Polyunsaturated fatty acids-PUFA -have surprised scientists once again. Supplementation with these compounds already supports the treatment of conditions such as Sjogren’s syndrome, atopic dermatitis, or easing morning stiffness in reumatoid arthritis. This time researchers have found in them a solution to harness the destructive process of inflammation in periodontitis.

Periodontal inflammation has been a huge problem in dentistry through the ages: the associated bleeding gums is just one of the less distressing symptoms –nearly 50% of patients above 30 years of age are suffering from it. As the disease evolves, it is followed by the formation of pathological deep pockets, the loss of periodontal ligaments and ultimately – of the bone structure. The inflammatory process generated by the human body gets out of control and destroys its own tissues.

Periodontitis and deep loss of soft tissues carries along a great risk of developing other diseases in the oral cavity. By exposing the root surface it encourages caries to develop in cementum which may lead to tooth fractures. The loss of hard tissues leads to mobility and teeth loss difficult to repair with standard prosthodontic procedures. It is also widely understood that periodontal diseases are closely linked with systemic (mainly cardiovascular) diseases.

The presence of pathogens in oral cavity due to poor oral hygiene is a condition for the gingival inflammation to take place. However, periodontitis depends on host factors that alter the immune response and lead to the destruction of periodontal tissues. It turned out that a diet rich in PUFAs enables to alleviate ongoing inflammation processes.

Numerous studies have shown that both n-3 fatty acids (eg DHA) and n-6 fatty acids like γ-Linolenic Acid (GLA) inhibited or in some cases completely stopped the inflammation. Recent research carried out on a diverse group of volunteers showed that within 12 weeks of taking GLA in borage oil, there was a significant decrease in the average probing depth (PPD) and gingival bleeding index. Other studies have shown that among people not taking DHA risk of deterioration of periodontal diseases increased almost by half.
What determines the saving effects of polyunsaturated fatty acids on the periodontal tissues? Most important are: modulation of inflammatory processes taking place in the oral cavity and antimicrobal activity against bacteria.

Periodontal tissue inflammation at an early stage is characterized by the elevated levels of LTB4 – it supports the development of inflammation, whereas the PGE2 sustains inflammation in tissues. Reducing levels of eicosanoids by the use of nonsteroidal anti-inflammatory drugs (NSAIDs) supports the treatment of periodontitis. Chronic use of these drugs, however, involves the risk of stomach ulcers. Thanks to the latest findings, PUFA might become a safe alternative to NSAIDs. Offenbacher studies have shown that EPA or DHA may be as effective in inhibiting PGE2 as ibuprofen, indomethacin, or dexamethasone, but can be used without any concerns.

The way PUFA works on the inflammation process seems to be brilliant in its simplicity. PUFAs are potential substrates for the production of eicosanoids (instead of arachidonic acid) Therefore they modify the final products of pathways: they induce the production of substrat LTB5 instead of LTB4. This alternative product is a worse chemoattractant. Thanks to the alternative pathway the organism also produces TXA3, which compared to TXA2 (obtained from the arachidonic acid) has a smaller pro-inflammatory effect. Eicopentaenoic acid (EPA) and DHA seem to be ideal as anti-inflammatory supplements. In addition to these features they lower neutrophils adherence, minimize the proliferation of T-lymphocytes, and decrease production of pro-inflammatory factors (eg IL2, TNF, IL6).

Another beneficial effect of omega -6, -7, -9 for patients with periodontitis is their antimicrobal activity. Streptococcus mutans, Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis and many other bacteria can be inhibited by PUFA. Polyunsaturated fatty acids also inhibit the development of fungal infections caused by Candida Albicans. Short-chain fatty acids (eg. butyric acid) have no antibacterial activity while medium-chain and long-chain fatty acids have the ability to inhibit or kill certain pathogens. The most effective against S. mutants proved acids of PA, GLA, LA and ARA, although their Esters proved to be less effective. Studies have shown that although the FA have the greatest effect on gram-positive bacteria, we cannot forget that they inhibit the growth of C. albicans up to 60%.
The exact mechanism of bactericidal activity of n-6, n-7 and n-9 fatty acids is not yet fully understood. Scientists point at the structure similarities between the cell membrane and the bipolar fatty acids and suggest that fatty acids can impair the functions of the cell membrane of oral pathogens.

Recent discoveries concerning PUFA have opened new possibilities for prevention of periodontal diseases. It is considered to be used in local delivery: toothpastes, mouthrinses or even chewing gum as “antimicrobal agents in situ”.

References:

1. n-3 Fatty Acid Intake and Periodontal Disease; Journal of the American Dietetic Association Volume: 110, Issue: 11, November, 2010, pp. 1650-1652; Kaye, Elizabeth Krall
2. Antimicrobial activity of n-6, n-7 and n-9 fatty acids and their esters for oral microorganisms; Archives of Oral Biology Volume: 55, Issue: 8, August, 2010, pp. 555-560; Huang, Chifu B.; George, Brian; Ebersole, Jeffery L.
3. Pilot study of dietary fatty acid supplementation in the treatment of adult periodontitis; Prostaglandins, Leukotrienes and Essential Fatty Acids Volume: 68, Issue: 3, March, 2003, pp. 213-218; Rosenstein, Elliot D.; Kushner, Laura J.; Kramer, Neil; Kazandjian, Gregory
4. Longitudinal relationship between dietary w-3 fatty acids and periodontal disease Nutrition Volume: 26, Issue: 11-12, November – December, 2010, pp. 1105-1109 Iwasaki, Masanori; Yoshihara, Akihiro; Moynihan, Paula; Watanabe, Reiko; Taylor, George W.; et. al.

Author: Maria Bilińska