Does loading influence the severity of cartilage degeneration in the canine Groove‐model of OA?

Vos, P.A.J.M.; Interma, Femke; El, B. van; DeGroot, Jeroen; Bijlsma, J. W. J.; Lafeber, Floris P. J. G.; Mastbergen, S.C.

doi:10.1002/jor.20897

Cited by 6 publications

(7 citation statements)

References 26 publications

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“…The surgically induced cartilage damage was restricted to a maximum of four grooves on femoral condyles only, whereas in the regularly performed Groove model OA at least 10 grooves are made 18. Additionally, loading of the joints was minimized, knowing that loading adds to development of OA 23. In the present study, the animals were permanently housed individually in indoor pens (3.5 m 2 ), the minimal reasonably acceptable space, to keep movement and with that loading of the joints to a minimum.…”

Section: Discussionmentioning

confidence: 99%

Elevation of cartilage AGEs does not accelerate initiation of canine experimental osteoarthritis upon mild surgical damage

Vos

DeGroot

Rijbroek

et al. 2012

Journal Orthopaedic Research

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Osteoarthritis is a highly prevalent disease, age being the main risk factor. The age-related accumulation of advancedglycation-endproducts (AGEs) adversely affects the mechanical and biochemical properties of cartilage. The hypothesis that accumulation of cartilage AGEs in combination with surgically induced damage predisposes to the development of osteoarthritis was tested in vivo in a canine model. To artificially increase cartilage AGEs, right knee joints of eight dogs were repeatedly injected with ribose/ threose (AGEd-joints). Left joints with vehicle alone served as control. Subsequently, minimal surgically applied cartilage damage was induced and loading restrained as much as possible. Thirty weeks after surgery, joint tissues of all dogs were analyzed for biochemical and histological features of OA. Cartilage pentosidine levels were $5-fold enhanced (p ¼ 0.001 vs. control-joints). On average, no statistically significant differences in joint degeneration were found between AGEd and control-joints. Enhanced cartilage pentosidine levels did correlate with less cartilage proteoglycan release (R ¼ À0.762 and R ¼ À0.810 for total and newly-formed proteoglycans, respectively; p ¼ 0.028 and 0.015 for both). The current data support the diminished cartilage turnover, but only a tendency towards enhanced cartilage damage in AGEd articular cartilage was observed. As such, elevated AGEs do not unambiguously accelerate the development of early canine OA upon minimal surgical damage. Keywords: osteoarthritis; non-enzymatic glycation; canine; pentosidine; proteoglycan Osteoarthritis (OA), with a high prevalence and increasing incidence due to the aging population, having a large impact on the patient's quality of life, is characterized by progressive cartilage damage, bone changes, and secondary synovial inflammation. 1 As yet, the pathogenesis of OA is largely unknown. Several factors have been reported to predispose to the development of OA, such as genetic background, overweight, joint laxity, and muscle weakness. 2 However, undisputedly, the most important risk factor for development of OA is age. 3 The incidence of OA increases strongly with age: >50% of the population over 60 years of age is affected. 4,5 However, there are still many uncertainties how age contributes to the onset and progression of OA. Age-related changes in the articular cartilage are suggested to play an important role in the susceptibility of cartilage to OA.One of the major age-related changes in articular cartilage is the spontaneous modification of proteins by non-enzymatic glycation resulting in the accumulation of advanced glycation endproducts (AGEs). Nonenzymatic glycation is a post-translational modification of proteins by reducing sugars. The spontaneous condensation of reducing sugars with free amino groups in lysine or arginine residues on proteins leads to the formation of AGEs. 6 Pentosidine, a fluorescent AGE formed between lysine and arginine residues, is frequently used as marker for AGEs. AGEs are formed in all pr...

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Section: Discussionmentioning

confidence: 99%

Elevation of cartilage AGEs does not accelerate initiation of canine experimental osteoarthritis upon mild surgical damage

Vos

DeGroot

Rijbroek

et al. 2012

Journal Orthopaedic Research

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“…As such, subtly complex differences in joint geometry may not be detected and it may be these differences that contribute most to differences in mechanics that may lead to the development or progression of knee osteoarthritis. Numerous studies have demonstrated the role of mechanical loading factors in onset and advancement of OA (Andriacchi et al, 2004; Arokoski et al, 2000; Sharma et al, 1999; Vos et al, 2009; Yang et al, 2009), and clinical studies have demonstrated that joint incongruity is related to early cartilage degeneration (Harris, 1986; Hohe et al, 2002; Mankin et al, 1971). …”

Section: Discussionmentioning

confidence: 99%

Statistical shape modeling describes variation in tibia and femur surface geometry between Control and Incidence groups from the Osteoarthritis Initiative database

Bredbenner

Eliason

Potter

et al. 2010

Journal of Biomechanics

126

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We hypothesize that variability in knee subchondral bone surface geometry will differentiate between patients at risk and those not at risk for developing osteoarthritis (OA) and suggest that statistical shape modeling (SSM) methods form the basis for developing a diagnostic tool for predicting the onset of OA. Using a subset of clinical knee MRI data from the osteoarthritis initiative (OAI), the objectives of this study were to (1) utilize SSM to compactly and efficiently describe variability in knee subchondral bone surface geometry and (2) determine the efficacy of SSM and rigid body transformations to distinguish between patients who are not expected to develop osteoarthritis (i.e. Control group) and those with clinical risk factors for OA (i.e. Incidence group). Quantitative differences in femur and tibia surface geometry were demonstrated between groups, although differences in knee joint alignment measures were not statistically significant, suggesting that variability in individual bone geometry may play a greater role in determining joint space geometry and mechanics. SSM provides a means of explicitly describing complete articular surface geometry and allows the complex spatial variation in joint surface geometry and joint congruence between healthy subjects and those with clinical risk of developing or existing signs of OA to be statistically demonstrated.

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“…Canine IVD tissue was collected from dogs euthanized in studies investigating osteoarthritis (Experiment numbers DEC 2007.III.08.110 and DEC 2009.III.05.037; euthanasia performed by way of an intravenous overdose of pentobarbital) [31-33] and cardiovascular disease (Experiment number DEC 2007.II.01.029; euthanasia performed under general anesthesia by way of fibrillation and subsequent excision of the heart) [[34], other, unpublished data].…”

Section: Methodsmentioning

confidence: 99%

Gene expression profiling of early intervertebral disc degeneration reveals a down-regulation of canonical Wnt signaling and caveolin-1 expression: implications for development of regenerative strategies

et al. 2013

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IntroductionEarly degeneration of the intervertebral disc (IVD) involves a change in cellular differentiation from notochordal cells (NCs) in the nucleus pulposus (NP) to chondrocyte-like cells (CLCs). The purpose of this study was to investigate the gene expression profiles involved in this process using NP tissue from non-chondrodystrophic and chondrodystrophic dogs, a species with naturally occurring IVD degeneration.MethodsDual channel DNA microarrays were used to compare 1) healthy NP tissue containing only NCs (NC-rich), 2) NP tissue with a mixed population of NCs and CLCs (Mixed), and 3) NP tissue containing solely CLCs (CLC-rich) in both non-chondrodystrophic and chondrodystrophic dogs. Based on previous reports and the findings of the microarray analyses, canonical Wnt signaling was further evaluated using qPCR of relevant Wnt target genes. We hypothesized that caveolin-1, a regulator of Wnt signaling that showed significant changes in gene expression in the microarray analyses, played a significant role in early IVD degeneration. Caveolin-1 expression was investigated in IVD tissue sections and in cultured NCs. To investigate the significance of Caveolin-1 in IVD health and degeneration, the NP of 3-month-old Caveolin-1 knock-out mice was histopathologically evaluated and compared with the NP of wild-type mice of the same age.ResultsEarly IVD degeneration involved significant changes in numerous pathways, including Wnt/β-catenin signaling. With regard to Wnt/β-catenin signaling, axin2 gene expression was significantly higher in chondrodystrophic dogs compared with non-chondrodystrophic dogs. IVD degeneration involved significant down-regulation of axin2 gene expression. IVD degeneration involved significant down-regulation in Caveolin-1 gene and protein expression. NCs showed abundant caveolin-1 expression in vivo and in vitro, whereas CLCs did not. The NP of wild-type mice was rich in viable NCs, whereas the NP of Caveolin-1 knock-out mice contained chondroid-like matrix with mainly apoptotic, small, rounded cells.ConclusionsEarly IVD degeneration involves down-regulation of canonical Wnt signaling and Caveolin-1 expression, which appears to be essential to the physiology and preservation of NCs. Therefore, Caveolin-1 may be regarded an exciting target for developing strategies for IVD regeneration.

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Does loading influence the severity of cartilage degeneration in the canine Groove‐model of OA?

Cited by 6 publications

References 26 publications

Elevation of cartilage AGEs does not accelerate initiation of canine experimental osteoarthritis upon mild surgical damage

Elevation of cartilage AGEs does not accelerate initiation of canine experimental osteoarthritis upon mild surgical damage

Statistical shape modeling describes variation in tibia and femur surface geometry between Control and Incidence groups from the Osteoarthritis Initiative database

Gene expression profiling of early intervertebral disc degeneration reveals a down-regulation of canonical Wnt signaling and caveolin-1 expression: implications for development of regenerative strategies

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