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Fatty Acid Profiles in Smokers with Chronic Periodontitis

Buduneli, N.; Larsson, Lennart LU ; Biyikoglu, B.; Renaud, D. E.; Bagaitkar, J. and Scott, D. A. (2011) In Journal of Dental Research 90(1). p.47-52
Abstract
We hypothesized that tobacco smoke induces alterations to the 3-OH fatty acids present in lipid A in a manner consistent with a microflora of reduced inflammatory potential. Whole saliva samples and full-mouth clinical periodontal recordings were obtained from persons with (22 smokers; 15 nonsmokers) and without (14 smokers; 15 non-smokers) chronic periodontitis. Clear differences in the contributions of multiple saturated 3-OH fatty acid species were noted in the group with disease compared with healthy individuals. Increases in the long-chain fatty acids associated with anaerobic bacterial periodontopathogens, particularly 3-OH-C-i17.0 (146.7%, relative to controls), were apparent. Significant reductions in the 3-OH fatty acids... (More)
We hypothesized that tobacco smoke induces alterations to the 3-OH fatty acids present in lipid A in a manner consistent with a microflora of reduced inflammatory potential. Whole saliva samples and full-mouth clinical periodontal recordings were obtained from persons with (22 smokers; 15 nonsmokers) and without (14 smokers; 15 non-smokers) chronic periodontitis. Clear differences in the contributions of multiple saturated 3-OH fatty acid species were noted in the group with disease compared with healthy individuals. Increases in the long-chain fatty acids associated with anaerobic bacterial periodontopathogens, particularly 3-OH-C-i17.0 (146.7%, relative to controls), were apparent. Significant reductions in the 3-OH fatty acids associated with the consensus (high potency) enteric LPS structure (3-OH-C-12.0 and 3-OH-C-14.0; 33.3% and 15.8% reduction, respectively) were noted in smokers compared with non-smokers with chronic periodontitis. Thus, smoking is associated with specific structural alterations to the lipid-A-derived 3-OH fatty acid profile in saliva that are consistent with an oral microflora of reduced inflammatory potential. These findings provide much-needed mechanistic insight into the established clinical conundrum of increased infection with periodontal pathogens but reduced clinical inflammation in smokers. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
inflammation, lipid A, lipopolysaccharide, periodontitis, saliva, smoking
in
Journal of Dental Research
volume
90
issue
1
pages
47 - 52
publisher
International & American Associations for Dental Research
external identifiers
  • wos:000285577500009
  • scopus:78650991649
ISSN
0022-0345
DOI
10.1177/0022034510380695
language
English
LU publication?
yes
id
d4cd9aa4-dd6c-466c-93fd-c4f5189bea4d (old id 1791093)
date added to LUP
2011-03-02 14:18:58
date last changed
2017-01-01 03:47:44
@article{d4cd9aa4-dd6c-466c-93fd-c4f5189bea4d,
  abstract     = {We hypothesized that tobacco smoke induces alterations to the 3-OH fatty acids present in lipid A in a manner consistent with a microflora of reduced inflammatory potential. Whole saliva samples and full-mouth clinical periodontal recordings were obtained from persons with (22 smokers; 15 nonsmokers) and without (14 smokers; 15 non-smokers) chronic periodontitis. Clear differences in the contributions of multiple saturated 3-OH fatty acid species were noted in the group with disease compared with healthy individuals. Increases in the long-chain fatty acids associated with anaerobic bacterial periodontopathogens, particularly 3-OH-C-i17.0 (146.7%, relative to controls), were apparent. Significant reductions in the 3-OH fatty acids associated with the consensus (high potency) enteric LPS structure (3-OH-C-12.0 and 3-OH-C-14.0; 33.3% and 15.8% reduction, respectively) were noted in smokers compared with non-smokers with chronic periodontitis. Thus, smoking is associated with specific structural alterations to the lipid-A-derived 3-OH fatty acid profile in saliva that are consistent with an oral microflora of reduced inflammatory potential. These findings provide much-needed mechanistic insight into the established clinical conundrum of increased infection with periodontal pathogens but reduced clinical inflammation in smokers.},
  author       = {Buduneli, N. and Larsson, Lennart and Biyikoglu, B. and Renaud, D. E. and Bagaitkar, J. and Scott, D. A.},
  issn         = {0022-0345},
  keyword      = {inflammation,lipid A,lipopolysaccharide,periodontitis,saliva,smoking},
  language     = {eng},
  number       = {1},
  pages        = {47--52},
  publisher    = {International & American Associations for Dental Research},
  series       = {Journal of Dental Research},
  title        = {Fatty Acid Profiles in Smokers with Chronic Periodontitis},
  url          = {http://dx.doi.org/10.1177/0022034510380695},
  volume       = {90},
  year         = {2011},
}