Orthodontic forces add to nicotine-induced loss of periodontal bone: An in vivo and in vitro study
Objectives Nicotine is considered an etiologic factor for chronic inflammatory phenomena within the periodontal ligament that may result in loss of periodontal attachment. Considering that smokers account for 26 % of adult and 12 % of adolescent patients in orthodontic practice, we performed in vivo...
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| Veröffentlicht in: | Journal of orofacial orthopedics 2015-05, Vol.76 (3), p.195-212 |
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| creator | Kirschneck, C. Proff, P. Maurer, M. Reicheneder, C. Römer, P. |
| description | Objectives
Nicotine is considered an etiologic factor for chronic inflammatory phenomena within the periodontal ligament that may result in loss of periodontal attachment. Considering that smokers account for 26 % of adult and 12 % of adolescent patients in orthodontic practice, we performed in vivo and in vitro studies as to whether orthodontic forces may add to the nicotine-induced loss of periodontal bone.
Methods
Fourteen male rats (Fischer 344 inbred) were used. Seven of these served as controls, while the other seven received daily subcutaneous injections of 1.89 mg L-nicotine per kg body weight. Both groups were exposed to orthodontic mesialization of the first two upper left molars using a NiTi closed-coil spring, the contralateral side serving as control. Periodontal bone loss was assessed by cone-beam computed tomography (CBCT). Human periodontal fibroblasts were stressed by compression (2 g/cm
2
) and/or nicotine (3/5/7.5 µmol), and the expression of cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE
2
), interleukin-6 (IL-6), osteoprotegerin (OPG), and receptor activator of nuclear factor κB ligand (RANKL) was determined at the transcriptional level by quantitative real-time polymerase chain reaction (qRT-PCR) and at the translational level by enzyme-linked immunosorbent assay (ELISA). In addition, differentiation of co-cultured murine RAW264.7 cells to osteoclast-like cells was quantified by tartrate-resistant acid phosphatase (TRAP) staining.
Results
Orthodontic force application in vivo led to a significant increase in nicotine-induced periodontal bone loss, and cell compression in vitro to increased COX-2, PGE
2
, IL-6, and RANKL expression, reduced OPG expression, and enhanced differentiation of RAW264.7 cells to osteoclast-like cells compared to nicotine alone.
Conclusion
Additional loss of periodontal bone must be expected during orthodontic treatment of smokers. Clinicians should inform their patients of this increased risk and refrain from performing tooth movements before cessation of smoking. |
| doi_str_mv | 10.1007/s00056-015-0283-7 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1697215912</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1697215912</sourcerecordid><originalsourceid>FETCH-LOGICAL-c296t-f46c12db121764026430c957af744a0f5f30e850a1662f7b283b0e6b1ecbee303</originalsourceid><addsrcrecordid>eNp9kL1OwzAURi0EolB4ABbkkSVw7Th2PaKKP6lSF5gtx7mGVGlc7GTg7XFJYWSyLZ_v072HkCsGtwxA3SUAqGQBrCqAL8pCHZEzJvNLKiaO812Uoqi4LmfkPKXNnhYgT8mMV5prBfqMLNdx-AhN6IfWUR-iw0Rt09Ah0L51YWh7LNq-GR02tAsp0eDpDmP7E7EdrUOPF-TE2y7h5eGck7fHh9flc7FaP70s71eF41oOhRfSMd7UjDMlBXApSnC6UtYrISz4ypeAiwosk5J7VeeNakBZM3Q1YgnlnNxMvbsYPkdMg9m2yWHX2R7DmAyTWnFWacYzyibUxTx0RG92sd3a-GUYmL07M7kz2Z3ZuzMqZ64P9WO9xeYv8SsrA3wCUv7q3zGaTRhjn1f-p_Ub9ll4tA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1697215912</pqid></control><display><type>article</type><title>Orthodontic forces add to nicotine-induced loss of periodontal bone: An in vivo and in vitro study</title><source>MEDLINE</source><source>SpringerNature Journals</source><creator>Kirschneck, C. ; Proff, P. ; Maurer, M. ; Reicheneder, C. ; Römer, P.</creator><creatorcontrib>Kirschneck, C. ; Proff, P. ; Maurer, M. ; Reicheneder, C. ; Römer, P.</creatorcontrib><description>Objectives
Nicotine is considered an etiologic factor for chronic inflammatory phenomena within the periodontal ligament that may result in loss of periodontal attachment. Considering that smokers account for 26 % of adult and 12 % of adolescent patients in orthodontic practice, we performed in vivo and in vitro studies as to whether orthodontic forces may add to the nicotine-induced loss of periodontal bone.
Methods
Fourteen male rats (Fischer 344 inbred) were used. Seven of these served as controls, while the other seven received daily subcutaneous injections of 1.89 mg L-nicotine per kg body weight. Both groups were exposed to orthodontic mesialization of the first two upper left molars using a NiTi closed-coil spring, the contralateral side serving as control. Periodontal bone loss was assessed by cone-beam computed tomography (CBCT). Human periodontal fibroblasts were stressed by compression (2 g/cm
2
) and/or nicotine (3/5/7.5 µmol), and the expression of cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE
2
), interleukin-6 (IL-6), osteoprotegerin (OPG), and receptor activator of nuclear factor κB ligand (RANKL) was determined at the transcriptional level by quantitative real-time polymerase chain reaction (qRT-PCR) and at the translational level by enzyme-linked immunosorbent assay (ELISA). In addition, differentiation of co-cultured murine RAW264.7 cells to osteoclast-like cells was quantified by tartrate-resistant acid phosphatase (TRAP) staining.
Results
Orthodontic force application in vivo led to a significant increase in nicotine-induced periodontal bone loss, and cell compression in vitro to increased COX-2, PGE
2
, IL-6, and RANKL expression, reduced OPG expression, and enhanced differentiation of RAW264.7 cells to osteoclast-like cells compared to nicotine alone.
Conclusion
Additional loss of periodontal bone must be expected during orthodontic treatment of smokers. Clinicians should inform their patients of this increased risk and refrain from performing tooth movements before cessation of smoking.</description><identifier>ISSN: 1434-5293</identifier><identifier>EISSN: 1615-6714</identifier><identifier>DOI: 10.1007/s00056-015-0283-7</identifier><identifier>PMID: 25929709</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Alveolar Bone Loss - etiology ; Alveolar Bone Loss - immunology ; Alveolar Bone Loss - pathology ; Alveolar Process - drug effects ; Alveolar Process - immunology ; Animals ; Cell Line ; Cytokines - immunology ; Dental Stress Analysis - methods ; Dentistry ; Male ; Medicine ; Mice ; Nicotine - toxicity ; Oral and Maxillofacial Surgery ; Original Article ; Osteoclasts ; Rats ; Rats, Inbred F344 ; Stress, Mechanical ; Tensile Strength ; Tooth Movement Techniques - adverse effects ; Treatment Outcome</subject><ispartof>Journal of orofacial orthopedics, 2015-05, Vol.76 (3), p.195-212</ispartof><rights>Springer-Verlag Berlin Heidelberg 2015</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c296t-f46c12db121764026430c957af744a0f5f30e850a1662f7b283b0e6b1ecbee303</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00056-015-0283-7$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00056-015-0283-7$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25929709$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kirschneck, C.</creatorcontrib><creatorcontrib>Proff, P.</creatorcontrib><creatorcontrib>Maurer, M.</creatorcontrib><creatorcontrib>Reicheneder, C.</creatorcontrib><creatorcontrib>Römer, P.</creatorcontrib><title>Orthodontic forces add to nicotine-induced loss of periodontal bone: An in vivo and in vitro study</title><title>Journal of orofacial orthopedics</title><addtitle>J Orofac Orthop</addtitle><addtitle>J Orofac Orthop</addtitle><description>Objectives
Nicotine is considered an etiologic factor for chronic inflammatory phenomena within the periodontal ligament that may result in loss of periodontal attachment. Considering that smokers account for 26 % of adult and 12 % of adolescent patients in orthodontic practice, we performed in vivo and in vitro studies as to whether orthodontic forces may add to the nicotine-induced loss of periodontal bone.
Methods
Fourteen male rats (Fischer 344 inbred) were used. Seven of these served as controls, while the other seven received daily subcutaneous injections of 1.89 mg L-nicotine per kg body weight. Both groups were exposed to orthodontic mesialization of the first two upper left molars using a NiTi closed-coil spring, the contralateral side serving as control. Periodontal bone loss was assessed by cone-beam computed tomography (CBCT). Human periodontal fibroblasts were stressed by compression (2 g/cm
2
) and/or nicotine (3/5/7.5 µmol), and the expression of cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE
2
), interleukin-6 (IL-6), osteoprotegerin (OPG), and receptor activator of nuclear factor κB ligand (RANKL) was determined at the transcriptional level by quantitative real-time polymerase chain reaction (qRT-PCR) and at the translational level by enzyme-linked immunosorbent assay (ELISA). In addition, differentiation of co-cultured murine RAW264.7 cells to osteoclast-like cells was quantified by tartrate-resistant acid phosphatase (TRAP) staining.
Results
Orthodontic force application in vivo led to a significant increase in nicotine-induced periodontal bone loss, and cell compression in vitro to increased COX-2, PGE
2
, IL-6, and RANKL expression, reduced OPG expression, and enhanced differentiation of RAW264.7 cells to osteoclast-like cells compared to nicotine alone.
Conclusion
Additional loss of periodontal bone must be expected during orthodontic treatment of smokers. Clinicians should inform their patients of this increased risk and refrain from performing tooth movements before cessation of smoking.</description><subject>Alveolar Bone Loss - etiology</subject><subject>Alveolar Bone Loss - immunology</subject><subject>Alveolar Bone Loss - pathology</subject><subject>Alveolar Process - drug effects</subject><subject>Alveolar Process - immunology</subject><subject>Animals</subject><subject>Cell Line</subject><subject>Cytokines - immunology</subject><subject>Dental Stress Analysis - methods</subject><subject>Dentistry</subject><subject>Male</subject><subject>Medicine</subject><subject>Mice</subject><subject>Nicotine - toxicity</subject><subject>Oral and Maxillofacial Surgery</subject><subject>Original Article</subject><subject>Osteoclasts</subject><subject>Rats</subject><subject>Rats, Inbred F344</subject><subject>Stress, Mechanical</subject><subject>Tensile Strength</subject><subject>Tooth Movement Techniques - adverse effects</subject><subject>Treatment Outcome</subject><issn>1434-5293</issn><issn>1615-6714</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kL1OwzAURi0EolB4ABbkkSVw7Th2PaKKP6lSF5gtx7mGVGlc7GTg7XFJYWSyLZ_v072HkCsGtwxA3SUAqGQBrCqAL8pCHZEzJvNLKiaO812Uoqi4LmfkPKXNnhYgT8mMV5prBfqMLNdx-AhN6IfWUR-iw0Rt09Ah0L51YWh7LNq-GR02tAsp0eDpDmP7E7EdrUOPF-TE2y7h5eGck7fHh9flc7FaP70s71eF41oOhRfSMd7UjDMlBXApSnC6UtYrISz4ypeAiwosk5J7VeeNakBZM3Q1YgnlnNxMvbsYPkdMg9m2yWHX2R7DmAyTWnFWacYzyibUxTx0RG92sd3a-GUYmL07M7kz2Z3ZuzMqZ64P9WO9xeYv8SsrA3wCUv7q3zGaTRhjn1f-p_Ub9ll4tA</recordid><startdate>20150501</startdate><enddate>20150501</enddate><creator>Kirschneck, C.</creator><creator>Proff, P.</creator><creator>Maurer, M.</creator><creator>Reicheneder, C.</creator><creator>Römer, P.</creator><general>Springer Berlin Heidelberg</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>7X8</scope></search><sort><creationdate>20150501</creationdate><title>Orthodontic forces add to nicotine-induced loss of periodontal bone</title><author>Kirschneck, C. ; Proff, P. ; Maurer, M. ; Reicheneder, C. ; Römer, P.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c296t-f46c12db121764026430c957af744a0f5f30e850a1662f7b283b0e6b1ecbee303</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Alveolar Bone Loss - etiology</topic><topic>Alveolar Bone Loss - immunology</topic><topic>Alveolar Bone Loss - pathology</topic><topic>Alveolar Process - drug effects</topic><topic>Alveolar Process - immunology</topic><topic>Animals</topic><topic>Cell Line</topic><topic>Cytokines - immunology</topic><topic>Dental Stress Analysis - methods</topic><topic>Dentistry</topic><topic>Male</topic><topic>Medicine</topic><topic>Mice</topic><topic>Nicotine - toxicity</topic><topic>Oral and Maxillofacial Surgery</topic><topic>Original Article</topic><topic>Osteoclasts</topic><topic>Rats</topic><topic>Rats, Inbred F344</topic><topic>Stress, Mechanical</topic><topic>Tensile Strength</topic><topic>Tooth Movement Techniques - adverse effects</topic><topic>Treatment Outcome</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kirschneck, C.</creatorcontrib><creatorcontrib>Proff, P.</creatorcontrib><creatorcontrib>Maurer, M.</creatorcontrib><creatorcontrib>Reicheneder, C.</creatorcontrib><creatorcontrib>Römer, P.</creatorcontrib><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>Journal of orofacial orthopedics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kirschneck, C.</au><au>Proff, P.</au><au>Maurer, M.</au><au>Reicheneder, C.</au><au>Römer, P.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Orthodontic forces add to nicotine-induced loss of periodontal bone: An in vivo and in vitro study</atitle><jtitle>Journal of orofacial orthopedics</jtitle><stitle>J Orofac Orthop</stitle><addtitle>J Orofac Orthop</addtitle><date>2015-05-01</date><risdate>2015</risdate><volume>76</volume><issue>3</issue><spage>195</spage><epage>212</epage><pages>195-212</pages><issn>1434-5293</issn><eissn>1615-6714</eissn><abstract>Objectives
Nicotine is considered an etiologic factor for chronic inflammatory phenomena within the periodontal ligament that may result in loss of periodontal attachment. Considering that smokers account for 26 % of adult and 12 % of adolescent patients in orthodontic practice, we performed in vivo and in vitro studies as to whether orthodontic forces may add to the nicotine-induced loss of periodontal bone.
Methods
Fourteen male rats (Fischer 344 inbred) were used. Seven of these served as controls, while the other seven received daily subcutaneous injections of 1.89 mg L-nicotine per kg body weight. Both groups were exposed to orthodontic mesialization of the first two upper left molars using a NiTi closed-coil spring, the contralateral side serving as control. Periodontal bone loss was assessed by cone-beam computed tomography (CBCT). Human periodontal fibroblasts were stressed by compression (2 g/cm
2
) and/or nicotine (3/5/7.5 µmol), and the expression of cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE
2
), interleukin-6 (IL-6), osteoprotegerin (OPG), and receptor activator of nuclear factor κB ligand (RANKL) was determined at the transcriptional level by quantitative real-time polymerase chain reaction (qRT-PCR) and at the translational level by enzyme-linked immunosorbent assay (ELISA). In addition, differentiation of co-cultured murine RAW264.7 cells to osteoclast-like cells was quantified by tartrate-resistant acid phosphatase (TRAP) staining.
Results
Orthodontic force application in vivo led to a significant increase in nicotine-induced periodontal bone loss, and cell compression in vitro to increased COX-2, PGE
2
, IL-6, and RANKL expression, reduced OPG expression, and enhanced differentiation of RAW264.7 cells to osteoclast-like cells compared to nicotine alone.
Conclusion
Additional loss of periodontal bone must be expected during orthodontic treatment of smokers. Clinicians should inform their patients of this increased risk and refrain from performing tooth movements before cessation of smoking.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>25929709</pmid><doi>10.1007/s00056-015-0283-7</doi><tpages>18</tpages></addata></record> |
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| source | MEDLINE; SpringerNature Journals |
| subjects | Alveolar Bone Loss - etiology Alveolar Bone Loss - immunology Alveolar Bone Loss - pathology Alveolar Process - drug effects Alveolar Process - immunology Animals Cell Line Cytokines - immunology Dental Stress Analysis - methods Dentistry Male Medicine Mice Nicotine - toxicity Oral and Maxillofacial Surgery Original Article Osteoclasts Rats Rats, Inbred F344 Stress, Mechanical Tensile Strength Tooth Movement Techniques - adverse effects Treatment Outcome |
| title | Orthodontic forces add to nicotine-induced loss of periodontal bone: An in vivo and in vitro study |
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