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A histomorphometric study of cortical bone of the iliac crest in patients treated with glucocorticoids
The effects of glucocorticoids on cancellous bone remodeling and structure are well documented but there are no reported histomorphometric studies in human cortical bone in glucocorticoid-treated patients. We have performed a histomorphometric analysis of iliac crest cortical bone in 14 patients tre...
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Published in: | Calcified tissue international 2005-08, Vol.77 (2), p.79-83 |
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description | The effects of glucocorticoids on cancellous bone remodeling and structure are well documented but there are no reported histomorphometric studies in human cortical bone in glucocorticoid-treated patients. We have performed a histomorphometric analysis of iliac crest cortical bone in 14 patients treated with glucocorticoids, 9 females and 5 males, aged 18 to 48 years (34.1 +/- 7 years) (mean +/- standard deviation [SD]). The underlying disease was cystic fibrosis in 8 patients; asthma 3; and nephrotic syndrome; Crohn disease and inflammatory pseudotumor of the liver in one patient each. Results were compared with an age-matched control group of 10 premenopausal women and 4 men aged 22 to 38 years (30.1 +/- 4.8 years) who were not, however matched for underlying disease. Cortical bone indices were assessed by image analysis. Cortical width and area were similar in the two groups. However, cortical porosity, Haversian canal number, and density were higher in patients treated with glucocorticoids compared with controls (8.4 +/- 8.9% vs. 5.1 +/- 3.9%; P = 0.03) (45.9 +/- 23.2 vs. 31.9 +/- 24.4; P =0.003) (13.7 +/- 9.4 vs. 6.7 +/- 3.3/mm2; P = 0.00005). Haversian canal area did not differ significantly between groups. The mean wall width of the osteons, bone formation rate (microm2/microm/day) and mineral apposition rate (microm/day) were lower in treated patients compared to controls (48.8 +/- 7.1 microm vs. 59.8 +/- 12.9 microm; P = 0.01) (0.056 +/- 0.040 vs. 0.095 +/- 0.058; P = 0.05) and (0.59 +/- 0.12 vs. 0.75 +/- 0.11; P = 0.002). The proportion of canals with an eroded surface was lower in the treated compared with the control group, although this difference was not statistically significant. These results demonstrate that cortical porosity is increased in patients treated with long-term glucocorticoid therapy, due mainly to an increase in the number rather than size of Haversian canals. This may be because of increased bone resorption during the early stages of glucocorticoid therapy, in combination with long-term impairment of bone formation. Effects of the underlying disease on bone remodeling may also contributed to these changes and could not be excluded in the present study; since control subjects were not matched in terms of disease status. |
doi_str_mv | 10.1007/s00223-004-0205-y |
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We have performed a histomorphometric analysis of iliac crest cortical bone in 14 patients treated with glucocorticoids, 9 females and 5 males, aged 18 to 48 years (34.1 +/- 7 years) (mean +/- standard deviation [SD]). The underlying disease was cystic fibrosis in 8 patients; asthma 3; and nephrotic syndrome; Crohn disease and inflammatory pseudotumor of the liver in one patient each. Results were compared with an age-matched control group of 10 premenopausal women and 4 men aged 22 to 38 years (30.1 +/- 4.8 years) who were not, however matched for underlying disease. Cortical bone indices were assessed by image analysis. Cortical width and area were similar in the two groups. However, cortical porosity, Haversian canal number, and density were higher in patients treated with glucocorticoids compared with controls (8.4 +/- 8.9% vs. 5.1 +/- 3.9%; P = 0.03) (45.9 +/- 23.2 vs. 31.9 +/- 24.4; P =0.003) (13.7 +/- 9.4 vs. 6.7 +/- 3.3/mm2; P = 0.00005). Haversian canal area did not differ significantly between groups. The mean wall width of the osteons, bone formation rate (microm2/microm/day) and mineral apposition rate (microm/day) were lower in treated patients compared to controls (48.8 +/- 7.1 microm vs. 59.8 +/- 12.9 microm; P = 0.01) (0.056 +/- 0.040 vs. 0.095 +/- 0.058; P = 0.05) and (0.59 +/- 0.12 vs. 0.75 +/- 0.11; P = 0.002). The proportion of canals with an eroded surface was lower in the treated compared with the control group, although this difference was not statistically significant. These results demonstrate that cortical porosity is increased in patients treated with long-term glucocorticoid therapy, due mainly to an increase in the number rather than size of Haversian canals. This may be because of increased bone resorption during the early stages of glucocorticoid therapy, in combination with long-term impairment of bone formation. Effects of the underlying disease on bone remodeling may also contributed to these changes and could not be excluded in the present study; since control subjects were not matched in terms of disease status.</description><identifier>ISSN: 0171-967X</identifier><identifier>EISSN: 1432-0827</identifier><identifier>DOI: 10.1007/s00223-004-0205-y</identifier><identifier>PMID: 16086108</identifier><language>eng</language><publisher>United States: Springer Nature B.V</publisher><subject>Adolescent ; Adult ; Biopsy ; Bone Density - drug effects ; Bone Remodeling - drug effects ; Female ; Glucocorticoids - adverse effects ; Haversian System - drug effects ; Haversian System - pathology ; Humans ; Ilium - drug effects ; Ilium - metabolism ; Ilium - pathology ; Image Processing, Computer-Assisted ; Male ; Middle Aged ; Premenopause</subject><ispartof>Calcified tissue international, 2005-08, Vol.77 (2), p.79-83</ispartof><rights>Springer Science+Business Media, Inc. 2005</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c357t-8969217b8c6c341ffe6cb188abb1ab84dc6dfca7657d47cc34c5877772db93c33</citedby><cites>FETCH-LOGICAL-c357t-8969217b8c6c341ffe6cb188abb1ab84dc6dfca7657d47cc34c5877772db93c33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16086108$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Vedi, S</creatorcontrib><creatorcontrib>Elkin, S L</creatorcontrib><creatorcontrib>Compston, J E</creatorcontrib><title>A histomorphometric study of cortical bone of the iliac crest in patients treated with glucocorticoids</title><title>Calcified tissue international</title><addtitle>Calcif Tissue Int</addtitle><description>The effects of glucocorticoids on cancellous bone remodeling and structure are well documented but there are no reported histomorphometric studies in human cortical bone in glucocorticoid-treated patients. We have performed a histomorphometric analysis of iliac crest cortical bone in 14 patients treated with glucocorticoids, 9 females and 5 males, aged 18 to 48 years (34.1 +/- 7 years) (mean +/- standard deviation [SD]). The underlying disease was cystic fibrosis in 8 patients; asthma 3; and nephrotic syndrome; Crohn disease and inflammatory pseudotumor of the liver in one patient each. Results were compared with an age-matched control group of 10 premenopausal women and 4 men aged 22 to 38 years (30.1 +/- 4.8 years) who were not, however matched for underlying disease. Cortical bone indices were assessed by image analysis. Cortical width and area were similar in the two groups. However, cortical porosity, Haversian canal number, and density were higher in patients treated with glucocorticoids compared with controls (8.4 +/- 8.9% vs. 5.1 +/- 3.9%; P = 0.03) (45.9 +/- 23.2 vs. 31.9 +/- 24.4; P =0.003) (13.7 +/- 9.4 vs. 6.7 +/- 3.3/mm2; P = 0.00005). Haversian canal area did not differ significantly between groups. The mean wall width of the osteons, bone formation rate (microm2/microm/day) and mineral apposition rate (microm/day) were lower in treated patients compared to controls (48.8 +/- 7.1 microm vs. 59.8 +/- 12.9 microm; P = 0.01) (0.056 +/- 0.040 vs. 0.095 +/- 0.058; P = 0.05) and (0.59 +/- 0.12 vs. 0.75 +/- 0.11; P = 0.002). The proportion of canals with an eroded surface was lower in the treated compared with the control group, although this difference was not statistically significant. These results demonstrate that cortical porosity is increased in patients treated with long-term glucocorticoid therapy, due mainly to an increase in the number rather than size of Haversian canals. This may be because of increased bone resorption during the early stages of glucocorticoid therapy, in combination with long-term impairment of bone formation. Effects of the underlying disease on bone remodeling may also contributed to these changes and could not be excluded in the present study; since control subjects were not matched in terms of disease status.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Biopsy</subject><subject>Bone Density - drug effects</subject><subject>Bone Remodeling - drug effects</subject><subject>Female</subject><subject>Glucocorticoids - adverse effects</subject><subject>Haversian System - drug effects</subject><subject>Haversian System - pathology</subject><subject>Humans</subject><subject>Ilium - drug effects</subject><subject>Ilium - metabolism</subject><subject>Ilium - pathology</subject><subject>Image Processing, Computer-Assisted</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Premenopause</subject><issn>0171-967X</issn><issn>1432-0827</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><recordid>eNqFkcFq3DAQhkVJaTZpHyCXIHrozemM5JXkYwhpE1jIJYXehDyWuwq2tZFkyr59vexCoJfoMiC-_2ekj7ErhBsE0N8zgBCyAqgrELCu9h_YCmspKjBCn7EVoMaqUfr3ObvI-QUAa6XUJ3aOCoxCMCvW3_JtyCWOMe22cfQlBeK5zN2ex55TTCWQG3gbJ3-4KFvPwxAccUo-Fx4mvnMl-KlkXpJ3xXf8byhb_meYKR7jMXT5M_vYuyH7L6d5yX79uH--e6g2Tz8f7243Fcm1LpVpVCNQt4YUyRr73itq0RjXtuhaU3ekup6cVmvd1ZoWhtZGL0d0bSNJykv27di7S_F1Xja0Y8jkh8FNPs7ZKqNFAw2-C6IWsHzQofHrf-BLnNO0PMIKlKAkologPEKUYs7J93aXwujS3iLYgyp7VGUXVfagyu6XzPWpeG5H370lTm7kPxpdkEg</recordid><startdate>200508</startdate><enddate>200508</enddate><creator>Vedi, S</creator><creator>Elkin, S L</creator><creator>Compston, J E</creator><general>Springer Nature B.V</general><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>3V.</scope><scope>7QP</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>200508</creationdate><title>A histomorphometric study of cortical bone of the iliac crest in patients treated with glucocorticoids</title><author>Vedi, S ; Elkin, S L ; Compston, J E</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c357t-8969217b8c6c341ffe6cb188abb1ab84dc6dfca7657d47cc34c5877772db93c33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Biopsy</topic><topic>Bone Density - drug effects</topic><topic>Bone Remodeling - drug effects</topic><topic>Female</topic><topic>Glucocorticoids - adverse effects</topic><topic>Haversian System - drug effects</topic><topic>Haversian System - pathology</topic><topic>Humans</topic><topic>Ilium - drug effects</topic><topic>Ilium - metabolism</topic><topic>Ilium - pathology</topic><topic>Image Processing, Computer-Assisted</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Premenopause</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Vedi, S</creatorcontrib><creatorcontrib>Elkin, S L</creatorcontrib><creatorcontrib>Compston, J E</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Proquest Nursing & Allied Health Source</collection><collection>ProQuest Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Calcified tissue international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Vedi, S</au><au>Elkin, S L</au><au>Compston, J E</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A histomorphometric study of cortical bone of the iliac crest in patients treated with glucocorticoids</atitle><jtitle>Calcified tissue international</jtitle><addtitle>Calcif Tissue Int</addtitle><date>2005-08</date><risdate>2005</risdate><volume>77</volume><issue>2</issue><spage>79</spage><epage>83</epage><pages>79-83</pages><issn>0171-967X</issn><eissn>1432-0827</eissn><abstract>The effects of glucocorticoids on cancellous bone remodeling and structure are well documented but there are no reported histomorphometric studies in human cortical bone in glucocorticoid-treated patients. We have performed a histomorphometric analysis of iliac crest cortical bone in 14 patients treated with glucocorticoids, 9 females and 5 males, aged 18 to 48 years (34.1 +/- 7 years) (mean +/- standard deviation [SD]). The underlying disease was cystic fibrosis in 8 patients; asthma 3; and nephrotic syndrome; Crohn disease and inflammatory pseudotumor of the liver in one patient each. Results were compared with an age-matched control group of 10 premenopausal women and 4 men aged 22 to 38 years (30.1 +/- 4.8 years) who were not, however matched for underlying disease. Cortical bone indices were assessed by image analysis. Cortical width and area were similar in the two groups. However, cortical porosity, Haversian canal number, and density were higher in patients treated with glucocorticoids compared with controls (8.4 +/- 8.9% vs. 5.1 +/- 3.9%; P = 0.03) (45.9 +/- 23.2 vs. 31.9 +/- 24.4; P =0.003) (13.7 +/- 9.4 vs. 6.7 +/- 3.3/mm2; P = 0.00005). Haversian canal area did not differ significantly between groups. The mean wall width of the osteons, bone formation rate (microm2/microm/day) and mineral apposition rate (microm/day) were lower in treated patients compared to controls (48.8 +/- 7.1 microm vs. 59.8 +/- 12.9 microm; P = 0.01) (0.056 +/- 0.040 vs. 0.095 +/- 0.058; P = 0.05) and (0.59 +/- 0.12 vs. 0.75 +/- 0.11; P = 0.002). The proportion of canals with an eroded surface was lower in the treated compared with the control group, although this difference was not statistically significant. These results demonstrate that cortical porosity is increased in patients treated with long-term glucocorticoid therapy, due mainly to an increase in the number rather than size of Haversian canals. This may be because of increased bone resorption during the early stages of glucocorticoid therapy, in combination with long-term impairment of bone formation. Effects of the underlying disease on bone remodeling may also contributed to these changes and could not be excluded in the present study; since control subjects were not matched in terms of disease status.</abstract><cop>United States</cop><pub>Springer Nature B.V</pub><pmid>16086108</pmid><doi>10.1007/s00223-004-0205-y</doi><tpages>5</tpages></addata></record> |
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subjects | Adolescent Adult Biopsy Bone Density - drug effects Bone Remodeling - drug effects Female Glucocorticoids - adverse effects Haversian System - drug effects Haversian System - pathology Humans Ilium - drug effects Ilium - metabolism Ilium - pathology Image Processing, Computer-Assisted Male Middle Aged Premenopause |
title | A histomorphometric study of cortical bone of the iliac crest in patients treated with glucocorticoids |
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