Hyperglycemia and xerostomia are key determinants of tooth decay in type 1 diabetic mice
Insulin-dependent type 1 diabetes mellitus (DM) and oral diseases are closely interrelated. Poor metabolic control in diabetics is associated with a high risk of gingivitis, periodontitis and tooth loss. Salivary flow declines in diabetics and patients suffer from xerostomia. Reduced saliva predispo...
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| Veröffentlicht in: | Laboratory investigation 2012-06, Vol.92 (6), p.868-882 |
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| creator | Yeh, Chih-Ko Harris, Stephen E Mohan, Sumathy Horn, Diane Fajardo, Roberto Chun, Yong-Hee Patricia Jorgensen, James MacDougall, Mary Abboud-Werner, Sherry |
| description | Insulin-dependent type 1 diabetes mellitus (DM) and oral diseases are closely interrelated. Poor metabolic control in diabetics is associated with a high risk of gingivitis, periodontitis and tooth loss. Salivary flow declines in diabetics and patients suffer from xerostomia. Reduced saliva predisposes to enamel hypomineralization and caries formation; however, the mechanisms that initiate and lead to progression of tooth decay and periodontitis in type 1 DM have not been explored. To address this issue, we analyzed tooth morphology in Akita −/− mice that harbor a point mutation in the Ins2 insulin gene, which leads to progressive hyperglycemia. Mandibles from Akita −/− and wild-type littermates were analyzed by microCT, scanning EM and histology; teeth were examined for amelogenin (Amel) and ameloblastin (Ambn) expression. Mice were injected with pilocarpine to assess saliva production. As hyperglycemia may alter pulp repair, the effect of high glucose levels on the proliferation/differentiation of cultured MD10-F2 pulp cells was also analyzed. Results showed that Akita −/− mice at 6 weeks of age showed chalky white incisors that correlated with marked hyperglycemia and impaired saliva production. MicroCT of Akita −/− teeth revealed excessive enamel wearing and hypomineralization; immunostaining for Amel and Ambn was decreased. A striking feature was invasion of dentinal tubules with Streptococcus mitis and microabcesses that originated in the coronal pulp and progressed to pulp necrosis and periapical periodontitis. High levels of glucose also inhibited MD10-F2 cell proliferation and differentiation. Our findings provide the first evidence that hyperglycemia in combination with reduced saliva in a model of type1 DM leads to decreased enamel mineralization/matrix proteins and predisposes to excessive wearing and decay. Importantly, hyperglycemia adversely affects enamel matrix proteins and pulp repair. Early detection and treatment of hyperglycemia and hyposalivation may provide a useful strategy for preventing the dental complications of diabetes and promoting oral health in this population. |
| doi_str_mv | 10.1038/labinvest.2012.60 |
| format | Article |
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Poor metabolic control in diabetics is associated with a high risk of gingivitis, periodontitis and tooth loss. Salivary flow declines in diabetics and patients suffer from xerostomia. Reduced saliva predisposes to enamel hypomineralization and caries formation; however, the mechanisms that initiate and lead to progression of tooth decay and periodontitis in type 1 DM have not been explored. To address this issue, we analyzed tooth morphology in Akita −/− mice that harbor a point mutation in the Ins2 insulin gene, which leads to progressive hyperglycemia. Mandibles from Akita −/− and wild-type littermates were analyzed by microCT, scanning EM and histology; teeth were examined for amelogenin (Amel) and ameloblastin (Ambn) expression. Mice were injected with pilocarpine to assess saliva production. As hyperglycemia may alter pulp repair, the effect of high glucose levels on the proliferation/differentiation of cultured MD10-F2 pulp cells was also analyzed. Results showed that Akita −/− mice at 6 weeks of age showed chalky white incisors that correlated with marked hyperglycemia and impaired saliva production. MicroCT of Akita −/− teeth revealed excessive enamel wearing and hypomineralization; immunostaining for Amel and Ambn was decreased. A striking feature was invasion of dentinal tubules with Streptococcus mitis and microabcesses that originated in the coronal pulp and progressed to pulp necrosis and periapical periodontitis. High levels of glucose also inhibited MD10-F2 cell proliferation and differentiation. Our findings provide the first evidence that hyperglycemia in combination with reduced saliva in a model of type1 DM leads to decreased enamel mineralization/matrix proteins and predisposes to excessive wearing and decay. Importantly, hyperglycemia adversely affects enamel matrix proteins and pulp repair. Early detection and treatment of hyperglycemia and hyposalivation may provide a useful strategy for preventing the dental complications of diabetes and promoting oral health in this population.</description><identifier>ISSN: 0023-6837</identifier><identifier>EISSN: 1530-0307</identifier><identifier>DOI: 10.1038/labinvest.2012.60</identifier><identifier>PMID: 22449801</identifier><identifier>CODEN: LAINAW</identifier><language>eng</language><publisher>New York: Elsevier Inc</publisher><subject>692/699 ; 692/699/2743/137/1418 ; Amelogenin - metabolism ; Animals ; Biological and medical sciences ; Biotechnology ; Dental Caries - diagnosis ; Dental Caries - etiology ; Dental Enamel Proteins - metabolism ; diabetes ; Diabetes Mellitus, Type 1 - complications ; Diabetes Mellitus, Type 1 - diagnosis ; Diabetes. Impaired glucose tolerance ; enamel ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; Female ; Fundamental and applied biological sciences. Psychology ; hyperglycemia ; Hyperglycemia - diagnosis ; Hyperglycemia - etiology ; Investigative techniques, diagnostic techniques (general aspects) ; Laboratory Medicine ; Male ; Mandible - diagnostic imaging ; Mandible - pathology ; Mandible - ultrastructure ; Medical sciences ; Medicine ; Medicine & Public Health ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Pathology ; Pilocarpine - pharmacology ; pulpitis ; Radiography ; research-article ; saliva ; Saliva - metabolism ; Salivation - drug effects ; Streptococcus mitis ; Tooth - metabolism ; Tooth - pathology ; Xerostomia - diagnosis ; Xerostomia - etiology</subject><ispartof>Laboratory investigation, 2012-06, Vol.92 (6), p.868-882</ispartof><rights>2012 United States & Canadian Academy of Pathology</rights><rights>United States and Canadian Academy of Pathology, Inc. 2012</rights><rights>2015 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Jun 2012</rights><rights>2012 USCAP, Inc All rights reserved 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c651t-49a7aa68100ab7e5ccf369f853611cd2bdc3e6bd6c117e5369e9505a2dce78c33</citedby><cites>FETCH-LOGICAL-c651t-49a7aa68100ab7e5ccf369f853611cd2bdc3e6bd6c117e5369e9505a2dce78c33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=26049595$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22449801$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yeh, Chih-Ko</creatorcontrib><creatorcontrib>Harris, Stephen E</creatorcontrib><creatorcontrib>Mohan, Sumathy</creatorcontrib><creatorcontrib>Horn, Diane</creatorcontrib><creatorcontrib>Fajardo, Roberto</creatorcontrib><creatorcontrib>Chun, Yong-Hee Patricia</creatorcontrib><creatorcontrib>Jorgensen, James</creatorcontrib><creatorcontrib>MacDougall, Mary</creatorcontrib><creatorcontrib>Abboud-Werner, Sherry</creatorcontrib><title>Hyperglycemia and xerostomia are key determinants of tooth decay in type 1 diabetic mice</title><title>Laboratory investigation</title><addtitle>Lab Invest</addtitle><addtitle>Lab Invest</addtitle><description>Insulin-dependent type 1 diabetes mellitus (DM) and oral diseases are closely interrelated. Poor metabolic control in diabetics is associated with a high risk of gingivitis, periodontitis and tooth loss. Salivary flow declines in diabetics and patients suffer from xerostomia. Reduced saliva predisposes to enamel hypomineralization and caries formation; however, the mechanisms that initiate and lead to progression of tooth decay and periodontitis in type 1 DM have not been explored. To address this issue, we analyzed tooth morphology in Akita −/− mice that harbor a point mutation in the Ins2 insulin gene, which leads to progressive hyperglycemia. Mandibles from Akita −/− and wild-type littermates were analyzed by microCT, scanning EM and histology; teeth were examined for amelogenin (Amel) and ameloblastin (Ambn) expression. Mice were injected with pilocarpine to assess saliva production. As hyperglycemia may alter pulp repair, the effect of high glucose levels on the proliferation/differentiation of cultured MD10-F2 pulp cells was also analyzed. Results showed that Akita −/− mice at 6 weeks of age showed chalky white incisors that correlated with marked hyperglycemia and impaired saliva production. MicroCT of Akita −/− teeth revealed excessive enamel wearing and hypomineralization; immunostaining for Amel and Ambn was decreased. A striking feature was invasion of dentinal tubules with Streptococcus mitis and microabcesses that originated in the coronal pulp and progressed to pulp necrosis and periapical periodontitis. High levels of glucose also inhibited MD10-F2 cell proliferation and differentiation. Our findings provide the first evidence that hyperglycemia in combination with reduced saliva in a model of type1 DM leads to decreased enamel mineralization/matrix proteins and predisposes to excessive wearing and decay. Importantly, hyperglycemia adversely affects enamel matrix proteins and pulp repair. Early detection and treatment of hyperglycemia and hyposalivation may provide a useful strategy for preventing the dental complications of diabetes and promoting oral health in this population.</description><subject>692/699</subject><subject>692/699/2743/137/1418</subject><subject>Amelogenin - metabolism</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Biotechnology</subject><subject>Dental Caries - diagnosis</subject><subject>Dental Caries - etiology</subject><subject>Dental Enamel Proteins - metabolism</subject><subject>diabetes</subject><subject>Diabetes Mellitus, Type 1 - complications</subject><subject>Diabetes Mellitus, Type 1 - diagnosis</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>enamel</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Etiopathogenesis. Screening. Investigations. Target tissue resistance</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>hyperglycemia</subject><subject>Hyperglycemia - diagnosis</subject><subject>Hyperglycemia - etiology</subject><subject>Investigative techniques, diagnostic techniques (general aspects)</subject><subject>Laboratory Medicine</subject><subject>Male</subject><subject>Mandible - diagnostic imaging</subject><subject>Mandible - pathology</subject><subject>Mandible - ultrastructure</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Pathology</subject><subject>Pilocarpine - pharmacology</subject><subject>pulpitis</subject><subject>Radiography</subject><subject>research-article</subject><subject>saliva</subject><subject>Saliva - metabolism</subject><subject>Salivation - drug effects</subject><subject>Streptococcus mitis</subject><subject>Tooth - metabolism</subject><subject>Tooth - pathology</subject><subject>Xerostomia - diagnosis</subject><subject>Xerostomia - etiology</subject><issn>0023-6837</issn><issn>1530-0307</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqNUV2L1DAULaK44-oP8EUCIvjS8ab5aIsgyKKusOCLgm8hTW9ns7bJmGQG--9NnXFcBcWnkHs-cnJPUTymsKbAmhej7qzbY0zrCmi1lnCnWFHBoAQG9d1iBVCxUjasPisexHgDQDmX4n5xVlWctw3QVfH5ct5i2Iyzwclqol1PvmHwMfkf14DkC86kx4Rhsk67FIkfSPI-Xeep0TOxjqTsQSjpre4wWUMma_BhcW_QY8RHx_O8-PT2zceLy_Lqw7v3F6-vSiMFTSVvda21bCiA7moUxgxMtkMjmKTU9FXXG4ay66WhNMMZw1aA0FVvsG4MY-fFq4PvdtdNmKcuBT2qbbCTDrPy2qrfEWev1cbvFReUtVxkg-dHg-C_7vIy1WSjwXHUDv0uKgot44LX0PwHldZtU9ewuD79g3rjd8HlTSysBiAbLuHpgWXyymPA4ZSbgloqVqeK1VKxkpA1T25_-KT42WkmPDsSdDR6HIJ2xsZfPAm8Fe0SsTrwYobcBsPtiH9__eVBhLnTvc2iaCw6g70NaJLqvf2H-jvRPdfU</recordid><startdate>20120601</startdate><enddate>20120601</enddate><creator>Yeh, Chih-Ko</creator><creator>Harris, Stephen E</creator><creator>Mohan, Sumathy</creator><creator>Horn, Diane</creator><creator>Fajardo, Roberto</creator><creator>Chun, Yong-Hee Patricia</creator><creator>Jorgensen, James</creator><creator>MacDougall, Mary</creator><creator>Abboud-Werner, Sherry</creator><general>Elsevier Inc</general><general>Nature Publishing Group US</general><general>Nature Publishing Group</general><scope>6I.</scope><scope>AAFTH</scope><scope>IQODW</scope><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>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</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>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20120601</creationdate><title>Hyperglycemia and xerostomia are key determinants of tooth decay in type 1 diabetic mice</title><author>Yeh, Chih-Ko ; Harris, Stephen E ; Mohan, Sumathy ; Horn, Diane ; Fajardo, Roberto ; Chun, Yong-Hee Patricia ; Jorgensen, James ; MacDougall, Mary ; Abboud-Werner, Sherry</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c651t-49a7aa68100ab7e5ccf369f853611cd2bdc3e6bd6c117e5369e9505a2dce78c33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>692/699</topic><topic>692/699/2743/137/1418</topic><topic>Amelogenin - metabolism</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Biotechnology</topic><topic>Dental Caries - diagnosis</topic><topic>Dental Caries - etiology</topic><topic>Dental Enamel Proteins - metabolism</topic><topic>diabetes</topic><topic>Diabetes Mellitus, Type 1 - complications</topic><topic>Diabetes Mellitus, Type 1 - diagnosis</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>enamel</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Etiopathogenesis. Screening. Investigations. Target tissue resistance</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>hyperglycemia</topic><topic>Hyperglycemia - diagnosis</topic><topic>Hyperglycemia - etiology</topic><topic>Investigative techniques, diagnostic techniques (general aspects)</topic><topic>Laboratory Medicine</topic><topic>Male</topic><topic>Mandible - diagnostic imaging</topic><topic>Mandible - pathology</topic><topic>Mandible - ultrastructure</topic><topic>Medical sciences</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Pathology</topic><topic>Pilocarpine - pharmacology</topic><topic>pulpitis</topic><topic>Radiography</topic><topic>research-article</topic><topic>saliva</topic><topic>Saliva - metabolism</topic><topic>Salivation - drug effects</topic><topic>Streptococcus mitis</topic><topic>Tooth - metabolism</topic><topic>Tooth - pathology</topic><topic>Xerostomia - diagnosis</topic><topic>Xerostomia - etiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yeh, Chih-Ko</creatorcontrib><creatorcontrib>Harris, Stephen E</creatorcontrib><creatorcontrib>Mohan, Sumathy</creatorcontrib><creatorcontrib>Horn, Diane</creatorcontrib><creatorcontrib>Fajardo, Roberto</creatorcontrib><creatorcontrib>Chun, Yong-Hee Patricia</creatorcontrib><creatorcontrib>Jorgensen, James</creatorcontrib><creatorcontrib>MacDougall, Mary</creatorcontrib><creatorcontrib>Abboud-Werner, Sherry</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Pascal-Francis</collection><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>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</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 Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</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><collection>PubMed Central (Full Participant titles)</collection><jtitle>Laboratory investigation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yeh, Chih-Ko</au><au>Harris, Stephen E</au><au>Mohan, Sumathy</au><au>Horn, Diane</au><au>Fajardo, Roberto</au><au>Chun, Yong-Hee Patricia</au><au>Jorgensen, James</au><au>MacDougall, Mary</au><au>Abboud-Werner, Sherry</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hyperglycemia and xerostomia are key determinants of tooth decay in type 1 diabetic mice</atitle><jtitle>Laboratory investigation</jtitle><stitle>Lab Invest</stitle><addtitle>Lab Invest</addtitle><date>2012-06-01</date><risdate>2012</risdate><volume>92</volume><issue>6</issue><spage>868</spage><epage>882</epage><pages>868-882</pages><issn>0023-6837</issn><eissn>1530-0307</eissn><coden>LAINAW</coden><abstract>Insulin-dependent type 1 diabetes mellitus (DM) and oral diseases are closely interrelated. Poor metabolic control in diabetics is associated with a high risk of gingivitis, periodontitis and tooth loss. Salivary flow declines in diabetics and patients suffer from xerostomia. Reduced saliva predisposes to enamel hypomineralization and caries formation; however, the mechanisms that initiate and lead to progression of tooth decay and periodontitis in type 1 DM have not been explored. To address this issue, we analyzed tooth morphology in Akita −/− mice that harbor a point mutation in the Ins2 insulin gene, which leads to progressive hyperglycemia. Mandibles from Akita −/− and wild-type littermates were analyzed by microCT, scanning EM and histology; teeth were examined for amelogenin (Amel) and ameloblastin (Ambn) expression. Mice were injected with pilocarpine to assess saliva production. As hyperglycemia may alter pulp repair, the effect of high glucose levels on the proliferation/differentiation of cultured MD10-F2 pulp cells was also analyzed. Results showed that Akita −/− mice at 6 weeks of age showed chalky white incisors that correlated with marked hyperglycemia and impaired saliva production. MicroCT of Akita −/− teeth revealed excessive enamel wearing and hypomineralization; immunostaining for Amel and Ambn was decreased. A striking feature was invasion of dentinal tubules with Streptococcus mitis and microabcesses that originated in the coronal pulp and progressed to pulp necrosis and periapical periodontitis. High levels of glucose also inhibited MD10-F2 cell proliferation and differentiation. Our findings provide the first evidence that hyperglycemia in combination with reduced saliva in a model of type1 DM leads to decreased enamel mineralization/matrix proteins and predisposes to excessive wearing and decay. Importantly, hyperglycemia adversely affects enamel matrix proteins and pulp repair. Early detection and treatment of hyperglycemia and hyposalivation may provide a useful strategy for preventing the dental complications of diabetes and promoting oral health in this population.</abstract><cop>New York</cop><pub>Elsevier Inc</pub><pmid>22449801</pmid><doi>10.1038/labinvest.2012.60</doi><tpages>15</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0023-6837 |
| ispartof | Laboratory investigation, 2012-06, Vol.92 (6), p.868-882 |
| issn | 0023-6837 1530-0307 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4513945 |
| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | 692/699 692/699/2743/137/1418 Amelogenin - metabolism Animals Biological and medical sciences Biotechnology Dental Caries - diagnosis Dental Caries - etiology Dental Enamel Proteins - metabolism diabetes Diabetes Mellitus, Type 1 - complications Diabetes Mellitus, Type 1 - diagnosis Diabetes. Impaired glucose tolerance enamel Endocrine pancreas. Apud cells (diseases) Endocrinopathies Etiopathogenesis. Screening. Investigations. Target tissue resistance Female Fundamental and applied biological sciences. Psychology hyperglycemia Hyperglycemia - diagnosis Hyperglycemia - etiology Investigative techniques, diagnostic techniques (general aspects) Laboratory Medicine Male Mandible - diagnostic imaging Mandible - pathology Mandible - ultrastructure Medical sciences Medicine Medicine & Public Health Mice Mice, Inbred C57BL Mice, Knockout Pathology Pilocarpine - pharmacology pulpitis Radiography research-article saliva Saliva - metabolism Salivation - drug effects Streptococcus mitis Tooth - metabolism Tooth - pathology Xerostomia - diagnosis Xerostomia - etiology |
| title | Hyperglycemia and xerostomia are key determinants of tooth decay in type 1 diabetic mice |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-06T18%3A00%3A04IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Hyperglycemia%20and%20xerostomia%20are%20key%20determinants%20of%20tooth%20decay%20in%20type%201%20diabetic%20mice&rft.jtitle=Laboratory%20investigation&rft.au=Yeh,%20Chih-Ko&rft.date=2012-06-01&rft.volume=92&rft.issue=6&rft.spage=868&rft.epage=882&rft.pages=868-882&rft.issn=0023-6837&rft.eissn=1530-0307&rft.coden=LAINAW&rft_id=info:doi/10.1038/labinvest.2012.60&rft_dat=%3Cproquest_pubme%3E2675067661%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1018004703&rft_id=info:pmid/22449801&rft_els_id=S0023683722026861&rfr_iscdi=true |