilage destruction resulting from low-grade inflammation, such as that triggered by a high-fat diet or endotoxemia.

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Does a high-fat diet affect the development and progression of osteoarthritis in mice? A systematic review

Cited by 28 publications

References 39 publications

Less mechanical loading attenuates osteoarthritis by reducing cartilage degeneration, subchondral bone remodelling, secondary inflammation, and activation of NLRP3 inflammasome

Less mechanical loading attenuates osteoarthritis by reducing cartilage degeneration, subchondral bone remodelling, secondary inflammation, and activation of NLRP3 inflammasome

Pathogenesis of Osteoarthritis: Risk Factors, Regulatory Pathways in Chondrocytes, and Experimental Models

Lipopolysaccharide Binding Protein and CD14, Cofactors of Toll‐like Receptors, Are Essential for Low‐Grade Inflammation–Induced Exacerbation of Cartilage Damage in Mouse Models of Posttraumatic Osteoarthritis

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