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<title>UTas ePrints - Smoking interacts with family history with regard to change in knee cartilage volume and cartilage defect development</title>
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<meta content="Ding, Changhai" name="eprints.creators_name" />
<meta content="Cicuttini, Flavia" name="eprints.creators_name" />
<meta content="Blizzard, Leigh" name="eprints.creators_name" />
<meta content="Jones, Graeme" name="eprints.creators_name" />
<meta content="chding@utas.edu.au" name="eprints.creators_id" />
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<meta content="Smoking interacts with family history with regard to change in knee cartilage volume and cartilage defect development" name="eprints.title" />
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<meta content="321028" name="eprints.subjects" />
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<meta content="knee, osteoarthritis, family history, smoking" name="eprints.keywords" />
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<meta content="Objective
To describe the effects of smoking on change in knee cartilage volume and increases in knee cartilage defects, and to test for interaction between smoking and family history of osteoarthritis (OA).
Methods
Subjects with at least 1 parent having severe primary knee OA (offspring) and randomly selected controls without this history (a total of 325 subjects with a mean age of 45 years) were measured at baseline and 2.3 years later. Knee cartilage volume and defect score (on a 0-4 scale) were determined using T1-weighted fat-saturated magnetic resonance imaging. Smoking status and duration and number of cigarettes were recorded by questionnaire.
Results
In offspring, smoking was associated with annual change in medial and lateral tibial cartilage volume (beta = -2.20% and beta = -1.45%, respectively, for current smokers versus former smokers and those who had never smoked; beta = -0.07%/pack-year at both tibial sites, for smoking severity) in multivariate analysis. Smoking was also associated with increases (change 1) in medial and lateral tibiofemoral cartilage defect scores (odds ratio [OR] 4.91 and OR 2.98, respectively, for current smokers versus those who had never smoked; OR 9.90 and OR 12.98, respectively, for heavy smoking [total of >20 pack-years] versus never smoking) (all P < 0.05). In contrast, smoking was not associated with any of the above in controls except for change in lateral tibial cartilage volume. There was significant interaction between smoking and offspring-control status for change in medial tibial cartilage volume (P = 0.047) and increases in medial (P = 0.03) and lateral (P = 0.049) tibiofemoral cartilage defects.
Conclusion
Smoking leads to knee cartilage loss and defect development primarily in individuals with a family history of knee OA. This provides evidence for a gene-environment interaction in the etiology of knee OA.
" name="eprints.abstract" />
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<meta content="Ding, Changhai and Cicuttini, Flavia and Blizzard, Leigh and Jones, Graeme (2007) Smoking interacts with family history with regard to change in knee cartilage volume and cartilage defect development. Arthritis & Rheumatism, 56 (5). pp. 1521-1528. ISSN 1529-0131" name="eprints.citation" />
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<meta content="Ding, Changhai" name="DC.creator" />
<meta content="Cicuttini, Flavia" name="DC.creator" />
<meta content="Blizzard, Leigh" name="DC.creator" />
<meta content="Jones, Graeme" name="DC.creator" />
<meta content="321028 Rheumatology and Arthritis" name="DC.subject" />
<meta content="Objective
To describe the effects of smoking on change in knee cartilage volume and increases in knee cartilage defects, and to test for interaction between smoking and family history of osteoarthritis (OA).
Methods
Subjects with at least 1 parent having severe primary knee OA (offspring) and randomly selected controls without this history (a total of 325 subjects with a mean age of 45 years) were measured at baseline and 2.3 years later. Knee cartilage volume and defect score (on a 0-4 scale) were determined using T1-weighted fat-saturated magnetic resonance imaging. Smoking status and duration and number of cigarettes were recorded by questionnaire.
Results
In offspring, smoking was associated with annual change in medial and lateral tibial cartilage volume (beta = -2.20% and beta = -1.45%, respectively, for current smokers versus former smokers and those who had never smoked; beta = -0.07%/pack-year at both tibial sites, for smoking severity) in multivariate analysis. Smoking was also associated with increases (change 1) in medial and lateral tibiofemoral cartilage defect scores (odds ratio [OR] 4.91 and OR 2.98, respectively, for current smokers versus those who had never smoked; OR 9.90 and OR 12.98, respectively, for heavy smoking [total of >20 pack-years] versus never smoking) (all P < 0.05). In contrast, smoking was not associated with any of the above in controls except for change in lateral tibial cartilage volume. There was significant interaction between smoking and offspring-control status for change in medial tibial cartilage volume (P = 0.047) and increases in medial (P = 0.03) and lateral (P = 0.049) tibiofemoral cartilage defects.
Conclusion
Smoking leads to knee cartilage loss and defect development primarily in individuals with a family history of knee OA. This provides evidence for a gene-environment interaction in the etiology of knee OA.
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<h1 class="ep_tm_pagetitle">Smoking interacts with family history with regard to change in knee cartilage volume and cartilage defect development</h1>
<p style="margin-bottom: 1em" class="not_ep_block"><span class="person_name">Ding, Changhai</span> and <span class="person_name">Cicuttini, Flavia</span> and <span class="person_name">Blizzard, Leigh</span> and <span class="person_name">Jones, Graeme</span> (2007) <xhtml:em>Smoking interacts with family history with regard to change in knee cartilage volume and cartilage defect development.</xhtml:em> Arthritis & Rheumatism, 56 (5). pp. 1521-1528. ISSN 1529-0131</p><p style="margin-bottom: 1em" class="not_ep_block"></p><table style="margin-bottom: 1em" class="not_ep_block"><tr><td valign="top" style="text-align:center"><a href="http://eprints.utas.edu.au/936/1/A%26R2007.pdf"><img alt="[img]" src="http://eprints.utas.edu.au/style/images/fileicons/application_pdf.png" class="ep_doc_icon" border="0" /></a></td><td valign="top"><a href="http://eprints.utas.edu.au/936/1/A%26R2007.pdf"><span class="ep_document_citation">PDF</span></a> - Full text restricted - Requires a PDF viewer<br />247Kb</td></tr></table><p style="margin-bottom: 1em" class="not_ep_block">Official URL: <a href="http://dx.doi.org/10.1002/art.22591">http://dx.doi.org/10.1002/art.22591</a></p><div class="not_ep_block"><h2>Abstract</h2><p style="padding-bottom: 16px; text-align: left; margin: 1em auto 0em auto">Objective
To describe the effects of smoking on change in knee cartilage volume and increases in knee cartilage defects, and to test for interaction between smoking and family history of osteoarthritis (OA).
Methods
Subjects with at least 1 parent having severe primary knee OA (offspring) and randomly selected controls without this history (a total of 325 subjects with a mean age of 45 years) were measured at baseline and 2.3 years later. Knee cartilage volume and defect score (on a 0-4 scale) were determined using T1-weighted fat-saturated magnetic resonance imaging. Smoking status and duration and number of cigarettes were recorded by questionnaire.
Results
In offspring, smoking was associated with annual change in medial and lateral tibial cartilage volume (beta = -2.20% and beta = -1.45%, respectively, for current smokers versus former smokers and those who had never smoked; beta = -0.07%/pack-year at both tibial sites, for smoking severity) in multivariate analysis. Smoking was also associated with increases (change 1) in medial and lateral tibiofemoral cartilage defect scores (odds ratio [OR] 4.91 and OR 2.98, respectively, for current smokers versus those who had never smoked; OR 9.90 and OR 12.98, respectively, for heavy smoking [total of >20 pack-years] versus never smoking) (all P < 0.05). In contrast, smoking was not associated with any of the above in controls except for change in lateral tibial cartilage volume. There was significant interaction between smoking and offspring-control status for change in medial tibial cartilage volume (P = 0.047) and increases in medial (P = 0.03) and lateral (P = 0.049) tibiofemoral cartilage defects.
Conclusion
Smoking leads to knee cartilage loss and defect development primarily in individuals with a family history of knee OA. This provides evidence for a gene-environment interaction in the etiology of knee OA.
</p></div><table style="margin-bottom: 1em" cellpadding="3" class="not_ep_block" border="0"><tr><th valign="top" class="ep_row">Item Type:</th><td valign="top" class="ep_row">Article</td></tr><tr><th valign="top" class="ep_row">Additional Information:</th><td valign="top" class="ep_row">http://www3.interscience.wiley.com/cgi-bin/fulltext/114229165/HTMLSTART</td></tr><tr><th valign="top" class="ep_row">Keywords:</th><td valign="top" class="ep_row">knee, osteoarthritis, family history, smoking</td></tr><tr><th valign="top" class="ep_row">Subjects:</th><td valign="top" class="ep_row"><a href="http://eprints.utas.edu.au/view/subjects/321028.html">320000 Medical and Health Sciences > 321000 Clinical Sciences > 321028 Rheumatology and Arthritis</a></td></tr><tr><th valign="top" class="ep_row">ID Code:</th><td valign="top" class="ep_row">936</td></tr><tr><th valign="top" class="ep_row">Deposited By:</th><td valign="top" class="ep_row"><span class="ep_name_citation"><span class="person_name">Dr Changhai / C Ding</span></span></td></tr><tr><th valign="top" class="ep_row">Deposited On:</th><td valign="top" class="ep_row">02 May 2007</td></tr><tr><th valign="top" class="ep_row">Last Modified:</th><td valign="top" class="ep_row">09 Jan 2008 02:30</td></tr><tr><th valign="top" class="ep_row">ePrint Statistics:</th><td valign="top" class="ep_row"><a target="ePrintStats" href="/es/index.php?action=show_detail_eprint;id=936;">View statistics for this ePrint</a></td></tr></table><p align="right">Repository Staff Only: <a href="http://eprints.utas.edu.au/cgi/users/home?screen=EPrint::View&eprintid=936">item control page</a></p>
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