Genetic- and Lifestyle-dependent Dental Caries Defined by the Acidic Proline-rich Protein Genes PRH1 and PRH2
Dental caries is a chronic infectious disease that affects billions of people with large individual differences in activity. We investigated whether PRH1 and PRH2 polymorphisms in saliva acidic proline-rich protein (PRP) receptors for indigenous bacteria match and predict individual differences in t...
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Elsevier
2017-12-01
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author | Nicklas Strömberg Anders Esberg Nongfei Sheng Lena Mårell Anna Löfgren-Burström Karin Danielsson Carina Källestål |
author_facet | Nicklas Strömberg Anders Esberg Nongfei Sheng Lena Mårell Anna Löfgren-Burström Karin Danielsson Carina Källestål |
author_sort | Nicklas Strömberg |
collection | DOAJ |
description | Dental caries is a chronic infectious disease that affects billions of people with large individual differences in activity. We investigated whether PRH1 and PRH2 polymorphisms in saliva acidic proline-rich protein (PRP) receptors for indigenous bacteria match and predict individual differences in the development of caries. PRH1 and PRH2 variation and adhesion of indigenous and cariogenic (Streptococcus mutans) model bacteria were measured in 452 12-year-old Swedish children along with traditional risk factors and related to caries at baseline and after 5-years. The children grouped into low-to-moderate and high susceptibility phenotypes for caries based on allelic PRH1, PRH2 variation. The low-to-moderate susceptibility children (P1 and P4a−) experienced caries from eating sugar or bad oral hygiene or infection by S. mutans. The high susceptibility P4a (Db, PIF, PRP12) children had more caries despite receiving extra prevention and irrespective of eating sugar or bad oral hygiene or S. mutans-infection. They instead developed 3.9-fold more caries than P1 children from plaque accumulation in general when treated with orthodontic multibrackets; and had basic PRP polymorphisms and low DMBT1-mediated S. mutans adhesion as additional susceptibility traits. The present findings thus suggest genetic autoimmune-like (P4a) and traditional life style (P1) caries, providing a rationale for individualized oral care. |
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issn | 2352-3964 |
language | English |
last_indexed | 2024-12-12T23:36:21Z |
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spelling | doaj.art-89ffe5c379c1442a8d5166e6a98605ee2022-12-22T00:07:26ZengElsevierEBioMedicine2352-39642017-12-0126C384610.1016/j.ebiom.2017.11.019Genetic- and Lifestyle-dependent Dental Caries Defined by the Acidic Proline-rich Protein Genes PRH1 and PRH2Nicklas Strömberg0Anders Esberg1Nongfei Sheng2Lena Mårell3Anna Löfgren-Burström4Karin Danielsson5Carina Källestål6Department of Odontology/Cariology, Umeå University, SE-901 87 Umeå, SwedenDepartment of Odontology/Cariology, Umeå University, SE-901 87 Umeå, SwedenDepartment of Odontology/Cariology, Umeå University, SE-901 87 Umeå, SwedenDepartment of Odontology/Cariology, Umeå University, SE-901 87 Umeå, SwedenDepartment of Odontology/Cariology, Umeå University, SE-901 87 Umeå, SwedenDepartment of Odontology/Cariology, Umeå University, SE-901 87 Umeå, SwedenDepartment of Odontology/Cariology, Umeå University, SE-901 87 Umeå, SwedenDental caries is a chronic infectious disease that affects billions of people with large individual differences in activity. We investigated whether PRH1 and PRH2 polymorphisms in saliva acidic proline-rich protein (PRP) receptors for indigenous bacteria match and predict individual differences in the development of caries. PRH1 and PRH2 variation and adhesion of indigenous and cariogenic (Streptococcus mutans) model bacteria were measured in 452 12-year-old Swedish children along with traditional risk factors and related to caries at baseline and after 5-years. The children grouped into low-to-moderate and high susceptibility phenotypes for caries based on allelic PRH1, PRH2 variation. The low-to-moderate susceptibility children (P1 and P4a−) experienced caries from eating sugar or bad oral hygiene or infection by S. mutans. The high susceptibility P4a (Db, PIF, PRP12) children had more caries despite receiving extra prevention and irrespective of eating sugar or bad oral hygiene or S. mutans-infection. They instead developed 3.9-fold more caries than P1 children from plaque accumulation in general when treated with orthodontic multibrackets; and had basic PRP polymorphisms and low DMBT1-mediated S. mutans adhesion as additional susceptibility traits. The present findings thus suggest genetic autoimmune-like (P4a) and traditional life style (P1) caries, providing a rationale for individualized oral care.http://www.sciencedirect.com/science/article/pii/S2352396417304620Dental cariesChronic infectionsPRH1PRH2Host susceptibilityAcidic proline-rich proteins |
spellingShingle | Nicklas Strömberg Anders Esberg Nongfei Sheng Lena Mårell Anna Löfgren-Burström Karin Danielsson Carina Källestål Genetic- and Lifestyle-dependent Dental Caries Defined by the Acidic Proline-rich Protein Genes PRH1 and PRH2 EBioMedicine Dental caries Chronic infections PRH1 PRH2 Host susceptibility Acidic proline-rich proteins |
title | Genetic- and Lifestyle-dependent Dental Caries Defined by the Acidic Proline-rich Protein Genes PRH1 and PRH2 |
title_full | Genetic- and Lifestyle-dependent Dental Caries Defined by the Acidic Proline-rich Protein Genes PRH1 and PRH2 |
title_fullStr | Genetic- and Lifestyle-dependent Dental Caries Defined by the Acidic Proline-rich Protein Genes PRH1 and PRH2 |
title_full_unstemmed | Genetic- and Lifestyle-dependent Dental Caries Defined by the Acidic Proline-rich Protein Genes PRH1 and PRH2 |
title_short | Genetic- and Lifestyle-dependent Dental Caries Defined by the Acidic Proline-rich Protein Genes PRH1 and PRH2 |
title_sort | genetic and lifestyle dependent dental caries defined by the acidic proline rich protein genes prh1 and prh2 |
topic | Dental caries Chronic infections PRH1 PRH2 Host susceptibility Acidic proline-rich proteins |
url | http://www.sciencedirect.com/science/article/pii/S2352396417304620 |
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