Age‐related changes in immune function (immune senescence) in caries and periodontal diseases: a systematic review

Aim To systematically review the evidence regarding immune senescence in the pathogenesis of periodontitis and dental caries. Methods A systematic search of electronic databases utilizing medical subject headings (MeSH terms) supplemented by screening of review articles and other relevant texts was...

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Published inJournal of clinical periodontology Vol. 44; no. S18; pp. S153 - S177
Main Authors Preshaw, Philip M., Henne, Karsten, Taylor, John J., Valentine, Ruth A., Conrads, Georg
Format Journal Article
LanguageEnglish
Published United States Blackwell Publishing Ltd 01.03.2017
Subjects
Adaptive immunity
Age
Age Factors
Aged
Animal research
Biofilms
caries
Cytokines
Dental caries
Dental Caries - immunology
Dentistry
Gum disease
Humans
immune function
Immune response
immune senescence
Immunosenescence
Inflammation
Interleukin 1
Interleukin 6
Medical Subject Headings-MeSH
mucosal immunity
Periodontal diseases
Periodontal Diseases - immunology
Periodontitis
Prostaglandin E2
Reviews
Saliva
Senescence
Systematic review
immune function
periodontitis
caries
immune senescence
mucosal immunity
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Abstract Aim To systematically review the evidence regarding immune senescence in the pathogenesis of periodontitis and dental caries. Methods A systematic search of electronic databases utilizing medical subject headings (MeSH terms) supplemented by screening of review articles and other relevant texts was undertaken. Results Seventy‐three articles were included (43 for periodontitis, 30 for caries). Study results were found to be generally heterogeneous. Regarding periodontitis, human studies suggest evidence for altered neutrophil function and increased production of pro‐inflammatory mediators (e.g. interleukin‐1β, interleukin‐6 and prostaglandin E2) in older compared to younger subjects, and animal experiments suggest increased expression of genes that contribute to a pro‐inflammatory state in older compared to younger animals. Regarding dental caries, research relating to changes in immune functioning and the impact of ageing is in its infancy. A small number of studies have reported components of innate and adaptive immunity that affect the composition of saliva and dental biofilms with possible impacts on caries progression. Conclusion There is evidence that immune functioning related to periodontitis and (less investigated) dental caries alters with increasing age. In both conditions, age‐associated mechanistic changes in immune functioning are complex and incompletely understood and it is not clear how these relate to disease susceptibility.
AbstractList To systematically review the evidence regarding immune senescence in the pathogenesis of periodontitis and dental caries. A systematic search of electronic databases utilizing medical subject headings (MeSH terms) supplemented by screening of review articles and other relevant texts was undertaken. Seventy-three articles were included (43 for periodontitis, 30 for caries). Study results were found to be generally heterogeneous. Regarding periodontitis, human studies suggest evidence for altered neutrophil function and increased production of pro-inflammatory mediators (e.g. interleukin-1β, interleukin-6 and prostaglandin E ) in older compared to younger subjects, and animal experiments suggest increased expression of genes that contribute to a pro-inflammatory state in older compared to younger animals. Regarding dental caries, research relating to changes in immune functioning and the impact of ageing is in its infancy. A small number of studies have reported components of innate and adaptive immunity that affect the composition of saliva and dental biofilms with possible impacts on caries progression. There is evidence that immune functioning related to periodontitis and (less investigated) dental caries alters with increasing age. In both conditions, age-associated mechanistic changes in immune functioning are complex and incompletely understood and it is not clear how these relate to disease susceptibility.
Aim To systematically review the evidence regarding immune senescence in the pathogenesis of periodontitis and dental caries. Methods A systematic search of electronic databases utilizing medical subject headings (MeSH terms) supplemented by screening of review articles and other relevant texts was undertaken. Results Seventy-three articles were included (43 for periodontitis, 30 for caries). Study results were found to be generally heterogeneous. Regarding periodontitis, human studies suggest evidence for altered neutrophil function and increased production of pro-inflammatory mediators (e.g. interleukin-1[beta], interleukin-6 and prostaglandin E2) in older compared to younger subjects, and animal experiments suggest increased expression of genes that contribute to a pro-inflammatory state in older compared to younger animals. Regarding dental caries, research relating to changes in immune functioning and the impact of ageing is in its infancy. A small number of studies have reported components of innate and adaptive immunity that affect the composition of saliva and dental biofilms with possible impacts on caries progression. Conclusion There is evidence that immune functioning related to periodontitis and (less investigated) dental caries alters with increasing age. In both conditions, age-associated mechanistic changes in immune functioning are complex and incompletely understood and it is not clear how these relate to disease susceptibility.
To systematically review the evidence regarding immune senescence in the pathogenesis of periodontitis and dental caries.AIMTo systematically review the evidence regarding immune senescence in the pathogenesis of periodontitis and dental caries.A systematic search of electronic databases utilizing medical subject headings (MeSH terms) supplemented by screening of review articles and other relevant texts was undertaken.METHODSA systematic search of electronic databases utilizing medical subject headings (MeSH terms) supplemented by screening of review articles and other relevant texts was undertaken.Seventy-three articles were included (43 for periodontitis, 30 for caries). Study results were found to be generally heterogeneous. Regarding periodontitis, human studies suggest evidence for altered neutrophil function and increased production of pro-inflammatory mediators (e.g. interleukin-1β, interleukin-6 and prostaglandin E2 ) in older compared to younger subjects, and animal experiments suggest increased expression of genes that contribute to a pro-inflammatory state in older compared to younger animals. Regarding dental caries, research relating to changes in immune functioning and the impact of ageing is in its infancy. A small number of studies have reported components of innate and adaptive immunity that affect the composition of saliva and dental biofilms with possible impacts on caries progression.RESULTSSeventy-three articles were included (43 for periodontitis, 30 for caries). Study results were found to be generally heterogeneous. Regarding periodontitis, human studies suggest evidence for altered neutrophil function and increased production of pro-inflammatory mediators (e.g. interleukin-1β, interleukin-6 and prostaglandin E2 ) in older compared to younger subjects, and animal experiments suggest increased expression of genes that contribute to a pro-inflammatory state in older compared to younger animals. Regarding dental caries, research relating to changes in immune functioning and the impact of ageing is in its infancy. A small number of studies have reported components of innate and adaptive immunity that affect the composition of saliva and dental biofilms with possible impacts on caries progression.There is evidence that immune functioning related to periodontitis and (less investigated) dental caries alters with increasing age. In both conditions, age-associated mechanistic changes in immune functioning are complex and incompletely understood and it is not clear how these relate to disease susceptibility.CONCLUSIONThere is evidence that immune functioning related to periodontitis and (less investigated) dental caries alters with increasing age. In both conditions, age-associated mechanistic changes in immune functioning are complex and incompletely understood and it is not clear how these relate to disease susceptibility.
Aim To systematically review the evidence regarding immune senescence in the pathogenesis of periodontitis and dental caries. Methods A systematic search of electronic databases utilizing medical subject headings (MeSH terms) supplemented by screening of review articles and other relevant texts was undertaken. Results Seventy‐three articles were included (43 for periodontitis, 30 for caries). Study results were found to be generally heterogeneous. Regarding periodontitis, human studies suggest evidence for altered neutrophil function and increased production of pro‐inflammatory mediators (e.g. interleukin‐1β, interleukin‐6 and prostaglandin E2) in older compared to younger subjects, and animal experiments suggest increased expression of genes that contribute to a pro‐inflammatory state in older compared to younger animals. Regarding dental caries, research relating to changes in immune functioning and the impact of ageing is in its infancy. A small number of studies have reported components of innate and adaptive immunity that affect the composition of saliva and dental biofilms with possible impacts on caries progression. Conclusion There is evidence that immune functioning related to periodontitis and (less investigated) dental caries alters with increasing age. In both conditions, age‐associated mechanistic changes in immune functioning are complex and incompletely understood and it is not clear how these relate to disease susceptibility.
Author Taylor, John J.
Valentine, Ruth A.
Conrads, Georg
Henne, Karsten
Preshaw, Philip M.
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  fullname: Preshaw, Philip M.
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  givenname: Ruth A.
  surname: Valentine
  fullname: Valentine, Ruth A.
  organization: Newcastle University
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  givenname: Georg
  surname: Conrads
  fullname: Conrads, Georg
  email: gconrads@ukaachen.de
  organization: RWTH Aachen University Hospital
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Keywords immune function
periodontitis
caries
immune senescence
mucosal immunity
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Notes Conflict of interest and source of funding statement
Dr. Conrads reports Other from LCL biokey GmbH company, outside the submitted work. In addition, Dr. Conrads has a patent ‘Detektionsverfahren für kariogene Keime, Method for detection of cariogenic bacteria. Deutsches Patent‐ und Markenamt, Nr. 101 09 012’ issued. Dr. Taylor reports Grants from Philips Research, outside the submitted work. Dr. Preshaw reports Grants from Colgate‐Palmolive, grants from Philips Research, outside the submitted work. Dr. Henne and Dr. Valentine have nothing to disclose.
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Snippet Aim To systematically review the evidence regarding immune senescence in the pathogenesis of periodontitis and dental caries. Methods A systematic search of...
To systematically review the evidence regarding immune senescence in the pathogenesis of periodontitis and dental caries. A systematic search of electronic...
Aim To systematically review the evidence regarding immune senescence in the pathogenesis of periodontitis and dental caries. Methods A systematic search of...
To systematically review the evidence regarding immune senescence in the pathogenesis of periodontitis and dental caries.AIMTo systematically review the...
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SubjectTerms Adaptive immunity
Age
Age Factors
Aged
Animal research
Biofilms
caries
Cytokines
Dental caries
Dental Caries - immunology
Dentistry
Gum disease
Humans
immune function
Immune response
immune senescence
Immunosenescence
Inflammation
Interleukin 1
Interleukin 6
Medical Subject Headings-MeSH
mucosal immunity
Periodontal diseases
Periodontal Diseases - immunology
Periodontitis
Prostaglandin E2
Reviews
Saliva
Senescence
Systematic review
Title Age‐related changes in immune function (immune senescence) in caries and periodontal diseases: a systematic review
URI https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fjcpe.12675
https://www.ncbi.nlm.nih.gov/pubmed/28266110
https://www.proquest.com/docview/1874570531
https://www.proquest.com/docview/1935169385
https://www.proquest.com/docview/1875145366
Volume 44
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