The Skinny on Fats: A report from IADR Miami
© Juliette Reeves 2010

Abstract
The Miami Beach Convention Centre opened its doors at 7 am on a beautiful and sunny April morning for the 87 General Session of the International Association for Dental Research. This is the opportunity for dental researchers from all over the world to meet in order to present and debate their current research. A significant amount of research and discussion regarding nutritional biochemistry and periodontal health was presented, highlighting the growing importance of this area of research. Juliette Reeves attended the four day conference, and in the first of a series of articles,reports back on some of the latest research presented at this convention.
Introduction
The annual IADR conference is a key date in the diaries of dental researchers all over the world. Thousands of research papers are presented and discussed over this four day event, with presentations taking place in over 30 lecture halls. Absolutely every aspect of dentistry is represented with papers ranging from dental materials to TMJ problems, craniofacial biology, oral medicine and periodontal research to name but a few.
A significant amount of research and discussion regarding nutritional biochemistry and periodontal health was presented, highlighting the growing importance of this area of research. Of particular interest was a study presented by a group from Boston University and Brigham Women’s Hospital regarding the topical application of an essential fatty acid derivative in the treatment of inflammatory periodontal disease. Resolvin D1 (RvD1) was shown to resolve experimental periodontitis (1).
Fats and Essential Fatty Acids
Fats are an important source of energy, containing twice as many calories as carbohydrate. Fats are also needed to obtain and metabolise fat soluble vitamins such as vitamins A,D and E. Fats prolong the process of digestion by slowing down stomach secretions of HCL, thus creating a longer lasting sensation of fullness after a meal. Polyunsaturated Fatty acids (PUFA’s) are the main components of cellular membranes and sub cellular organelles. Fatty acids play key roles in the construction and maintenance of all healthy cells.
Classification of Fats
Saturated Fats Saturated fats are short chain fatty acids. A saturated fat is one in which all the covalent carbon bonds are taken up with other atoms: carbon, hydrogen, oxygen or hydroxyl ions. The bonds therefore, are saturated with other ions. Saturated fats are usually solid at room temperature.
Unsaturated Fats An unsaturated fat is a long chain fatty acid that does not have all it’s available covalent carbon bonds taken up with other atoms, and thus forms double carbon bonds.
Mono unsaturated Fats These have one double bond per carbon chain e.g. Olive Oil
Polyunsaturated Fats These have more than one double bond per carbon chain e.g. Sunflower Oil.
Essential Fatty Acids These are polyunsaturated fats (PUFA’s). These must be supplied from the diet as the body is unable to synthesise them. Two main families are needed: Omega 3 (n-3) and Omega 6 (n-6) fatty acids. These fats perform a wide variety of functions in the body, ranging from structural components of cell membranes, to the synthesis of male and female hormones and the highly reactive prostaglandins which regulate the immuno-inflammatory pathways.
Cis Fatty Acids The cis configuration of a fatty acid occurs in all PUFA’s in their natural undamaged form. In this state wherever there is a double bond, the hydrogen atoms occur on the same side of each other. Cis fatty acids are health giving PUFA’s and in this configuration, make up a significant part of the cell membrane.
Trans Fatty Acids When a PUFA is exposed to high temperatures such as deep frying, the hydrogen atoms at the double bond are flipped to opposite sides., in effect twisting the molecule. Once a cis fatty acid has been transformed into a trans fat it is unlikely to change back. Trans fats are therefore damaged fats, which also behave like saturated fats in the body. They also have an affinity for the cell membrane and disrupt or damage the PUFA’s in the cell membrane.
Hydrogenated fats Hydrogenation changes an unsaturated fat into a saturated fat by filling all the carbon bonds with hydrogen. This process takes place at high temperature and in the presence of a metal catalyst, mainly nickel, which is 50% aluminium. The reason for this is to provide cheap spreadable products, which remain solid at room temperature but spread easily. As this process takes place at high temperatures, all hydrogenated fats are also damaged, trans fats.
Essential Fatty Acids and Oral Health
Many people are under the misconception that all fats are unhealthy and are to be avoided. To this end the fat free diet is the goal. Whilst this is true of animal and other saturated fats, essential fatty acids are just that: Essential. The relevance of essential fatty acids (EFA’s) in oral health lies in their requirement for:
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Wound healing and connective tissue integrity.
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Membrane integrity, in particular the skin.
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Immune function and host susceptibility.
Linoleic acid and Linolenic acid are essential dietary components for humans, as the body can synthesise the remainder. EFA deficiency is manifested by the inability to synthesise prostaglandins. Some of the best known
mediators of the immuno-inflammatory pathways are prostaglandins. PGE1 and 3 are known to be anti-inflammatory and oppose the excess production of the pro-inflammatory PGE2. GLA works as an anti-inflammatory agent, by blocking the mobilisation of arachidonic acid (AA). EPA and DHA from fish oils and its metabolites appears to compete with AA and so prevent the synthesis of AA to inflammatory metabolites.
The prostaglandins group PGE2 and other pro inflammatory metabolites of AA are released into gingival tissue in response to tissue damage, which in the progression of periodontal disease is caused by bacterial plaque.
Studies have shown that levels of AA metabolites are significantly elevated in periodontally diseased tissue when compared to healthy periodontal tissue. PGE2 levels have been found at 10-20 times higher than in healthy gingival tissue. (2,3) Adequate production of the anti inflammatory prostaglandins PGE1 and PGE3 are needed to regulate pro inflammatory cytokines and oppose long term chronic inflammatory tissue damage.
A series of recent studies have shown that n-3 fatty acids can reduce inflammation in the oral cavity of rats challenged with specific oral bacteria (4,5). It has also been suggested that dietary fish oil supplementation may have potential benefits in modulating the immuno-inflammatory pathways of the host in the prevention and adjunctive management of periodontitis (6,7).
Porphyromonas gingivalis infected rats treated with n-3 fatty acids had significantly less alveolar bone resorption. These results demonstrated the effectiveness of an n-3 supplemented diet in modulating alveolar bone resorption following
P. gingivalis infection, and supported the idea that n-3 fatty acids may be a useful adjunct in the treatment of periodontal disease. In addition, n-3 fatty acids were shown to reduce the inflammation in the oral cavity by modulating gene expression and decreasing proinflammatory cytokine production (interleukin-1, tumour necrosis factor) and the up regulation of protective bio mechanisms, compared with rats fed a corn oil diet (8). All these studies support the idea that host inflammatory reactions may be modified through dietary intervention and supplementation with essential PUFA’s.
Latest Research
DHA and Periodontal Inflammation
Resolvin D1 is a newly identified lipid mediator with potent anti-inflammatory properties derived from docosahexaenoic acid (DHA) (1). RvD1 provides protection against tissue damage in several systemic inflammation models. The purpose of the study presented was to evaluate the resolving actions of topically applied RvD1 in experimental periodontitis. Local RvD1 application reduced the inflammatory changes and osteoclastic activity induced by
P. gingivalis and the RvD1 treatment resulted in significant bone gain ,compared to control, with complete resolution of inflammatory changes and bone fill in the treated group.
The group concluded that in a rabbit model of human periodontal disease, local application of RvD1 in small amounts resulted in complete resolution of inflammation and regeneration of bone.
A longitudinal relationship between DHA and periodontal disease was demonstrated in another study presented from Japan and the UK (9). DHA from fish oil is recognized as having anti inflammatory actions which may be beneficial to oral health. A study of 55 subjects aged 74 years was undertaken. Dietary intakes of energy and DHA were calculated and dental examinations were carried out at baseline and once a year for 4 years.
The results showed that the number of teeth present had a significant relationship with the intake of DHA at baseline . In addition, DHA intake at baseline was significantly correlated with the number of periodontal disease events. The conclusion was made that the findings of the present study suggest that there was a significant relationship between dietary DHA and periodontal disease progression among elderly.
More recently a new study has demonstrated the anti-bacterial effects of EPA, DHA and ALA ( Alpha-Linolenic Acid) on periodontal pathogens such as AA (Aggregatibacter Actinomycetemcomitans) and PG (Porphyromonas gingivalis) (10). This study demonstrated a novel bioactivity of the three major n-3 fatty acids, (EPA, DHA, and ALA), and their ester derivatives. The research showed that n-3 fatty acids and their ester derivatives exhibited strong antibacterial activity against various oral pathogens including AA and PG.
To date, this is the first study to demonstrate the significant antibacterial activity of n-3 fatty acids and their esters against oral pathogens. This could indicate that the target of the n-3 fatty acids could be the cellular membrane because fatty acids could possibly penetrate into the cell membrane of the bacteria disrupting normal cell membrane functions and leading to bacterial death. Although the in vitro effect was demonstrated, the in vivo effects still need to be determined. However, the researchers suggest that as EPA and ALA had a much stronger antibacterial activity than DHA in vitro ,it is expected that EPA and ALA will have stronger in vivo effects than DHA.
This study suggests that n-3 fatty acids could have a positive therapeutic effect for improving oral health via their antimicrobial activities, in addition to their anti-inflammatory effects. Future research will be carried out to study the mechanism of their antimicrobial activity.
Conclusion
Government recommendations suggest about 10% of our food energy comes from saturated fats 6% from polyunsaturated fats 12% from mono-unsaturated fats (11) Poor diet, eating disorders and micronutrient deficiencies can have ramifications for oral health. Nutritional deficiencies may also exist and exacerbate oral symptoms. The effect of diet, nutrition and malnutrition on the oral cavity is receiving more and more attention, as these factors are being considered to be potential contributors to oral disease. As the link between systemic and oral health becomes more established, so too will the role of nutrition prove more significant. Continuing to build the body of research will also improve our understanding of this important issue. Whilst more research is required to establish the therapeutic role PUFA’s may have in the treatment of periodontal disease, it is easy to see how a deficiency may modify the host’s response to bacterial plaque.
Recommended food sources include nuts, seeds, oily fish, avocados. EFA deficiency symptoms may include: Dry, cracked lips, dry skin and poor wound healing.
References
1 Hasturk H, Kantarci A, Goguet-Surmenian E, Van Dyke TE, and Serhan CN: Resolvin D1 a novel docosahexanoic acid derived mediator resolves experimental periodontitis. IADR 2009.
2 Goodson,J.M., Dewhirst,F.C., Brunetti,A: Prostagandin E2 Levels and human periodontal disease. Prostaglandins 1974 6:81-85.
3 El-Attar,T.M.A., Lin,H.S: Prostaglandins in gingivae of patients with periodontal disease. J.Periodontol. 1981 52:16-19.
4 Campan P., Planchand P.O., Duran D: Pilot study on n-3 polyunsaturated fatty acids in the treatment of human experimental gingivitis. J Clin Periodontol 1997 24: 907–913.
5 Hasturk H., Kantarci A., Ohira T. et al: RvE1 protects from local inflammation and osteoclast- mediated bone destruction in periodontitis. FASEB J 2006 20: 401–413.
6 Bendyk A., Marino V., Zilm P.S., Howe P., Bartold P.M: Effect of dietary omega-3 polyunsaturated fatty acids on experimental periodontitis in the mouse. J Periodontal Res 2009 44: 211–216.
7. Eberhard J., Heilmann F., Acil Y., Albers H.K., Jepsen S: Local application of n-3 or n-6 polyunsaturated fatty acids in the treatment of human experimental gingivitis. J Clin Periodontol 2002 29: 364–369.
8 Kesavalu L., Bakthavatchalu V., Rahman M.M. et al: Omega-3 fatty acid regulates inflammatory cytokine/mediator messenger RNA expression in Porphyromonas gingivalis-induced experimental periodontal disease. Oral Microbiol Immunol 2007 22: 232–239.
9 Iwasaki M, Yoshihara A, Moynihan, P.J, Watanabe R, Miyazaki H: Longitudinal relationship between dietry docosahexanoic acid and the dental condition. IADR 2009
10 C.B. Huang and J.L. Ebersole : A novel bioactivity of omega-3 polyunsaturated fatty acids and their ester derivatives. Molecular Oral Microbiology 2010 25 (1);75-80.
11 Manual of Nutrition10 Edn : Dietary reference values for fat and carbohydrate intake for adults. Table 26Pg 70 HMSO