Aging, inflammation, immunity and periodontal disease

The increased prevalence and severity of periodontal disease have long been associated with aging, such that this oral condition affects the majority of the adult population over 50 years of age. Although the immune system is a critical component for maintaining health, aging can be characterized by...

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Published in:Periodontology 2000 Vol. 72; no. 1; pp. 54 - 75
Main Authors: Ebersole, Jeffrey L., Graves, Christina L., Gonzalez, Octavio A., Dawson III, Dolph, Morford, Lorri A., Huja, Pinar Emecen, Hartsfield Jr, James K., Huja, Sarandeep S., Pandruvada, Subramanya, Wallet, Shannon M.
Format: Journal Article
Language:English
Published: Denmark Blackwell Publishing Ltd 01-10-2016
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Abstract The increased prevalence and severity of periodontal disease have long been associated with aging, such that this oral condition affects the majority of the adult population over 50 years of age. Although the immune system is a critical component for maintaining health, aging can be characterized by quantitative and qualitative modifications of the immune system. This process, termed ‘immunosenescence’, is a progressive modification of the immune system that leads to greater susceptibility to infections, neoplasia and autoimmunity, presumably reflecting the prolonged antigenic stimulation and/or stress responses that occur across the lifespan. Interestingly, the global reduction in the host capability to respond effectively to these challenges is coupled with a progressive increase in the general proinflammatory status, termed ‘inflammaging’. Consistent with the definition of immunosenescence, it has been suggested that the cumulative effect of prolonged exposure of the periodontium to microbial challenge is, at least in part, a contributor to the effects of aging on these tissues. Thus, it has also been hypothesized that alterations in the function of resident immune and nonimmune cells of the periodontium contribute to the expression of inflammaging in periodontal disease. Although the majority of aging research has focused on the adaptive immune response, it is becoming increasingly clear that the innate immune compartment is also highly affected by aging. Thus, the phenomenon of immunosenescence and inflammaging, expressed as age‐associated changes within the periodontium, needs to be more fully understood in this era of precision and personalized medicine and dentistry.
AbstractList The increased prevalence and severity of periodontal disease have long been associated with aging, such that this oral condition affects the majority of the adult population over 50 years of age. Although the immune system is a critical component for maintaining health, aging can be characterized by quantitative and qualitative modifications of the immune system. This process, termed ‘immunosenescence’, is a progressive modification of the immune system that leads to greater susceptibility to infections, neoplasia and autoimmunity, presumably reflecting the prolonged antigenic stimulation and/or stress responses that occur across the lifespan. Interestingly, the global reduction in the host capability to respond effectively to these challenges is coupled with a progressive increase in the general proinflammatory status, termed ‘inflammaging’. Consistent with the definition of immunosenescence, it has been suggested that the cumulative effect of prolonged exposure of the periodontium to microbial challenge is, at least in part, a contributor to the effects of aging on these tissues. Thus, it has also been hypothesized that alterations in the function of resident immune and nonimmune cells of the periodontium contribute to the expression of inflammaging in periodontal disease. Although the majority of aging research has focused on the adaptive immune response, it is becoming increasingly clear that the innate immune compartment is also highly affected by aging. Thus, the phenomenon of immunosenescence and inflammaging, expressed as age‐associated changes within the periodontium, needs to be more fully understood in this era of precision and personalized medicine and dentistry.
Author Gonzalez, Octavio A.
Pandruvada, Subramanya
Morford, Lorri A.
Huja, Sarandeep S.
Graves, Christina L.
Hartsfield Jr, James K.
Ebersole, Jeffrey L.
Huja, Pinar Emecen
Wallet, Shannon M.
Dawson III, Dolph
Author_xml – sequence: 1
  givenname: Jeffrey L.
  surname: Ebersole
  fullname: Ebersole, Jeffrey L.
– sequence: 2
  givenname: Christina L.
  surname: Graves
  fullname: Graves, Christina L.
– sequence: 3
  givenname: Octavio A.
  surname: Gonzalez
  fullname: Gonzalez, Octavio A.
– sequence: 4
  givenname: Dolph
  surname: Dawson III
  fullname: Dawson III, Dolph
– sequence: 5
  givenname: Lorri A.
  surname: Morford
  fullname: Morford, Lorri A.
– sequence: 6
  givenname: Pinar Emecen
  surname: Huja
  fullname: Huja, Pinar Emecen
– sequence: 7
  givenname: James K.
  surname: Hartsfield Jr
  fullname: Hartsfield Jr, James K.
– sequence: 8
  givenname: Sarandeep S.
  surname: Huja
  fullname: Huja, Sarandeep S.
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  givenname: Subramanya
  surname: Pandruvada
  fullname: Pandruvada, Subramanya
– sequence: 10
  givenname: Shannon M.
  surname: Wallet
  fullname: Wallet, Shannon M.
BackLink https://www.ncbi.nlm.nih.gov/pubmed/27501491$$D View this record in MEDLINE/PubMed
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1991; 18
1989; 44
2010; 107
2013; 62
2007; 581
2004; 3
2004; 6
2004; 5
2008; 105
2010; 184
2014; 29
2012; 13
2012; 11
2014; 23
1994; 62
2009; 12
1824; 2002
2007; 178
2010; 25
2006; 24
2013; 57
2005; 102
2004; 39
2007; 8
2008; 113
2008; 112
2008; 111
2012; 24
1998; 12
2010; 30
1994; 74
2006; 169
2011; 121
2003; 284
2014; 124
2004; 43
1989; 60
2009; 69
2010; 37
1989; 1
2011; 2
2009; 64
2000; 67
2009; 182
2013; 84
1992; 663
1991; 292
2014; 49
2005; 84
2011; 74
2002; 3
2003; 38
2010; 161
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2014; 41
2011; 6
2004; 305
2011; 132
2012; 30
2007; 16
2010; 42
2004; 50
2000; 908
2009; 70
1997; 160
2005; 366
2000; 106
2005; 8
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2003; 24
1999; 34
1956; 27
1969; 24
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2000; 100
2005; 16
2005; 17
2005; 11
1996; 87
2001; 31
2009; 106
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2007; 148
2013; 25
2006; 77
2015; 30
1993; 64
2000; 51
2008; 7
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2008; 79
2011; 10
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1996; 348
2011; 203
2004; 75
2011; 208
2004; 72
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1997; 93
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1997; 98
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2009; 8
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e_1_2_7_153_1
e_1_2_7_176_1
Franceschi C (e_1_2_7_57_1) 1989; 1
e_1_2_7_138_1
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Snippet The increased prevalence and severity of periodontal disease have long been associated with aging, such that this oral condition affects the majority of the...
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SubjectTerms Adaptive Immunity - immunology
Aging - immunology
Aging - physiology
Autoimmune Diseases - complications
Autoimmune Diseases - immunology
Autoimmunity - immunology
Cytokines - genetics
Cytokines - immunology
Dentistry
Disease Susceptibility - immunology
Epigenomics
Humans
Immune System
Immunity, Innate - genetics
Immunity, Innate - immunology
Immunosenescence - physiology
Inflammation - immunology
Neoplasms - complications
Neoplasms - immunology
Periodontal Diseases - immunology
Periodontium - immunology
Periodontium - microbiology
Polymorphism, Genetic
Title Aging, inflammation, immunity and periodontal disease
URI https://api.istex.fr/ark:/67375/WNG-S59GCFTR-W/fulltext.pdf
https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fprd.12135
https://www.ncbi.nlm.nih.gov/pubmed/27501491
https://search.proquest.com/docview/1810557452
Volume 72
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