Skeletal fluorosis: Histomorphometric analysis of bone changes and bone fluoride content in 29 patients
Identifieur interne : 000978 ( Istex/Corpus ); précédent : 000977; suivant : 000979Skeletal fluorosis: Histomorphometric analysis of bone changes and bone fluoride content in 29 patients
Auteurs : G. Boivin ; P. Chavassieux ; M. C. Chapuy ; C. A. Baud ; P. J. MeunierSource :
- Bone [ 8756-3282 ] ; 1989.
Abstract
Bone fluoride content (BFC) was measured and histomorphometric analysis of undecalcified sections was performed in transiliac biopsy cores from 29 patients (16 men, 13 women, aged 51 ± 17 years) suffering from skeletal fluorosis due to chronic exposure to fluoride. The origin of the exposure, known in 20 patients, was either hydric (endemic or sporadic) or industrial, or in a few cases iatrogenic. Measured on calcined bone using a specific ion electrode, BFC was significantly high in each specimen (mean ± SD; 0.79 ± 0.36% on bone ash). The radiologically evident osteosclerosis observed in each patient was confirmed by a significant increase in cancellous bone volume (40.1 ± 11.2% vs. 19.0 ± 2.8% in controls, p < 0.0001). There were significant increases in cortical width (1292 ± 395 mem vs. 934 ± 173 mcm, p < 0.0001) and porosity (14.4 ± 6.4% vs. 6.5 ± 1.7%, p < 0.002), but without reduction of cortical bone mass. Cancellous osteoid volume and perimeter, as well as width of osteoid seams, were significantly increased in fluorotic patients. The increase in cancellous osteoid perimeter was almost three-fold greater than that noted in cancellous eroded perimeter. In 15 patients doubly labeled with tetracycline, the mineral apposition rate was significantly decreased, mineralization lag time was significantly increased. The fluorotic group had a greater number of osteoblasts than controls with a very high proportion of flat osteoblasts. The ultrastructural characteristics reflecting the activity of the bone cells were clearly visible on electron microscopy. Bone formation rate and adjusted apposition rate were significantly decreased in skeletal fluorosis. On stained sections and microradiographs, bone tissue showed typical modifications for skeletal fluorosis (linear formation defects, mottled bone). The volume of cancellous interstitial mineralization defects and the proportion of mottled periosteocytic lacunae were markedly increased in skeletal fluorosis. These two parameters were significantly correlated together but neither of these was significantly correlated with BFC. Renal function did not significantly influence the changes in BFC and histomorphometry of fluorotic patients. Skeletal fluorosis is thus characterized by an unbalanced coupling in favor of bone formation, and a great number of osteoblasts with a high proportion of flat osteoblasts. This may explain the mineralization impairment proven by thick osteoid seams and reduced mineral apposition rate, and supports the view that fluoride may have a dual effect on osteoblasts: a probable increased birthrate at the tissue-level due to a mitogenic effect of fluoride on precursors of osteoblasts, and a toxic effect at the individual cell-level. The addition of these two effects represents, however, a marked increase of bone formation at the organ level.
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DOI: 10.1016/8756-3282(89)90004-5
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title>Skeletal fluorosis: Histomorphometric analysis of bone changes and bone fluoride content in 29 patients</title><author><name sortKey="Boivin, G" sort="Boivin, G" uniqKey="Boivin G" first="G." last="Boivin">G. Boivin</name><affiliation><mods:affiliation>INSERM Unité 234, Faculté Alexis Carrel, 69008 Lyon, France</mods:affiliation></affiliation></author><author><name sortKey="Chavassieux, P" sort="Chavassieux, P" uniqKey="Chavassieux P" first="P." last="Chavassieux">P. Chavassieux</name><affiliation><mods:affiliation>INSERM Unité 234, Faculté Alexis Carrel, 69008 Lyon, France</mods:affiliation></affiliation></author><author><name sortKey="Chapuy, M C" sort="Chapuy, M C" uniqKey="Chapuy M" first="M. C." last="Chapuy">M. C. Chapuy</name><affiliation><mods:affiliation>INSERM Unité 234, Faculté Alexis Carrel, 69008 Lyon, France</mods:affiliation></affiliation></author><author><name sortKey="Baud, C A" sort="Baud, C A" uniqKey="Baud C" first="C. A." last="Baud">C. A. Baud</name><affiliation><mods:affiliation>Institut de Morphologie, Centre Médical Universitaire, 1211 Genève 4, Switzerland</mods:affiliation></affiliation></author><author><name sortKey="Meunier, P J" sort="Meunier, P J" uniqKey="Meunier P" first="P. J." last="Meunier">P. J. 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Boivin</name><affiliation><mods:affiliation>INSERM Unité 234, Faculté Alexis Carrel, 69008 Lyon, France</mods:affiliation></affiliation></author><author><name sortKey="Chavassieux, P" sort="Chavassieux, P" uniqKey="Chavassieux P" first="P." last="Chavassieux">P. Chavassieux</name><affiliation><mods:affiliation>INSERM Unité 234, Faculté Alexis Carrel, 69008 Lyon, France</mods:affiliation></affiliation></author><author><name sortKey="Chapuy, M C" sort="Chapuy, M C" uniqKey="Chapuy M" first="M. C." last="Chapuy">M. C. Chapuy</name><affiliation><mods:affiliation>INSERM Unité 234, Faculté Alexis Carrel, 69008 Lyon, France</mods:affiliation></affiliation></author><author><name sortKey="Baud, C A" sort="Baud, C A" uniqKey="Baud C" first="C. A." last="Baud">C. A. Baud</name><affiliation><mods:affiliation>Institut de Morphologie, Centre Médical Universitaire, 1211 Genève 4, Switzerland</mods:affiliation></affiliation></author><author><name sortKey="Meunier, P J" sort="Meunier, P J" uniqKey="Meunier P" first="P. J." last="Meunier">P. J. Meunier</name><affiliation><mods:affiliation>INSERM Unité 234, Faculté Alexis Carrel, 69008 Lyon, France</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Bone</title><title level="j" type="abbrev">BON</title><idno type="ISSN">8756-3282</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1989">1989</date><biblScope unit="volume">10</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="89">89</biblScope><biblScope unit="page" to="99">99</biblScope></imprint><idno type="ISSN">8756-3282</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">8756-3282</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Bone fluoride content (BFC) was measured and histomorphometric analysis of undecalcified sections was performed in transiliac biopsy cores from 29 patients (16 men, 13 women, aged 51 ± 17 years) suffering from skeletal fluorosis due to chronic exposure to fluoride. The origin of the exposure, known in 20 patients, was either hydric (endemic or sporadic) or industrial, or in a few cases iatrogenic. Measured on calcined bone using a specific ion electrode, BFC was significantly high in each specimen (mean ± SD; 0.79 ± 0.36% on bone ash). The radiologically evident osteosclerosis observed in each patient was confirmed by a significant increase in cancellous bone volume (40.1 ± 11.2% vs. 19.0 ± 2.8% in controls, p < 0.0001). There were significant increases in cortical width (1292 ± 395 mem vs. 934 ± 173 mcm, p < 0.0001) and porosity (14.4 ± 6.4% vs. 6.5 ± 1.7%, p < 0.002), but without reduction of cortical bone mass. Cancellous osteoid volume and perimeter, as well as width of osteoid seams, were significantly increased in fluorotic patients. The increase in cancellous osteoid perimeter was almost three-fold greater than that noted in cancellous eroded perimeter. In 15 patients doubly labeled with tetracycline, the mineral apposition rate was significantly decreased, mineralization lag time was significantly increased. The fluorotic group had a greater number of osteoblasts than controls with a very high proportion of flat osteoblasts. The ultrastructural characteristics reflecting the activity of the bone cells were clearly visible on electron microscopy. Bone formation rate and adjusted apposition rate were significantly decreased in skeletal fluorosis. On stained sections and microradiographs, bone tissue showed typical modifications for skeletal fluorosis (linear formation defects, mottled bone). The volume of cancellous interstitial mineralization defects and the proportion of mottled periosteocytic lacunae were markedly increased in skeletal fluorosis. These two parameters were significantly correlated together but neither of these was significantly correlated with BFC. Renal function did not significantly influence the changes in BFC and histomorphometry of fluorotic patients. Skeletal fluorosis is thus characterized by an unbalanced coupling in favor of bone formation, and a great number of osteoblasts with a high proportion of flat osteoblasts. This may explain the mineralization impairment proven by thick osteoid seams and reduced mineral apposition rate, and supports the view that fluoride may have a dual effect on osteoblasts: a probable increased birthrate at the tissue-level due to a mitogenic effect of fluoride on precursors of osteoblasts, and a toxic effect at the individual cell-level. The addition of these two effects represents, however, a marked increase of bone formation at the organ level.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>G. Boivin</name><affiliations><json:string>INSERM Unité 234, Faculté Alexis Carrel, 69008 Lyon, France</json:string></affiliations></json:item><json:item><name>P. Chavassieux</name><affiliations><json:string>INSERM Unité 234, Faculté Alexis Carrel, 69008 Lyon, France</json:string></affiliations></json:item><json:item><name>M.C. Chapuy</name><affiliations><json:string>INSERM Unité 234, Faculté Alexis Carrel, 69008 Lyon, France</json:string></affiliations></json:item><json:item><name>C.A. Baud</name><affiliations><json:string>Institut de Morphologie, Centre Médical Universitaire, 1211 Genève 4, Switzerland</json:string></affiliations></json:item><json:item><name>P.J. Meunier</name><affiliations><json:string>INSERM Unité 234, Faculté Alexis Carrel, 69008 Lyon, France</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Iliac bone tissue</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Skeletal fluorosis</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Bone fluoride content</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Histomorphometry</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Renal function</value></json:item></subject><language><json:string>eng</json:string></language><originalGenre><json:string>Full-length article</json:string></originalGenre><abstract>Bone fluoride content (BFC) was measured and histomorphometric analysis of undecalcified sections was performed in transiliac biopsy cores from 29 patients (16 men, 13 women, aged 51 ± 17 years) suffering from skeletal fluorosis due to chronic exposure to fluoride. The origin of the exposure, known in 20 patients, was either hydric (endemic or sporadic) or industrial, or in a few cases iatrogenic. Measured on calcined bone using a specific ion electrode, BFC was significantly high in each specimen (mean ± SD; 0.79 ± 0.36% on bone ash). The radiologically evident osteosclerosis observed in each patient was confirmed by a significant increase in cancellous bone volume (40.1 ± 11.2% vs. 19.0 ± 2.8% in controls, p > 0.0001). There were significant increases in cortical width (1292 ± 395 mem vs. 934 ± 173 mcm, p > 0.0001) and porosity (14.4 ± 6.4% vs. 6.5 ± 1.7%, p > 0.002), but without reduction of cortical bone mass. Cancellous osteoid volume and perimeter, as well as width of osteoid seams, were significantly increased in fluorotic patients. The increase in cancellous osteoid perimeter was almost three-fold greater than that noted in cancellous eroded perimeter. In 15 patients doubly labeled with tetracycline, the mineral apposition rate was significantly decreased, mineralization lag time was significantly increased. The fluorotic group had a greater number of osteoblasts than controls with a very high proportion of flat osteoblasts. The ultrastructural characteristics reflecting the activity of the bone cells were clearly visible on electron microscopy. Bone formation rate and adjusted apposition rate were significantly decreased in skeletal fluorosis. On stained sections and microradiographs, bone tissue showed typical modifications for skeletal fluorosis (linear formation defects, mottled bone). The volume of cancellous interstitial mineralization defects and the proportion of mottled periosteocytic lacunae were markedly increased in skeletal fluorosis. These two parameters were significantly correlated together but neither of these was significantly correlated with BFC. Renal function did not significantly influence the changes in BFC and histomorphometry of fluorotic patients. Skeletal fluorosis is thus characterized by an unbalanced coupling in favor of bone formation, and a great number of osteoblasts with a high proportion of flat osteoblasts. This may explain the mineralization impairment proven by thick osteoid seams and reduced mineral apposition rate, and supports the view that fluoride may have a dual effect on osteoblasts: a probable increased birthrate at the tissue-level due to a mitogenic effect of fluoride on precursors of osteoblasts, and a toxic effect at the individual cell-level. The addition of these two effects represents, however, a marked increase of bone formation at the organ level.</abstract><qualityIndicators><score>8.5</score><pdfVersion>1.4</pdfVersion><pdfPageSize>576 x 792 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>5</keywordCount><abstractCharCount>2860</abstractCharCount><pdfWordCount>8628</pdfWordCount><pdfCharCount>44240</pdfCharCount><pdfPageCount>11</pdfPageCount><abstractWordCount>428</abstractWordCount></qualityIndicators><title>Skeletal fluorosis: Histomorphometric analysis of bone changes and bone fluoride content in 29 patients</title><pii><json:string>8756-3282(89)90004-5</json:string></pii><genre><json:string>research-article</json:string></genre><serie><volume>Vol. 4</volume><pages><last>439</last><first>424</first></pages><language><json:string>unknown</json:string></language><title>Fluorine chemistry</title></serie><host><volume>10</volume><pii><json:string>S8756-3282(00)X0135-4</json:string></pii><pages><last>99</last><first>89</first></pages><issn><json:string>8756-3282</json:string></issn><issue>2</issue><genre><json:string>journal</json:string></genre><language><json:string>unknown</json:string></language><title>Bone</title><publicationDate>1989</publicationDate></host><categories><wos><json:string>science</json:string><json:string>endocrinology & metabolism</json:string></wos><scienceMetrix><json:string>health sciences</json:string><json:string>clinical medicine</json:string><json:string>endocrinology & metabolism</json:string></scienceMetrix><inist><json:string>sciences appliquees, technologies et medecines</json:string><json:string>sciences biologiques et medicales</json:string><json:string>sciences medicales</json:string><json:string>cardiologie. appareil circulatoire</json:string></inist></categories><publicationDate>1989</publicationDate><copyrightDate>1989</copyrightDate><doi><json:string>10.1016/8756-3282(89)90004-5</json:string></doi><id>919D9E869C3BE406C5BA259303FFCF67413EF46A</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/document/919D9E869C3BE406C5BA259303FFCF67413EF46A/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/document/919D9E869C3BE406C5BA259303FFCF67413EF46A/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/919D9E869C3BE406C5BA259303FFCF67413EF46A/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a">Skeletal fluorosis: Histomorphometric analysis of bone changes and bone fluoride content in 29 patients</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>ELSEVIER</publisher><availability><p>ELSEVIER</p></availability><date>1989</date></publicationStmt><notesStmt><note type="content">Section title: Original article</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a">Skeletal fluorosis: Histomorphometric analysis of bone changes and bone fluoride content in 29 patients</title><author xml:id="author-0000"><persName><forename type="first">G.</forename><surname>Boivin</surname></persName><affiliation>Address for correspondence and reprints: Georges Boivin, Ph.D., INSERM Unité 234, Faculté Alexis Carrel, rue G. Paradin, 69008 Lyon, France.</affiliation><affiliation>INSERM Unité 234, Faculté Alexis Carrel, 69008 Lyon, France</affiliation></author><author xml:id="author-0001"><persName><forename type="first">P.</forename><surname>Chavassieux</surname></persName><affiliation>INSERM Unité 234, Faculté Alexis Carrel, 69008 Lyon, France</affiliation></author><author xml:id="author-0002"><persName><forename type="first">M.C.</forename><surname>Chapuy</surname></persName><affiliation>INSERM Unité 234, Faculté Alexis Carrel, 69008 Lyon, France</affiliation></author><author xml:id="author-0003"><persName><forename type="first">C.A.</forename><surname>Baud</surname></persName><affiliation>Institut de Morphologie, Centre Médical Universitaire, 1211 Genève 4, Switzerland</affiliation></author><author xml:id="author-0004"><persName><forename type="first">P.J.</forename><surname>Meunier</surname></persName><affiliation>INSERM Unité 234, Faculté Alexis Carrel, 69008 Lyon, France</affiliation></author><idno type="istex">919D9E869C3BE406C5BA259303FFCF67413EF46A</idno><idno type="DOI">10.1016/8756-3282(89)90004-5</idno><idno type="PII">8756-3282(89)90004-5</idno></analytic><monogr><title level="j">Bone</title><title level="j" type="abbrev">BON</title><idno type="pISSN">8756-3282</idno><idno type="PII">S8756-3282(00)X0135-4</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1989"></date><biblScope unit="volume">10</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="89">89</biblScope><biblScope unit="page" to="99">99</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1989</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Bone fluoride content (BFC) was measured and histomorphometric analysis of undecalcified sections was performed in transiliac biopsy cores from 29 patients (16 men, 13 women, aged 51 ± 17 years) suffering from skeletal fluorosis due to chronic exposure to fluoride. The origin of the exposure, known in 20 patients, was either hydric (endemic or sporadic) or industrial, or in a few cases iatrogenic. Measured on calcined bone using a specific ion electrode, BFC was significantly high in each specimen (mean ± SD; 0.79 ± 0.36% on bone ash). The radiologically evident osteosclerosis observed in each patient was confirmed by a significant increase in cancellous bone volume (40.1 ± 11.2% vs. 19.0 ± 2.8% in controls, p < 0.0001). There were significant increases in cortical width (1292 ± 395 mem vs. 934 ± 173 mcm, p < 0.0001) and porosity (14.4 ± 6.4% vs. 6.5 ± 1.7%, p < 0.002), but without reduction of cortical bone mass. Cancellous osteoid volume and perimeter, as well as width of osteoid seams, were significantly increased in fluorotic patients. The increase in cancellous osteoid perimeter was almost three-fold greater than that noted in cancellous eroded perimeter. In 15 patients doubly labeled with tetracycline, the mineral apposition rate was significantly decreased, mineralization lag time was significantly increased. The fluorotic group had a greater number of osteoblasts than controls with a very high proportion of flat osteoblasts. The ultrastructural characteristics reflecting the activity of the bone cells were clearly visible on electron microscopy. Bone formation rate and adjusted apposition rate were significantly decreased in skeletal fluorosis. On stained sections and microradiographs, bone tissue showed typical modifications for skeletal fluorosis (linear formation defects, mottled bone). The volume of cancellous interstitial mineralization defects and the proportion of mottled periosteocytic lacunae were markedly increased in skeletal fluorosis. These two parameters were significantly correlated together but neither of these was significantly correlated with BFC. Renal function did not significantly influence the changes in BFC and histomorphometry of fluorotic patients. Skeletal fluorosis is thus characterized by an unbalanced coupling in favor of bone formation, and a great number of osteoblasts with a high proportion of flat osteoblasts. This may explain the mineralization impairment proven by thick osteoid seams and reduced mineral apposition rate, and supports the view that fluoride may have a dual effect on osteoblasts: a probable increased birthrate at the tissue-level due to a mitogenic effect of fluoride on precursors of osteoblasts, and a toxic effect at the individual cell-level. The addition of these two effects represents, however, a marked increase of bone formation at the organ level.</p></abstract><textClass><keywords scheme="keyword"><list><head>Keywords</head><item><term>Iliac bone tissue</term></item><item><term>Skeletal fluorosis</term></item><item><term>Bone fluoride content</term></item><item><term>Histomorphometry</term></item><item><term>Renal function</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1988-12-05">Modified</change><change when="1989">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/919D9E869C3BE406C5BA259303FFCF67413EF46A/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: tail"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla"><item-info><jid>BON</jid><aid>89900045</aid><ce:pii>8756-3282(89)90004-5</ce:pii><ce:doi>10.1016/8756-3282(89)90004-5</ce:doi><ce:copyright type="unknown" year="1989"></ce:copyright></item-info><head><ce:dochead><ce:textfn>Original article</ce:textfn></ce:dochead><ce:title>Skeletal fluorosis: Histomorphometric analysis of bone changes and bone fluoride content in 29 patients</ce:title><ce:author-group><ce:author><ce:given-name>G.</ce:given-name><ce:surname>Boivin</ce:surname><ce:cross-ref refid="COR1"><ce:sup>∗</ce:sup></ce:cross-ref><ce:cross-ref refid="AFF1"><ce:sup>1</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>P.</ce:given-name><ce:surname>Chavassieux</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>1</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>M.C.</ce:given-name><ce:surname>Chapuy</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>1</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>C.A.</ce:given-name><ce:surname>Baud</ce:surname><ce:cross-ref refid="AFF2"><ce:sup>2</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>P.J.</ce:given-name><ce:surname>Meunier</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>1</ce:sup></ce:cross-ref></ce:author><ce:affiliation id="AFF1"><ce:label>a</ce:label><ce:textfn>INSERM Unité 234, Faculté Alexis Carrel, 69008 Lyon, France</ce:textfn></ce:affiliation><ce:affiliation id="AFF2"><ce:label>b</ce:label><ce:textfn>Institut de Morphologie, Centre Médical Universitaire, 1211 Genève 4, Switzerland</ce:textfn></ce:affiliation><ce:correspondence id="COR1"><ce:label>∗</ce:label><ce:text>Address for correspondence and reprints: Georges Boivin, Ph.D., INSERM Unité 234, Faculté Alexis Carrel, rue G. Paradin, 69008 Lyon, France.</ce:text></ce:correspondence></ce:author-group><ce:date-received day="3" month="5" year="1988"></ce:date-received><ce:date-revised day="5" month="12" year="1988"></ce:date-revised><ce:date-accepted day="10" month="12" year="1988"></ce:date-accepted><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>Bone fluoride content (BFC) was measured and histomorphometric analysis of undecalcified sections was performed in transiliac biopsy cores from 29 patients (16 men, 13 women, aged 51 ± 17 years) suffering from skeletal fluorosis due to chronic exposure to fluoride. The origin of the exposure, known in 20 patients, was either hydric (endemic or sporadic) or industrial, or in a few cases iatrogenic. Measured on calcined bone using a specific ion electrode, BFC was significantly high in each specimen (<ce:italic>mean</ce:italic> ± <ce:italic>SD</ce:italic>; 0.79 ± 0.36% on bone ash). The radiologically evident osteosclerosis observed in each patient was confirmed by a significant increase in cancellous bone volume (40.1 ± 11.2% vs. 19.0 ± 2.8% in controls, <ce:italic>p</ce:italic> < 0.0001). There were significant increases in cortical width (1292 ± 395 mem vs. 934 ± 173 mcm, <ce:italic>p</ce:italic> < 0.0001) and porosity (14.4 ± 6.4% vs. 6.5 ± 1.7%, <ce:italic>p</ce:italic> < 0.002), but without reduction of cortical bone mass. Cancellous osteoid volume and perimeter, as well as width of osteoid seams, were significantly increased in fluorotic patients. The increase in cancellous osteoid perimeter was almost three-fold greater than that noted in cancellous eroded perimeter. In 15 patients doubly labeled with tetracycline, the mineral apposition rate was significantly decreased, mineralization lag time was significantly increased. The fluorotic group had a greater number of osteoblasts than controls with a very high proportion of flat osteoblasts. The ultrastructural characteristics reflecting the activity of the bone cells were clearly visible on electron microscopy. Bone formation rate and adjusted apposition rate were significantly decreased in skeletal fluorosis. On stained sections and microradiographs, bone tissue showed typical modifications for skeletal fluorosis (linear formation defects, mottled bone). The volume of cancellous interstitial mineralization defects and the proportion of mottled periosteocytic lacunae were markedly increased in skeletal fluorosis. These two parameters were significantly correlated together but neither of these was significantly correlated with BFC. Renal function did not significantly influence the changes in BFC and histomorphometry of fluorotic patients. Skeletal fluorosis is thus characterized by an unbalanced coupling in favor of bone formation, and a great number of osteoblasts with a high proportion of flat osteoblasts. This may explain the mineralization impairment proven by thick osteoid seams and reduced mineral apposition rate, and supports the view that fluoride may have a dual effect on osteoblasts: a probable increased birthrate at the tissue-level due to a mitogenic effect of fluoride on precursors of osteoblasts, and a toxic effect at the individual cell-level. The addition of these two effects represents, however, a marked increase of bone formation at the organ level.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>Iliac bone tissue</ce:text></ce:keyword><ce:keyword><ce:text>Skeletal fluorosis</ce:text></ce:keyword><ce:keyword><ce:text>Bone fluoride content</ce:text></ce:keyword><ce:keyword><ce:text>Histomorphometry</ce:text></ce:keyword><ce:keyword><ce:text>Renal function</ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Skeletal fluorosis: Histomorphometric analysis of bone changes and bone fluoride content in 29 patients</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Skeletal fluorosis: Histomorphometric analysis of bone changes and bone fluoride content in 29 patients</title></titleInfo><name type="personal"><namePart type="given">G.</namePart><namePart type="family">Boivin</namePart><affiliation>INSERM Unité 234, Faculté Alexis Carrel, 69008 Lyon, France</affiliation><description>Address for correspondence and reprints: Georges Boivin, Ph.D., INSERM Unité 234, Faculté Alexis Carrel, rue G. Paradin, 69008 Lyon, France.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P.</namePart><namePart type="family">Chavassieux</namePart><affiliation>INSERM Unité 234, Faculté Alexis Carrel, 69008 Lyon, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M.C.</namePart><namePart type="family">Chapuy</namePart><affiliation>INSERM Unité 234, Faculté Alexis Carrel, 69008 Lyon, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C.A.</namePart><namePart type="family">Baud</namePart><affiliation>Institut de Morphologie, Centre Médical Universitaire, 1211 Genève 4, Switzerland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P.J.</namePart><namePart type="family">Meunier</namePart><affiliation>INSERM Unité 234, Faculté Alexis Carrel, 69008 Lyon, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article"></genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1989</dateIssued><dateModified encoding="w3cdtf">1988-12-05</dateModified><copyrightDate encoding="w3cdtf">1989</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">Bone fluoride content (BFC) was measured and histomorphometric analysis of undecalcified sections was performed in transiliac biopsy cores from 29 patients (16 men, 13 women, aged 51 ± 17 years) suffering from skeletal fluorosis due to chronic exposure to fluoride. The origin of the exposure, known in 20 patients, was either hydric (endemic or sporadic) or industrial, or in a few cases iatrogenic. Measured on calcined bone using a specific ion electrode, BFC was significantly high in each specimen (mean ± SD; 0.79 ± 0.36% on bone ash). The radiologically evident osteosclerosis observed in each patient was confirmed by a significant increase in cancellous bone volume (40.1 ± 11.2% vs. 19.0 ± 2.8% in controls, p < 0.0001). There were significant increases in cortical width (1292 ± 395 mem vs. 934 ± 173 mcm, p < 0.0001) and porosity (14.4 ± 6.4% vs. 6.5 ± 1.7%, p < 0.002), but without reduction of cortical bone mass. Cancellous osteoid volume and perimeter, as well as width of osteoid seams, were significantly increased in fluorotic patients. The increase in cancellous osteoid perimeter was almost three-fold greater than that noted in cancellous eroded perimeter. In 15 patients doubly labeled with tetracycline, the mineral apposition rate was significantly decreased, mineralization lag time was significantly increased. The fluorotic group had a greater number of osteoblasts than controls with a very high proportion of flat osteoblasts. The ultrastructural characteristics reflecting the activity of the bone cells were clearly visible on electron microscopy. Bone formation rate and adjusted apposition rate were significantly decreased in skeletal fluorosis. On stained sections and microradiographs, bone tissue showed typical modifications for skeletal fluorosis (linear formation defects, mottled bone). The volume of cancellous interstitial mineralization defects and the proportion of mottled periosteocytic lacunae were markedly increased in skeletal fluorosis. These two parameters were significantly correlated together but neither of these was significantly correlated with BFC. Renal function did not significantly influence the changes in BFC and histomorphometry of fluorotic patients. Skeletal fluorosis is thus characterized by an unbalanced coupling in favor of bone formation, and a great number of osteoblasts with a high proportion of flat osteoblasts. This may explain the mineralization impairment proven by thick osteoid seams and reduced mineral apposition rate, and supports the view that fluoride may have a dual effect on osteoblasts: a probable increased birthrate at the tissue-level due to a mitogenic effect of fluoride on precursors of osteoblasts, and a toxic effect at the individual cell-level. The addition of these two effects represents, however, a marked increase of bone formation at the organ level.</abstract><note type="content">Section title: Original article</note><subject><genre>Keywords</genre><topic>Iliac bone tissue</topic><topic>Skeletal fluorosis</topic><topic>Bone fluoride content</topic><topic>Histomorphometry</topic><topic>Renal function</topic></subject><relatedItem type="host"><titleInfo><title>Bone</title></titleInfo><titleInfo type="abbreviated"><title>BON</title></titleInfo><genre type="journal">journal</genre><originInfo><dateIssued encoding="w3cdtf">1989</dateIssued></originInfo><identifier type="ISSN">8756-3282</identifier><identifier type="PII">S8756-3282(00)X0135-4</identifier><part><date>1989</date><detail type="volume"><number>10</number><caption>vol.</caption></detail><detail type="issue"><number>2</number><caption>no.</caption></detail><extent unit="issue pages"><start>75</start><end>155</end></extent><extent unit="pages"><start>89</start><end>99</end></extent></part></relatedItem><identifier type="istex">919D9E869C3BE406C5BA259303FFCF67413EF46A</identifier><identifier type="DOI">10.1016/8756-3282(89)90004-5</identifier><identifier type="PII">8756-3282(89)90004-5</identifier><recordInfo><recordContentSource>ELSEVIER</recordContentSource></recordInfo></mods></metadata></istex></record>Pour manipuler ce document sous Unix (Dilib)
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