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      Collagen Damage Location in Articular Cartilage Differs if Damage is Caused by Excessive Loading Magnitude or Rate

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          Abstract

          Collagen damage in articular cartilage is considered nearly irreversible and may be an early indication of cartilage degeneration. Surface fibrillation and internal collagen damage may both develop after overloading. This study hypothesizes that damage develops at these different locations, because the distribution of excessive strains varies with loading rate as a consequence of time-dependent cartilage properties. The objective is to explore whether collagen damage could preferentially occur superficially or internally, depending on the magnitude and rate of overloading. Bovine osteochondral plugs were compressed with a 2 mm diameter indenter to 15, 25, 35 and 45 N, and at 5, 60 and 120 mm/min. Surface fibrillation and internal collagen damage were graded by four observers, based on histology and staining of collagen damage. Results show that loading magnitude affects the degree of collagen damage, while loading rate dominates the location of network damage: low rates predominantly damage superficial collagen, while at high rates, internal collagen damage occurs. The proposed explanation for the rate-dependent location is that internal fluid flows govern the time-dependent internal tissue deformation and therewith the location of overstained and damaged areas. This supports the hypothesis that collagen damage development is influenced by the time-dependent material behaviour of cartilage.

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          Most cited references 33

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          Biochemical and metabolic abnormalities in articular cartilage from osteo-arthritic human hips. II. Correlation of morphology with biochemical and metabolic data.

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            Increased stromelysin-1 (MMP-3), proteoglycan degradation (3B3- and 7D4) and collagen damage in cyclically load-injured articular cartilage.

            To determine whether load-induced injury causes alterations in proteoglycan (PG), stromelysin-1 (MMP-3) and collagen in articular cartilage. Mature bovine cartilage was cyclically loaded at 0.5 Hz with 1 and 5 MPa for 1, 6 and 24h. Immediately after loading explants were evaluated for cell viability. Alterations in matrix integrity were determined by measuring PG content, PG degradation using 7D4 and 3B3(-) antibodies, broken collagen using COL2-3/4m antibody, and stromelysin-1 content using a MMP-3 antibody. Mechanical load caused cell death and PG loss starting from the articular surface and increasing in depth with loading time. There was a decrease in the 7D4 epitope (native chondroitin sulfate) in the superficial zone of cartilage loaded for longer than 1h, but an increase around chondrocytes in the deep zone. The 3B3(-) staining for degraded/abnormal chondroitin-4-sulfate neoepitope appeared only in cartilage loaded under the most severe condition (5 MPa, 24 h). The elevation of stromelysin-1 was co-localized with broken collagen (COL2-3/4m) at the articular surface in explants loaded with 1 and 5 MPa for 24 h. Cell death and PG loss occurred within 6h of cyclic loading. The elevation of MMP-3 following cell death was consistently found in the superficial zone of loaded cartilage. Since MMP-3 can degrade PG and super-activate procollagenase, the increase of MMP-3 can therefore induce matrix degradation and PG depletion in mechanically injured articular cartilage, both of which are important to the development of osteoarthritis.
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              Effect of impact load on articular cartilage: cell metabolism and viability, and matrix water content.

              Significant evidence exists that trauma to a joint produced by a single impact load below that which causes subchondral bone fracture can result in permanent damage to the cartilage matrix, including surface fissures, loss of proteoglycan, and cell death. Limited information exists, however, on the effect of a varying impact stress on chondrocyte biophysiology and matrix integrity. Based on our previous work, we hypothesized that a stress-dependent response exists for both the chondrocyte's metabolic activity and viability and the matrix's hydration. This hypothesis was tested by impacting bovine cartilage explants with nominal stresses ranging from 0.5 to 65 MPa and measuring proteoglycan biosynthesis, cell viability, and water content immediately after impaction and 24 hours later. We found that proteoglycan biosynthesis decreased and water content increased with increasing impact stress. However, there appeared to be a critical threshold stress (15-20 MPa) that caused cell death and apparent rupture of the collagen fiber matrix at the time of impaction. We concluded that the cell death and collagen rupture are responsible for the observed alterations in the tissue's metabolism and water content, respectively, although the exact mechanism causing this damage could not be determined.
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                Author and article information

                Contributors
                +31 40 2473135 , c.c.v.donkelaar@tue.nl
                Journal
                Ann Biomed Eng
                Ann Biomed Eng
                Annals of Biomedical Engineering
                Springer US (New York )
                0090-6964
                1573-9686
                8 February 2018
                8 February 2018
                2018
                : 46
                : 4
                : 605-615
                Affiliations
                [1 ]ISNI 0000 0004 0398 8763, GRID grid.6852.9, Department of Biomedical Engineering, , Eindhoven University of Technology, ; Gemini-Zuid 4.101, P.O. Box 513, 5600 MB Eindhoven, The Netherlands
                [2 ]GRID grid.441739.c, Department of Electronics and Industrial Automation, , Universidad Autónoma de Manizales, ; Manizales, Colombia
                [3 ]ISNI 0000000090126352, GRID grid.7692.a, Department of Orthopaedics, , University Medical Center Utrecht, ; Utrecht, The Netherlands
                Author notes

                Associate Editor Michael S. Detamore oversaw the review of this article.

                Article
                1986
                10.1007/s10439-018-1986-x
                5861170
                29423727
                © The Author(s) 2018

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

                Funding
                Funded by: Colciencias
                Award ID: LASPAU ID 20110290
                Award Recipient :
                Categories
                Article
                Custom metadata
                © Biomedical Engineering Society 2018

                Biomedical engineering

                surface roughening, indentation, mechanical loading, cartilage damage

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