Fatty Acid Profiles in Smokers with Chronic Periodontitis
(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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1791093
- author
- Buduneli, N. ; Larsson, Lennart LU ; Biyikoglu, B. ; Renaud, D. E. ; Bagaitkar, J. and Scott, D. A.
- organization
- publishing date
- 2011
- 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
- pmid:21041552
- 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
- 2016-04-01 10:40:07
- date last changed
- 2022-01-26 01:18:59
@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}},
keywords = {{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}},
doi = {{10.1177/0022034510380695}},
volume = {{90}},
year = {{2011}},
}