Longitudinal Characterization of Synovial Fluid Biomarkers in the Canine Meniscectomy Model of Osteoarthritis

Lindhorst, E.; Vail, Thomas P.; Guilak, Farshid; Wang, H.; Setton, L.A.; Vilı́m, Vladimı́r; Kraus, Virginia B.

doi:10.2106/00004623-200006000-00051

Cited by 20 publications

(26 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Glycosaminoglycan, collagen, nitric oxide, PGE-2, and MMPs have each been reported to be significantly elevated in the synovial fluid of dogs, horses, and/or humans [4,5,9,11,19,27,36,37]. While synovial fluid was not collected from dogs in this study for comparison to culture media in the models, the changes noted in the measured variables in the liquid media from OA groups corresponded well to changes reported in the synovial fluid of osteoarthritic joints.…”

Section: Discussionsupporting

confidence: 63%

Review of In Vitro Models and Development and Initial Validation of a Novel Co-Culture Model for the Study of Osteoarthritis

Cook¹,

Kuroki²,

Stoker³

et al. 2007

CRR

View full text Add to dashboard Cite

Objective: Provide an overview of models used for the study of osteoarthritis (OA) and describe a novel in vitro model of OA using synovial and cartilage explants from dogs which we compared to spontaneously occurring OA in dogs.Design: Controlled laboratory study.Methods: Articular cartilage and synovial explants were created from canine cadaveric tissues (n=38 dogs) or tissues excised during surgery on clinical canine patients (n=17 hips). Matched cartilage and synovial explant co-cultures were compared to articular cartilage explant culture. Four groups were created based on presence or absence of synovium and presence or absence of IL-1 : Cartilage Culture Control (n=48), Cartilage Culture OA (n=48), Co-Culture Control (n=76), Co-Culture OA (n=76). Explants and media were evaluated on days 1, 3, 6, 12, and/or 20 of culture. For comparison to spontaneously occurring OA, articular cartilage and synovial tissues from dogs that had no evidence of OA, Clinical Control, and dogs that had OA, Clinical OA, were evaluated. Outcome measures included molecular, biochemical, and histologic assessments.Results: Gene expression levels in articular tissues correlated well between Co-Culture and Clinical Control and OA groups. GAG and collagen in normal and OA cartilage also corresponded well between Co-Culture and Clinical groups. Subjective histologic assessment revealed consistent similarities in cell and matrix characteristics between these groups. Changes in the media of the Co-Culture OA group were consistent with what has been reported for changes in synovial fluid of OA in dogs and humans.Conclusions: This co-culture model allows for assessment of cartilage and synovium, and can be used to provide a relatively comprehensive picture of spontaneously occurring OA in dogs. This model may have advantages over other models of OA in that the influences of both synovium and articular cartilage can be investigated at many levels and initial validation of the model using tissues from spontaneously occurring OA in dogs as the gold standard has been performed.

show abstract

Section: Discussionsupporting

confidence: 63%

Review of In Vitro Models and Development and Initial Validation of a Novel Co-Culture Model for the Study of Osteoarthritis

Cook¹,

Kuroki²,

Stoker³

et al. 2007

CRR

View full text Add to dashboard Cite

show abstract

“…Joint instability, induced by meniscectomy or ligand transection, increase hydration, collagen disruption, and matrix turnover accompanied by a decrease in the tissue stiffness in tension, compression, and shear . Both articular cartilage and synovial fluid (SF) from these OA models show an increase of biomarkers correlated with joint histological damage …”

mentioning

confidence: 99%

Biomechanics, obesity, and osteoarthritis. The role of adipokines: When the levee breaks

Francisco

Pérez

Pino

et al. 2017

Journal Orthopaedic Research

View full text Add to dashboard Cite

Osteoarthritis is a high-incidence painful and debilitating disease characterized by progressive degeneration of articular joints, which indicates a breakdown in joint homeostasis favoring catabolic processes. Biomechanical loading, associated with inflammatory and metabolic imbalances of joint, strongly contributes to the initiation and progression of the disease. Obesity is a primary risk factor for disease onset, and mechanical factors increased the risk for disease progression. Moreover, inflammatory mediators, in particular, adipose tissue-derived cytokines (better known as adipokines) play a critical role linking obesity and osteoarthritis. The present article summarizes the knowledge about the role of adipokines in cartilage and bone function, highlighting their contribution to the imbalance of joint homeostasis and, consequently, pathogenesis of osteoarthritis. © 2017 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 36:594-604, 2018.

show abstract

“…Inflammatory cytokines have been shown to upregulate catabolic mediators of cartilage degeneration, such as nitric oxide (NO) and prostaglandin E2, and also extracellular matrix (ECM) degrading enzymes, such as matrix metalloproteases (MMPs) and aggrecanases . Molecular biomarkers of cartilage degradation products are significantly increased following knee injury in patients and are upregulated in animal models of joint injury and in vitro models of injury to articular cartilage …”

mentioning

confidence: 99%

CXCL10 is upregulated in synovium and cartilage following articular fracture

Furman

Kent

Huebner³

et al. 2017

Journal Orthopaedic Research

View full text Add to dashboard Cite

The objective of this study was to investigate the expression of the chemokine CXCL10 and its role in joint tissues following articular fracture. We hypothesized that CXCL10 is upregulated following articular fracture and contributes to cartilage degradation associated with posttraumatic arthritis (PTA). To evaluate CXCL10 expression following articular fracture, gene expression was quantified in synovial tissue from knee joints of C57BL/6 mice that develop PTA following articular fracture, and MRL/MpJ mice that are protected from PTA. CXCL10 protein expression was assessed in human cartilage in normal, osteoarthritic (OA), and post-traumatic tissue using immunohistochemistry. The effects of exogenous CXCL10, alone and in combination with IL-1, on porcine cartilage explants were assessed by quantifying the release of catabolic mediators. Synovial tissue gene expression of CXCL10 was upregulated by joint trauma, peaking one day in C57BL/6 mice (25-fold) vs. three days post-fracture in MRL/MpJ mice (15-fold). CXCL10 protein in articular cartilage was most highly expressed following trauma compared with normal and OA tissue. In a dose dependent manner, exogenous CXCL10 significantly reduced total matrix metalloproteinase (MMP) and aggrecanase activity of culture media from cartilage explants. CXCL10 also trended toward a reduction in IL-1α-stimulated total MMP activity (p=0.09) and S-GAG (p=0.09), but not NO release. In conclusion, CXCL10 was upregulated in synovium and chondrocytes following trauma. However, exogenous CXCL10 did not induce a catabolic response in cartilage. CXCL10 may play a role in modulating the chondrocyte response to inflammatory stimuli associated with joint injury and the progression of PTA. This article is protected by copyright. All rights reserved

show abstract

Longitudinal Characterization of Synovial Fluid Biomarkers in the Canine Meniscectomy Model of Osteoarthritis

Cited by 20 publications

References 0 publications

Review of In Vitro Models and Development and Initial Validation of a Novel Co-Culture Model for the Study of Osteoarthritis

Review of In Vitro Models and Development and Initial Validation of a Novel Co-Culture Model for the Study of Osteoarthritis

Biomechanics, obesity, and osteoarthritis. The role of adipokines: When the levee breaks

CXCL10 is upregulated in synovium and cartilage following articular fracture

Contact Info

Product

Resources

About