Articular cartilage explant culture; an appropriate in vitro system to compare osteoarthritic and normal human cartilage

Lafeber, Floris P. J. G.; Kraan, P. M. Vander; Roy, J. L. A. M. Van; Huber-Bruning, O.; Bijlsma, J. W. J.

doi:10.3109/03008209309016834

Cited by 83 publications

(75 citation statements)

References 19 publications

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“…Cartilage was obtained from the femoral condyles of control and experimental knee joints of all dogs according to standardized procedures (41). Within 1 hour after dissection, full-thickness cartilage slices (excluding the subchondral bone) were cut into square pieces (3-10 mg) and processed for histologic and biochemical analyses (40).…”

Section: Methodsmentioning

confidence: 99%

Accumulation of advanced glycation end products as a molecular mechanism for aging as a risk factor in osteoarthritis

DeGroot¹,

Verzijl²,

Wijk

et al. 2004

Arthritis & Rheumatism

182

114

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Objective. Osteoarthritis (OA) is one of the most prevalent and disabling chronic conditions affecting the elderly. Its etiology is largely unknown, but age is the most prominent risk factor. The current study was designed to test whether accumulation of advanced glycation end products (AGEs), which are known to adversely affect cartilage turnover and mechanical properties, provides a molecular mechanism by which aging contributes to the development of OA.Methods. The hypothesis that elevated AGE levels predispose to the development of OA was tested in the canine anterior cruciate ligament transection (ACLT) model of experimental OA. Cartilage AGE levels were enhanced in young dogs by intraarticular injections of ribose. This mimics the accumulation of AGEs without the interference of other age-related changes. The severity of OA was then assessed 7 weeks after ACLT surgery in dogs with normal versus enhanced AGE levels.Results. Intraarticular injections of ribose enhanced cartilage AGE levels ϳ5-fold, which is similar to the normal increase that is observed in old dogs. ACLT surgery resulted in more-pronounced OA in dogs with enhanced AGE levels. This was observed as increased collagen damage and enhanced release of proteoglycans. The attempt to repair the matrix damage was impaired; proteoglycan synthesis and retention were decreased at enhanced AGE levels. Mankin grading of histology sections also revealed more-severe OA in animals with enhanced AGE levels.Conclusion. These findings demonstrate increased severity of OA at higher cartilage AGE levels and provide the first in vivo experimental evidence for a molecular mechanism by which aging may predispose to the development of OA.The population of Western society is aging rapidly. Consequently, age-related diseases will increase greatly over the coming decades and will have a great impact on the quality of life of the elderly. Osteoarthritis (OA) is one of the most prevalent and disabling chronic conditions affecting the elderly and poses a significant public health problem (1). The most prominent feature of OA is the progressive destruction of articular cartilage, resulting in impaired joint motion, severe pain, and, ultimately, disability (2). As yet, the etiology of OA remains largely unknown. The incidence of OA increases with age: Ͼ50% of the population over 60 years of age is affected (3,4). Although age is identified as the main risk factor for the development of OA, the mechanism by which aging is involved remains unclear. Age-related changes in the articular cartilage are expected to play an important role in the susceptibility of cartilage to OA.Articular cartilage derives its mechanical properties from its extracellular matrix. This matrix is composed of type II collagen, which forms a 3-dimensional network that provides the cartilage with resistance to tensile forces (5).

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Section: Methodsmentioning

confidence: 99%

Accumulation of advanced glycation end products as a molecular mechanism for aging as a risk factor in osteoarthritis

DeGroot¹,

Verzijl²,

Wijk

et al. 2004

Arthritis & Rheumatism

182

114

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“…Cartilage degeneration was evaluated in safranin-O/fast-green iron hematoxylin-stained sections by light microscopy according to the slightly modified (33) criteria of Mankin. (34) Specimens were graded in random order by two observers unaware of the source of the cartilage.…”

Section: Cartilage Analysismentioning

confidence: 99%

Similarities and discrepancies in subchondral bone structure in two differently induced canine models of osteoarthritis

Intema

Sniekers

Weinans

et al. 2010

Journal of Bone and Mineral Research

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In osteoarthritis (OA), cartilage degradation is accompanied by subchondral bone changes. The pathogenesis and physiology of bone changes in OA are still unclear. The changes in subchondral bone architecture and cartilage damage were compared in differently induced experimental models of OA. Experimental OA was induced bilaterally by anterior cruciate ligament transection (ACLT) or by cartilage trauma (Groove model); bilateral sham surgery served as control. Lysylpyridinoline (LP, bone resorption) and C-telopeptide of type II collagen (CTX-II, cartilage breakdown) were measured over time. At 20 weeks after surgery, the subchondral cortical plate and trabecular bone of the tibia were analyzed by micro-computed tomography (mCT) and cartilage degeneration was analyzed histologically and biochemically. In both models, cartilage degeneration and cortical subchondral plate thinning were present. CTX-II levels were elevated over time in both models. Subchondral trabecular bone changes were observed only in the ACLT model, not in the Groove model. Correspondingly, LP levels were elevated over time in the ACLT model and not in the Groove model. Interestingly, the trabecular bone changes in the ACLT model were extended to the metaphyseal area. The early decrease in plate thickness, present in both models, as was cartilage damage, suggests that plate thinning is a phenomenon that is intrinsic to the process of OA independent of the cause/induction of OA. On the other hand, trabecular changes in subchondral and metaphyseal bone are not part of a common pathway of OA development and may be induced biomechanically in the destabilized and less loaded ACLT joint. ß

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“…18,19 For biochemical analysis, cartilage samples were cultured according to standard procedures. 20 For femoral condyles and tibial plateau, cartilage proteoglycan content-synthesis, retention, release-and DNA content were determined for six explants per parameter. 5 …”

Section: Synovial Tissue Analysismentioning

confidence: 99%

“…20 Synthesis rate is expressed as nmol of sulphate incorporated per hour per mg DNA of the cartilage (nmol/h/g). As a measure of the retention of newly synthesized proteoglycans, the release of 35 SO 4 2À -labeled proteoglycans in the medium was determined, as described previously.…”

Section: Somentioning

confidence: 99%

“…As a measure of the retention of newly synthesized proteoglycans, the release of 35 SO 4 2À -labeled proteoglycans in the medium was determined, as described previously. 20 The release of newly formed proteoglycans is expressed as percentage release of newly formed proteoglycans in 3 days (% new proteoglycan release). For the total release of proteoglycans, Alcian blue (8-GX Sigma A5268) stained and precipitated proteoglycans were quantified photometrically with chondroitin sulphate (Sigma C4384) as a reference.…”

Section: Somentioning

confidence: 99%

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

Vos

Interma

El³

et al. 2009

Journal Orthopaedic Research

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Many animal models are used to study osteoarthritis (OA). In these models the role of joint loading in the development of OA is not fully understood. We studied the effect of loading on the development of OA in the canine Groove-model. In ten female beagle dogs OA was induced in one knee according to the Groove-model. The animals were divided in groups with and without forced-loading. Forced-loading was achieved by fixing the contra-lateral limb to the trunk 3 times a week for 4 hours. After 20 weeks joint tissues of all dogs were evaluated. Subjective evaluation revealed less movement with more loading in the forced-loading-group compared to the group without forced-loading. In both groups induction of OA resulted in macroscopical and microscopical OA changes as well as alterations in cartilage metabolism characteristics for OA. Although differences were small, for some parameters they were statistically significant for the forced-loading-group. There were no differences between the contra-lateral healthy joints of both groups. The present study demonstrates that in the Groove-model intensified loading is not a prerequisite for the development of OA, although it adds to some extent to the severity of the OA. ß

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Articular cartilage explant culture; an appropriate in vitro system to compare osteoarthritic and normal human cartilage

Cited by 83 publications

References 19 publications

Accumulation of advanced glycation end products as a molecular mechanism for aging as a risk factor in osteoarthritis

Accumulation of advanced glycation end products as a molecular mechanism for aging as a risk factor in osteoarthritis

Similarities and discrepancies in subchondral bone structure in two differently induced canine models of osteoarthritis

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

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