Increased matrix mineralization in the immature femoral head following ischemic osteonecrosis
Abstract Traditionally, it is believed that structural failure of the ischemic epiphysis as well as changes in radiodensity seen in the early stage of Legg–Calvé–Perthes disease is due to the repair process. However, little is known if matrix properties are altered following ischemic injury of the j...
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description | Abstract Traditionally, it is believed that structural failure of the ischemic epiphysis as well as changes in radiodensity seen in the early stage of Legg–Calvé–Perthes disease is due to the repair process. However, little is known if matrix properties are altered following ischemic injury of the juvenile femoral head. The purpose of this study was to determine the matrix mineralization density, an important determinant of material quality and strength, of the proximal femoral epiphysis in an experimental animal model of Perthes disease. Ten piglets were surgically induced with femoral head ischemia and euthanized at 4 and 8 weeks following surgery. Contralateral, unoperated femoral heads were used as controls. Bone and calcified cartilage mineralization density distribution parameters were determined using quantitative backscattered electron imaging (qBEI) in the epiphyseal calcified articular cartilage, subchondral bone and central trabecular bone region. Histological as well as radiographic assessment was also performed. In the necrotic calcified epiphyseal cartilage matrix, a significant increase in the mean degree of mineralization (CaMean: +24%, p < 0.0001) as well as the homogeneity of mineralization (CaWidth: − 21%, p < 0.05) and a significantly reduced amount of low mineralized matrix (CaLow: − 49%, p < 0.0001) were already present at 4 weeks post-ischemia induction. Similar changes, but more moderate, were also seen in the subchondral bone region. In contrast, in the necrotic central trabecular region, significant changes in matrix mineralization were found at 8 weeks (CaMean: +4%, p < 0.05; CaWidth: − 22%, p < 0.05; CaLow: − 8%, p < 0.05) but not at 4 weeks post-ischemia induction. Our findings indicate that the process of matrix mineralization continues in necrotic calcified articular cartilage and bone following femoral head ischemia, which leads to a higher and more homogenous mineralized tissue matrix altering its intrinsic material properties. This may also explain the increased radiodensity seen in the early stage of Perthes disease prior to the initiation of the repair process. |
doi_str_mv | 10.1016/j.bone.2009.10.006 |
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However, little is known if matrix properties are altered following ischemic injury of the juvenile femoral head. The purpose of this study was to determine the matrix mineralization density, an important determinant of material quality and strength, of the proximal femoral epiphysis in an experimental animal model of Perthes disease. Ten piglets were surgically induced with femoral head ischemia and euthanized at 4 and 8 weeks following surgery. Contralateral, unoperated femoral heads were used as controls. Bone and calcified cartilage mineralization density distribution parameters were determined using quantitative backscattered electron imaging (qBEI) in the epiphyseal calcified articular cartilage, subchondral bone and central trabecular bone region. Histological as well as radiographic assessment was also performed. In the necrotic calcified epiphyseal cartilage matrix, a significant increase in the mean degree of mineralization (CaMean: +24%, p < 0.0001) as well as the homogeneity of mineralization (CaWidth: − 21%, p < 0.05) and a significantly reduced amount of low mineralized matrix (CaLow: − 49%, p < 0.0001) were already present at 4 weeks post-ischemia induction. Similar changes, but more moderate, were also seen in the subchondral bone region. In contrast, in the necrotic central trabecular region, significant changes in matrix mineralization were found at 8 weeks (CaMean: +4%, p < 0.05; CaWidth: − 22%, p < 0.05; CaLow: − 8%, p < 0.05) but not at 4 weeks post-ischemia induction. Our findings indicate that the process of matrix mineralization continues in necrotic calcified articular cartilage and bone following femoral head ischemia, which leads to a higher and more homogenous mineralized tissue matrix altering its intrinsic material properties. This may also explain the increased radiodensity seen in the early stage of Perthes disease prior to the initiation of the repair process.]]></description><identifier>ISSN: 8756-3282</identifier><identifier>EISSN: 1873-2763</identifier><identifier>DOI: 10.1016/j.bone.2009.10.006</identifier><identifier>PMID: 19833243</identifier><language>eng</language><publisher>Amsterdam: Elsevier Inc</publisher><subject>Animals ; Backscattered electron imaging ; Biological and medical sciences ; Bone Density - physiology ; Bone material properties ; Bone Matrix - diagnostic imaging ; Bone Matrix - pathology ; Bone Matrix - physiopathology ; Calcification, Physiologic - physiology ; Calcinosis - complications ; Calcinosis - diagnostic imaging ; Calcinosis - physiopathology ; Cartilage - diagnostic imaging ; Cartilage - pathology ; Cartilage - physiopathology ; Cell physiology ; Diseases of the osteoarticular system ; Epiphyses - diagnostic imaging ; Epiphyses - pathology ; Epiphyses - physiopathology ; Femur Head - blood supply ; Femur Head - diagnostic imaging ; Femur Head - pathology ; Femur Head - physiopathology ; Fundamental and applied biological sciences. Psychology ; Ischemia - complications ; Ischemia - diagnostic imaging ; Ischemia - physiopathology ; Legg–Calvé–Perthes disease ; Medical sciences ; Mineralization ; Mineralization, calcification ; Molecular and cellular biology ; Orthopedics ; Osteonecrosis ; Osteonecrosis - complications ; Osteonecrosis - diagnostic imaging ; Osteonecrosis - physiopathology ; Radiography ; Sus scrofa ; Vascular bone diseases ; Vertebrates: anatomy and physiology, studies on body, several organs or systems</subject><ispartof>Bone (New York, N.Y.), 2010-02, Vol.46 (2), p.379-385</ispartof><rights>Elsevier Inc.</rights><rights>2009 Elsevier Inc.</rights><rights>2015 INIST-CNRS</rights><rights>(c) 2009 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c506t-bf54b48226e010cbf76019a1d16ae5bbb0f4463f7ae56bc782748499bff3282c3</citedby><cites>FETCH-LOGICAL-c506t-bf54b48226e010cbf76019a1d16ae5bbb0f4463f7ae56bc782748499bff3282c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.bone.2009.10.006$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=22474758$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19833243$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hofstaetter, Jochen G</creatorcontrib><creatorcontrib>Roschger, Paul</creatorcontrib><creatorcontrib>Klaushofer, Klaus</creatorcontrib><creatorcontrib>Kim, Harry K.W</creatorcontrib><title>Increased matrix mineralization in the immature femoral head following ischemic osteonecrosis</title><title>Bone (New York, N.Y.)</title><addtitle>Bone</addtitle><description><![CDATA[Abstract Traditionally, it is believed that structural failure of the ischemic epiphysis as well as changes in radiodensity seen in the early stage of Legg–Calvé–Perthes disease is due to the repair process. However, little is known if matrix properties are altered following ischemic injury of the juvenile femoral head. The purpose of this study was to determine the matrix mineralization density, an important determinant of material quality and strength, of the proximal femoral epiphysis in an experimental animal model of Perthes disease. Ten piglets were surgically induced with femoral head ischemia and euthanized at 4 and 8 weeks following surgery. Contralateral, unoperated femoral heads were used as controls. Bone and calcified cartilage mineralization density distribution parameters were determined using quantitative backscattered electron imaging (qBEI) in the epiphyseal calcified articular cartilage, subchondral bone and central trabecular bone region. Histological as well as radiographic assessment was also performed. In the necrotic calcified epiphyseal cartilage matrix, a significant increase in the mean degree of mineralization (CaMean: +24%, p < 0.0001) as well as the homogeneity of mineralization (CaWidth: − 21%, p < 0.05) and a significantly reduced amount of low mineralized matrix (CaLow: − 49%, p < 0.0001) were already present at 4 weeks post-ischemia induction. Similar changes, but more moderate, were also seen in the subchondral bone region. In contrast, in the necrotic central trabecular region, significant changes in matrix mineralization were found at 8 weeks (CaMean: +4%, p < 0.05; CaWidth: − 22%, p < 0.05; CaLow: − 8%, p < 0.05) but not at 4 weeks post-ischemia induction. Our findings indicate that the process of matrix mineralization continues in necrotic calcified articular cartilage and bone following femoral head ischemia, which leads to a higher and more homogenous mineralized tissue matrix altering its intrinsic material properties. This may also explain the increased radiodensity seen in the early stage of Perthes disease prior to the initiation of the repair process.]]></description><subject>Animals</subject><subject>Backscattered electron imaging</subject><subject>Biological and medical sciences</subject><subject>Bone Density - physiology</subject><subject>Bone material properties</subject><subject>Bone Matrix - diagnostic imaging</subject><subject>Bone Matrix - pathology</subject><subject>Bone Matrix - physiopathology</subject><subject>Calcification, Physiologic - physiology</subject><subject>Calcinosis - complications</subject><subject>Calcinosis - diagnostic imaging</subject><subject>Calcinosis - physiopathology</subject><subject>Cartilage - diagnostic imaging</subject><subject>Cartilage - pathology</subject><subject>Cartilage - physiopathology</subject><subject>Cell physiology</subject><subject>Diseases of the osteoarticular system</subject><subject>Epiphyses - diagnostic imaging</subject><subject>Epiphyses - pathology</subject><subject>Epiphyses - physiopathology</subject><subject>Femur Head - blood supply</subject><subject>Femur Head - diagnostic imaging</subject><subject>Femur Head - pathology</subject><subject>Femur Head - physiopathology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Ischemia - complications</subject><subject>Ischemia - diagnostic imaging</subject><subject>Ischemia - physiopathology</subject><subject>Legg–Calvé–Perthes disease</subject><subject>Medical sciences</subject><subject>Mineralization</subject><subject>Mineralization, calcification</subject><subject>Molecular and cellular biology</subject><subject>Orthopedics</subject><subject>Osteonecrosis</subject><subject>Osteonecrosis - complications</subject><subject>Osteonecrosis - diagnostic imaging</subject><subject>Osteonecrosis - physiopathology</subject><subject>Radiography</subject><subject>Sus scrofa</subject><subject>Vascular bone diseases</subject><subject>Vertebrates: anatomy and physiology, studies on body, several organs or systems</subject><issn>8756-3282</issn><issn>1873-2763</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU1rFTEUhoMo9rb6B1xINuJqrvmaZAZEkKK1UOiiupSQZE68uc4kNZmx1l9vhnux4MJVyDnPSd48QegFJVtKqHyz39oUYcsI6WthS4h8hDa0U7xhSvLHaNOpVjacdewEnZayJ4TwXtGn6IT2HedM8A36ehldBlNgwJOZc_iFpxAhmzH8NnNIEYeI5x3gMNX2kgF7mFJt4x2YAfs0jukuxG84FLeDKTicygw1lcuphPIMPfFmLPD8uJ6hLx8_fD7_1FxdX1yev79qXEvk3FjfCis6xiQQSpz1ShLaGzpQaaC11hIvhORe1Z20TnVMiU70vfV-fZ3jZ-j14dzbnH4sUGY91UAwjiZCWopWnPdEENFWkh3INWDJ4PVtDpPJ95oSvVrVe71a1avVtVat1qGXx-MXO8HwMHLUWIFXR8AUZ0afTXSh_OUYE0qotqvc2wMHVcbPAFkXFyA6GEIGN-shhf_nePfPuBtDDPXG73APZZ-WHKtmTXVhmuib9f9XQaSvOhXj_A9T1qvZ</recordid><startdate>20100201</startdate><enddate>20100201</enddate><creator>Hofstaetter, Jochen G</creator><creator>Roschger, Paul</creator><creator>Klaushofer, Klaus</creator><creator>Kim, Harry K.W</creator><general>Elsevier Inc</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20100201</creationdate><title>Increased matrix mineralization in the immature femoral head following ischemic osteonecrosis</title><author>Hofstaetter, Jochen G ; Roschger, Paul ; Klaushofer, Klaus ; Kim, Harry K.W</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c506t-bf54b48226e010cbf76019a1d16ae5bbb0f4463f7ae56bc782748499bff3282c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Animals</topic><topic>Backscattered electron imaging</topic><topic>Biological and medical sciences</topic><topic>Bone Density - physiology</topic><topic>Bone material properties</topic><topic>Bone Matrix - diagnostic imaging</topic><topic>Bone Matrix - pathology</topic><topic>Bone Matrix - physiopathology</topic><topic>Calcification, Physiologic - physiology</topic><topic>Calcinosis - complications</topic><topic>Calcinosis - diagnostic imaging</topic><topic>Calcinosis - physiopathology</topic><topic>Cartilage - diagnostic imaging</topic><topic>Cartilage - pathology</topic><topic>Cartilage - physiopathology</topic><topic>Cell physiology</topic><topic>Diseases of the osteoarticular system</topic><topic>Epiphyses - diagnostic imaging</topic><topic>Epiphyses - pathology</topic><topic>Epiphyses - physiopathology</topic><topic>Femur Head - blood supply</topic><topic>Femur Head - diagnostic imaging</topic><topic>Femur Head - pathology</topic><topic>Femur Head - physiopathology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Ischemia - complications</topic><topic>Ischemia - diagnostic imaging</topic><topic>Ischemia - physiopathology</topic><topic>Legg–Calvé–Perthes disease</topic><topic>Medical sciences</topic><topic>Mineralization</topic><topic>Mineralization, calcification</topic><topic>Molecular and cellular biology</topic><topic>Orthopedics</topic><topic>Osteonecrosis</topic><topic>Osteonecrosis - complications</topic><topic>Osteonecrosis - diagnostic imaging</topic><topic>Osteonecrosis - physiopathology</topic><topic>Radiography</topic><topic>Sus scrofa</topic><topic>Vascular bone diseases</topic><topic>Vertebrates: anatomy and physiology, studies on body, several organs or systems</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hofstaetter, Jochen G</creatorcontrib><creatorcontrib>Roschger, Paul</creatorcontrib><creatorcontrib>Klaushofer, Klaus</creatorcontrib><creatorcontrib>Kim, Harry K.W</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Bone (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hofstaetter, Jochen G</au><au>Roschger, Paul</au><au>Klaushofer, Klaus</au><au>Kim, Harry K.W</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Increased matrix mineralization in the immature femoral head following ischemic osteonecrosis</atitle><jtitle>Bone (New York, N.Y.)</jtitle><addtitle>Bone</addtitle><date>2010-02-01</date><risdate>2010</risdate><volume>46</volume><issue>2</issue><spage>379</spage><epage>385</epage><pages>379-385</pages><issn>8756-3282</issn><eissn>1873-2763</eissn><abstract><![CDATA[Abstract Traditionally, it is believed that structural failure of the ischemic epiphysis as well as changes in radiodensity seen in the early stage of Legg–Calvé–Perthes disease is due to the repair process. However, little is known if matrix properties are altered following ischemic injury of the juvenile femoral head. The purpose of this study was to determine the matrix mineralization density, an important determinant of material quality and strength, of the proximal femoral epiphysis in an experimental animal model of Perthes disease. Ten piglets were surgically induced with femoral head ischemia and euthanized at 4 and 8 weeks following surgery. Contralateral, unoperated femoral heads were used as controls. Bone and calcified cartilage mineralization density distribution parameters were determined using quantitative backscattered electron imaging (qBEI) in the epiphyseal calcified articular cartilage, subchondral bone and central trabecular bone region. Histological as well as radiographic assessment was also performed. In the necrotic calcified epiphyseal cartilage matrix, a significant increase in the mean degree of mineralization (CaMean: +24%, p < 0.0001) as well as the homogeneity of mineralization (CaWidth: − 21%, p < 0.05) and a significantly reduced amount of low mineralized matrix (CaLow: − 49%, p < 0.0001) were already present at 4 weeks post-ischemia induction. Similar changes, but more moderate, were also seen in the subchondral bone region. In contrast, in the necrotic central trabecular region, significant changes in matrix mineralization were found at 8 weeks (CaMean: +4%, p < 0.05; CaWidth: − 22%, p < 0.05; CaLow: − 8%, p < 0.05) but not at 4 weeks post-ischemia induction. Our findings indicate that the process of matrix mineralization continues in necrotic calcified articular cartilage and bone following femoral head ischemia, which leads to a higher and more homogenous mineralized tissue matrix altering its intrinsic material properties. This may also explain the increased radiodensity seen in the early stage of Perthes disease prior to the initiation of the repair process.]]></abstract><cop>Amsterdam</cop><pub>Elsevier Inc</pub><pmid>19833243</pmid><doi>10.1016/j.bone.2009.10.006</doi><tpages>7</tpages></addata></record> |
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subjects | Animals Backscattered electron imaging Biological and medical sciences Bone Density - physiology Bone material properties Bone Matrix - diagnostic imaging Bone Matrix - pathology Bone Matrix - physiopathology Calcification, Physiologic - physiology Calcinosis - complications Calcinosis - diagnostic imaging Calcinosis - physiopathology Cartilage - diagnostic imaging Cartilage - pathology Cartilage - physiopathology Cell physiology Diseases of the osteoarticular system Epiphyses - diagnostic imaging Epiphyses - pathology Epiphyses - physiopathology Femur Head - blood supply Femur Head - diagnostic imaging Femur Head - pathology Femur Head - physiopathology Fundamental and applied biological sciences. Psychology Ischemia - complications Ischemia - diagnostic imaging Ischemia - physiopathology Legg–Calvé–Perthes disease Medical sciences Mineralization Mineralization, calcification Molecular and cellular biology Orthopedics Osteonecrosis Osteonecrosis - complications Osteonecrosis - diagnostic imaging Osteonecrosis - physiopathology Radiography Sus scrofa Vascular bone diseases Vertebrates: anatomy and physiology, studies on body, several organs or systems |
title | Increased matrix mineralization in the immature femoral head following ischemic osteonecrosis |
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