Susceptibility of different mouse strains to peri‐implantitis
Background and Objective Peri‐implantitis (PI) is an inflammatory condition that affects the tissues surrounding dental implants. Although the pathogenesis of PI is not fully understood, evidence suggests that the etiology is multifactorial and may include a genetic component. The aim of this study...
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| Veröffentlicht in: | Journal of periodontal research 2018-02, Vol.53 (1), p.107-116 |
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| creator | Hiyari, S. Naghibi, A. Wong, R. Sadreshkevary, R. Yi‐Ling, L. Tetradis, S. Camargo, P. M. Pirih, F. Q. |
| description | Background and Objective
Peri‐implantitis (PI) is an inflammatory condition that affects the tissues surrounding dental implants. Although the pathogenesis of PI is not fully understood, evidence suggests that the etiology is multifactorial and may include a genetic component. The aim of this study was to investigate the role of genetics in the development of peri‐implantitis.
Material and Methods
Four‐week‐old C57BL/6J, C3H/HeJ and A/J male mice had their left maxillary molars extracted. Implants were placed in the healed extraction sockets. Upon osseointegration, ligatures were placed around the implant head for 1 or 4 weeks to induce PI. Micro‐computed tomography scanning was used to measure volumetric bone loss. Histological analyses were also performed to evaluate collagen organization and the presence of neutrophils and osteoclasts.
Results
Radiographically, comparing the ligature‐treated mice, C57BL/6J displayed the greatest amount of bone loss, followed by C3H/HeJ and A/J mice at 1 and 4 weeks. Histologically, at 1 week, C57BL/6J mice presented with the highest numbers of neutrophils and osteoclasts. At 4 weeks, C57BL/6J mice presented with the most active bone remodeling compared with the other two strains.
Conclusion
There were significant differences in the severity of peri‐implantitis among the different mouse strains, suggesting that the genetic framework can affect implant survival and success. Future work is needed to dissect the genetic contribution to the development of peri‐implantitis. |
| doi_str_mv | 10.1111/jre.12493 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5760471</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1984750718</sourcerecordid><originalsourceid>FETCH-LOGICAL-c5093-c40e5b53360de669d59e94a2ac1c455d77183953a93ec5e920fc763ff667d85f3</originalsourceid><addsrcrecordid>eNp1kctOGzEUhq0KVELaRV8AjcSmLCbY41u8AaEo3BSpUi9ry_EcF0dzw54pyo5H4Bl5EgyhUYvE2VhH_vTr_8-P0BeCJyTN8SrAhBRM0Q9oRATGOZaC76ARxkWRUzZle2g_xhVOu5DqI9orFGaMF3yETn8M0ULX-6WvfL_OWpeV3jkI0PRZ3Q4RstgH45uY9W3WQfCP9w--7irT9L738RPadaaK8Pn1HaNf5_Ofs8t88e3iana2yC3HiuaWYeBLTqnAJQihSq5AMVMYSyzjvJSSTKni1CgKloMqsLNSUOeEkOWUOzpGJxvdbljWUNpkL5hKd8HXJqx1a7z-_6fxN_p3-0dzKTCTJAl8fRUI7e0Asde1T8mrFARSTE1UugclSuGEHr5BV-0QmhQvUVMmOX52O0ZHG8qGNsYAbmuGYP1ci0616JdaEnvwr_st-beHBBxvgDtfwfp9JX39fb6RfAK055gh</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1984750718</pqid></control><display><type>article</type><title>Susceptibility of different mouse strains to peri‐implantitis</title><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><creator>Hiyari, S. ; Naghibi, A. ; Wong, R. ; Sadreshkevary, R. ; Yi‐Ling, L. ; Tetradis, S. ; Camargo, P. M. ; Pirih, F. Q.</creator><creatorcontrib>Hiyari, S. ; Naghibi, A. ; Wong, R. ; Sadreshkevary, R. ; Yi‐Ling, L. ; Tetradis, S. ; Camargo, P. M. ; Pirih, F. Q.</creatorcontrib><description>Background and Objective
Peri‐implantitis (PI) is an inflammatory condition that affects the tissues surrounding dental implants. Although the pathogenesis of PI is not fully understood, evidence suggests that the etiology is multifactorial and may include a genetic component. The aim of this study was to investigate the role of genetics in the development of peri‐implantitis.
Material and Methods
Four‐week‐old C57BL/6J, C3H/HeJ and A/J male mice had their left maxillary molars extracted. Implants were placed in the healed extraction sockets. Upon osseointegration, ligatures were placed around the implant head for 1 or 4 weeks to induce PI. Micro‐computed tomography scanning was used to measure volumetric bone loss. Histological analyses were also performed to evaluate collagen organization and the presence of neutrophils and osteoclasts.
Results
Radiographically, comparing the ligature‐treated mice, C57BL/6J displayed the greatest amount of bone loss, followed by C3H/HeJ and A/J mice at 1 and 4 weeks. Histologically, at 1 week, C57BL/6J mice presented with the highest numbers of neutrophils and osteoclasts. At 4 weeks, C57BL/6J mice presented with the most active bone remodeling compared with the other two strains.
Conclusion
There were significant differences in the severity of peri‐implantitis among the different mouse strains, suggesting that the genetic framework can affect implant survival and success. Future work is needed to dissect the genetic contribution to the development of peri‐implantitis.</description><identifier>ISSN: 0022-3484</identifier><identifier>EISSN: 1600-0765</identifier><identifier>DOI: 10.1111/jre.12493</identifier><identifier>PMID: 29044525</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Alveolar Bone Loss - diagnostic imaging ; Alveolar Bone Loss - pathology ; Animals ; Bone loss ; Bone remodeling ; Bone Remodeling - genetics ; Collagen ; Computed tomography ; dental implant ; Dental implants ; Dental prosthetics ; Dental restorative materials ; Dentistry ; Etiology ; Genetic Predisposition to Disease ; genetics ; Inflammation ; Leukocytes (neutrophilic) ; Maxilla ; Mice, Inbred Strains ; Molars ; murine ; Neutrophils ; Neutrophils - metabolism ; Osseointegration ; Osteoclasts ; Osteoclasts - metabolism ; Peri-Implantitis - genetics ; Rodents ; Teeth ; Transplants & implants</subject><ispartof>Journal of periodontal research, 2018-02, Vol.53 (1), p.107-116</ispartof><rights>2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd</rights><rights>2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.</rights><rights>Copyright © 2018 John Wiley & Sons A/S</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5093-c40e5b53360de669d59e94a2ac1c455d77183953a93ec5e920fc763ff667d85f3</citedby><cites>FETCH-LOGICAL-c5093-c40e5b53360de669d59e94a2ac1c455d77183953a93ec5e920fc763ff667d85f3</cites><orcidid>0000-0003-1670-7345</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fjre.12493$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fjre.12493$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,314,776,780,881,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29044525$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hiyari, S.</creatorcontrib><creatorcontrib>Naghibi, A.</creatorcontrib><creatorcontrib>Wong, R.</creatorcontrib><creatorcontrib>Sadreshkevary, R.</creatorcontrib><creatorcontrib>Yi‐Ling, L.</creatorcontrib><creatorcontrib>Tetradis, S.</creatorcontrib><creatorcontrib>Camargo, P. M.</creatorcontrib><creatorcontrib>Pirih, F. Q.</creatorcontrib><title>Susceptibility of different mouse strains to peri‐implantitis</title><title>Journal of periodontal research</title><addtitle>J Periodontal Res</addtitle><description>Background and Objective
Peri‐implantitis (PI) is an inflammatory condition that affects the tissues surrounding dental implants. Although the pathogenesis of PI is not fully understood, evidence suggests that the etiology is multifactorial and may include a genetic component. The aim of this study was to investigate the role of genetics in the development of peri‐implantitis.
Material and Methods
Four‐week‐old C57BL/6J, C3H/HeJ and A/J male mice had their left maxillary molars extracted. Implants were placed in the healed extraction sockets. Upon osseointegration, ligatures were placed around the implant head for 1 or 4 weeks to induce PI. Micro‐computed tomography scanning was used to measure volumetric bone loss. Histological analyses were also performed to evaluate collagen organization and the presence of neutrophils and osteoclasts.
Results
Radiographically, comparing the ligature‐treated mice, C57BL/6J displayed the greatest amount of bone loss, followed by C3H/HeJ and A/J mice at 1 and 4 weeks. Histologically, at 1 week, C57BL/6J mice presented with the highest numbers of neutrophils and osteoclasts. At 4 weeks, C57BL/6J mice presented with the most active bone remodeling compared with the other two strains.
Conclusion
There were significant differences in the severity of peri‐implantitis among the different mouse strains, suggesting that the genetic framework can affect implant survival and success. Future work is needed to dissect the genetic contribution to the development of peri‐implantitis.</description><subject>Alveolar Bone Loss - diagnostic imaging</subject><subject>Alveolar Bone Loss - pathology</subject><subject>Animals</subject><subject>Bone loss</subject><subject>Bone remodeling</subject><subject>Bone Remodeling - genetics</subject><subject>Collagen</subject><subject>Computed tomography</subject><subject>dental implant</subject><subject>Dental implants</subject><subject>Dental prosthetics</subject><subject>Dental restorative materials</subject><subject>Dentistry</subject><subject>Etiology</subject><subject>Genetic Predisposition to Disease</subject><subject>genetics</subject><subject>Inflammation</subject><subject>Leukocytes (neutrophilic)</subject><subject>Maxilla</subject><subject>Mice, Inbred Strains</subject><subject>Molars</subject><subject>murine</subject><subject>Neutrophils</subject><subject>Neutrophils - metabolism</subject><subject>Osseointegration</subject><subject>Osteoclasts</subject><subject>Osteoclasts - metabolism</subject><subject>Peri-Implantitis - genetics</subject><subject>Rodents</subject><subject>Teeth</subject><subject>Transplants & implants</subject><issn>0022-3484</issn><issn>1600-0765</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kctOGzEUhq0KVELaRV8AjcSmLCbY41u8AaEo3BSpUi9ry_EcF0dzw54pyo5H4Bl5EgyhUYvE2VhH_vTr_8-P0BeCJyTN8SrAhBRM0Q9oRATGOZaC76ARxkWRUzZle2g_xhVOu5DqI9orFGaMF3yETn8M0ULX-6WvfL_OWpeV3jkI0PRZ3Q4RstgH45uY9W3WQfCP9w--7irT9L738RPadaaK8Pn1HaNf5_Ofs8t88e3iana2yC3HiuaWYeBLTqnAJQihSq5AMVMYSyzjvJSSTKni1CgKloMqsLNSUOeEkOWUOzpGJxvdbljWUNpkL5hKd8HXJqx1a7z-_6fxN_p3-0dzKTCTJAl8fRUI7e0Asde1T8mrFARSTE1UugclSuGEHr5BV-0QmhQvUVMmOX52O0ZHG8qGNsYAbmuGYP1ci0616JdaEnvwr_st-beHBBxvgDtfwfp9JX39fb6RfAK055gh</recordid><startdate>201802</startdate><enddate>201802</enddate><creator>Hiyari, S.</creator><creator>Naghibi, A.</creator><creator>Wong, R.</creator><creator>Sadreshkevary, R.</creator><creator>Yi‐Ling, L.</creator><creator>Tetradis, S.</creator><creator>Camargo, P. M.</creator><creator>Pirih, F. Q.</creator><general>Wiley Subscription Services, Inc</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>7QP</scope><scope>K9.</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-1670-7345</orcidid></search><sort><creationdate>201802</creationdate><title>Susceptibility of different mouse strains to peri‐implantitis</title><author>Hiyari, S. ; Naghibi, A. ; Wong, R. ; Sadreshkevary, R. ; Yi‐Ling, L. ; Tetradis, S. ; Camargo, P. M. ; Pirih, F. Q.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5093-c40e5b53360de669d59e94a2ac1c455d77183953a93ec5e920fc763ff667d85f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Alveolar Bone Loss - diagnostic imaging</topic><topic>Alveolar Bone Loss - pathology</topic><topic>Animals</topic><topic>Bone loss</topic><topic>Bone remodeling</topic><topic>Bone Remodeling - genetics</topic><topic>Collagen</topic><topic>Computed tomography</topic><topic>dental implant</topic><topic>Dental implants</topic><topic>Dental prosthetics</topic><topic>Dental restorative materials</topic><topic>Dentistry</topic><topic>Etiology</topic><topic>Genetic Predisposition to Disease</topic><topic>genetics</topic><topic>Inflammation</topic><topic>Leukocytes (neutrophilic)</topic><topic>Maxilla</topic><topic>Mice, Inbred Strains</topic><topic>Molars</topic><topic>murine</topic><topic>Neutrophils</topic><topic>Neutrophils - metabolism</topic><topic>Osseointegration</topic><topic>Osteoclasts</topic><topic>Osteoclasts - metabolism</topic><topic>Peri-Implantitis - genetics</topic><topic>Rodents</topic><topic>Teeth</topic><topic>Transplants & implants</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hiyari, S.</creatorcontrib><creatorcontrib>Naghibi, A.</creatorcontrib><creatorcontrib>Wong, R.</creatorcontrib><creatorcontrib>Sadreshkevary, R.</creatorcontrib><creatorcontrib>Yi‐Ling, L.</creatorcontrib><creatorcontrib>Tetradis, S.</creatorcontrib><creatorcontrib>Camargo, P. M.</creatorcontrib><creatorcontrib>Pirih, F. Q.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of periodontal research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hiyari, S.</au><au>Naghibi, A.</au><au>Wong, R.</au><au>Sadreshkevary, R.</au><au>Yi‐Ling, L.</au><au>Tetradis, S.</au><au>Camargo, P. M.</au><au>Pirih, F. Q.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Susceptibility of different mouse strains to peri‐implantitis</atitle><jtitle>Journal of periodontal research</jtitle><addtitle>J Periodontal Res</addtitle><date>2018-02</date><risdate>2018</risdate><volume>53</volume><issue>1</issue><spage>107</spage><epage>116</epage><pages>107-116</pages><issn>0022-3484</issn><eissn>1600-0765</eissn><abstract>Background and Objective
Peri‐implantitis (PI) is an inflammatory condition that affects the tissues surrounding dental implants. Although the pathogenesis of PI is not fully understood, evidence suggests that the etiology is multifactorial and may include a genetic component. The aim of this study was to investigate the role of genetics in the development of peri‐implantitis.
Material and Methods
Four‐week‐old C57BL/6J, C3H/HeJ and A/J male mice had their left maxillary molars extracted. Implants were placed in the healed extraction sockets. Upon osseointegration, ligatures were placed around the implant head for 1 or 4 weeks to induce PI. Micro‐computed tomography scanning was used to measure volumetric bone loss. Histological analyses were also performed to evaluate collagen organization and the presence of neutrophils and osteoclasts.
Results
Radiographically, comparing the ligature‐treated mice, C57BL/6J displayed the greatest amount of bone loss, followed by C3H/HeJ and A/J mice at 1 and 4 weeks. Histologically, at 1 week, C57BL/6J mice presented with the highest numbers of neutrophils and osteoclasts. At 4 weeks, C57BL/6J mice presented with the most active bone remodeling compared with the other two strains.
Conclusion
There were significant differences in the severity of peri‐implantitis among the different mouse strains, suggesting that the genetic framework can affect implant survival and success. Future work is needed to dissect the genetic contribution to the development of peri‐implantitis.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>29044525</pmid><doi>10.1111/jre.12493</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0003-1670-7345</orcidid><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Wiley Online Library Journals Frontfile Complete |
| subjects | Alveolar Bone Loss - diagnostic imaging Alveolar Bone Loss - pathology Animals Bone loss Bone remodeling Bone Remodeling - genetics Collagen Computed tomography dental implant Dental implants Dental prosthetics Dental restorative materials Dentistry Etiology Genetic Predisposition to Disease genetics Inflammation Leukocytes (neutrophilic) Maxilla Mice, Inbred Strains Molars murine Neutrophils Neutrophils - metabolism Osseointegration Osteoclasts Osteoclasts - metabolism Peri-Implantitis - genetics Rodents Teeth Transplants & implants |
| title | Susceptibility of different mouse strains to peri‐implantitis |
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