Maturation of collagen fibril network structure in tibial and femoral cartilage of rabbits
ABSTRACT The structure and composition of articular cartilage change during development and growth, as well as in response to varying loading conditions. These changes modulate the functional properties of cartilage. We studied maturation-related changes in the collagen network organization of cartilage as a function of tissue depth.
Articular cartilage from the tibial medial plateaus and femoral medial condyles of female New Zealand white rabbits was collected from six age-groups: 4 weeks (n=30), 6 weeks (n=30), 3 months (n=24), 6 months (n=24), 9 months (n=27) and 18 months (n=19). Collagen fibril orientation, parallelism (anisotropy) and optical retardation were analyzed with polarized light microscopy. Differences in the development of depth-wise collagen organization in consecutive age-groups and the two joint locations were compared statistically.
The collagen fibril network of articular cartilage undergoes significant changes during maturation. The most prominent changes in collagen architecture, as assessed by orientation, parallelism and retardation were noticed between the ages of 4 and 6 weeks in tibial cartilage and between 6 weeks and 3 months in femoral cartilage, i.e., orientation became more perpendicular-to-surface, and parallelism and retardation increased with changes being most prominent in the deep zone. At the age of 6 weeks, tibial cartilage had a more perpendicular-to-surface orientation in the middle and deep zones than femoral cartilage (P<0.001) and higher parallelism throughout the tissue depth (P<0.001), while femoral cartilage exhibited more parallel-to-surface orientation (P<0.01) above the deep zone after maturation. Optical retardation of collagen was higher in tibial than in femoral cartilage at the ages of 4 and 6 weeks (P<0.001), while at older ages, retardation below the superficial zone in the femoral cartilage became higher than in the tibial cartilage.
During maturation, there is a significant modulation of collagen organization in articular cartilage which occurs earlier in tibial than in femoral cartilage, and is most pronounced in the deep zone.
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ABSTRACT: The function of articular cartilage depends on its structure and composition, sensitively impaired in disease (e.g. osteoarthritis, OA). Responses of chondrocytes to tissue loading are modulated by the structure. Altered cell responses as an effect of OA may regulate cartilage mechanotransduction and cell biosynthesis. To be able to evaluate cell responses and factors affecting the onset and progression of OA, local tissue and cell stresses and strains in cartilage need to be characterized. This is extremely challenging with the presently available experimental techniques and therefore computational modeling is required. Modern models of articular cartilage are inhomogeneous and anisotropic, and they include many aspects of the real tissue structure and composition. In this paper, we provide an overview of the computational applications that have been developed for modeling the mechanics of articular cartilage at the tissue and cellular level. We concentrate on the use of fibril-reinforced models of cartilage. Furthermore, we introduce practical considerations for modeling applications, including also experimental tests that can be combined with the modeling approach. At the end, we discuss the prospects for patient-specific models when aiming to use finite element modeling analysis and evaluation of articular cartilage function, cellular responses, failure points, OA progression, and rehabilitation.Computational and Mathematical Methods in Medicine 04/2013; 2013:326150. DOI:10.1155/2013/326150 · 1.02 Impact Factor
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ABSTRACT: Articular cartilage and subchondral bone act together, forming a unit as a weight-bearing loading-transmitting surface. A close interaction between both structures has been implicated during joint cartilage degeneration, but their coupling during normal growth and development is insufficiently understood. The purpose of the present study was to examine growth-related changes of cartilage mechanical properties and to relate these changes to alterations in cartilage biochemical composition and subchondral bone structure. Tibiae and femora of both hindlimbs from 7- and 13-week-old (each n = 12) female Sprague-Dawley rats were harvested. Samples were processed for structural, biochemical and mechanical analyses. Immunohistochemical staining and protein expression analyses of collagen II, collagen IX, COMP and matrilin-3, histomorphometry of cartilage thickness and COMP staining height were performed. Furthermore, mechanical testing of articular cartilage and micro-CT analysis of subchondral bone was conducted. Growth decreased cartilage thickness, paralleled by a functional condensation of the underlying subchondral bone due to enchondral ossification. Cartilage mechanical properties seem to be rather influenced by growth-related changes in the assembly of major ECM proteins such as collagen II, collagen IX and matrilin-3 than by growth-related alterations in its underlying subchondral bone structure. Importantly, the present study provides a first insight into the growth-related structural, biochemical and mechanical interaction of articular cartilage and subchondral bone. Finally, these data contribute to the general knowledge about the cooperation between the articular cartilage and subchondral bone.Journal of Anatomy 10/2012; 222(2). DOI:10.1111/joa.12003 · 2.23 Impact Factor
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ABSTRACT: There is an urgent demand for long term solutions to improve osteoarthritis treatments in the ageing population. There are drugs that control the pain but none that stop the progression of the disease in a safe and efficient way. Increased intervention efforts, augmented by early diagnosis and integrated biophysical therapies are therefore needed. Unfortunately, progress has been hampered due to the wide variety of experimental models which examine the effect of mechanical stimuli and inflammatory mediators on signal transduction pathways. Our understanding of the early mechanopathophysiology is poor, particularly the way in which mechanical stimuli influences cell function and regulates matrix synthesis. This makes it difficult to identify reliable targets and design new therapies. In addition, the effect of mechanical loading on matrix turnover is dependent on the nature of the mechanical stimulus. Accumulating evidence suggests that moderate mechanical loading helps to maintain cartilage integrity with a low turnover of matrix constituents. In contrast, nonphysiological mechanical signals are associated with increased cartilage damage and degenerative changes. This review will discuss the pathways regulated by compressive loading regimes and inflammatory signals in animal and in vitro 3D models. Identification of the chondroprotective pathways will reveal novel targets for osteoarthritis treatments.09/2011; 2011:979032. DOI:10.1155/2011/979032