Fatty Acid Profiles in Smokers with Chronic Periodontitis

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 non-smokers) 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.

Salivary Concentrations of Interleukin (IL)‐1β, IL‐17A, and IL‐23 Vary in Relation to Periodontal Status

“…It is hypothesized that in salivary supernatant LPS is mainly present in the form of shed bacterial outer membrane vesicles, and whole saliva may be more suitable for LPS measurements. In two previous studies using whole saliva, differences were observed between participants with and without periodontal disease when structural alterations in lipid‐A‐derived 3‐OH fatty acid profile were determined or bioassay for stimulants of Toll‐like receptors 2 and 4 was used 37 , 38 . It has been shown that LPS concentrations in GCF of ligature‐induced periodontitis‐affected rats are higher than those of control rats 39 …”

“…In two previous studies using whole saliva, differences were observed between participants with and without periodontal disease when structural alterations in lipid-A-derived 3-OH fatty acid profile were determined or bioassay for stimulants of Toll-like receptors 2 and 4 was used. 37,38 It has been shown that LPS concentrations in GCF of ligature-induced periodontitis-affected rats are higher than those of control rats. 39 There are only some reports [20][21][22] dealing with salivary concentrations of IL-17A in periodontitis and none on IL-23 concentrations in saliva.…”

Tobacco‐induced suppression of the vascular response to dental plaque

“…Variant LPS structures have differential capacities to engage the Toll‐like receptors (TLRs) that drive inflammatory mediator release from epithelial and immune cells. Certainly, the overall LPS profile in smokers, as measured in saliva, is composed of lower levels of LPS with the optimal TLR‐activating structure than that of nonsmokers …”

Smoking and Periodontal Disease

“…Studies find that former smokers (clinically defined as two or more years since quitting smoking) experience less attachment loss than current smokers but more than neversmokers. Furthermore, the likelihood of developing increasing periodontal disease exhibits dose dependency (5). …”