The Well Balanced Healthy Diet Systemic Implications on Oral Health

The food supplement industry is becoming one of the fastest growing industries in this country. According to figures from industry analysts Euromonitor, sales of vitamins and dietary supplements alone increased by 55% between 1994 and 1998. The total amount spent by Britons on food supplements in 1998 was £358.4 million, (with oral hygiene expenditure trailing in at £8.2m).

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The Department of Health (DoH) insists that the well-balanced healthy diet provides all the vitamins and minerals we need, and that supplementation is unnecessary. On the other hand the 1995 MAFF Food Survey (1) provides startling evidence that dietary micronutrient intake is falling in the UK with deficiencies for almost all micronutrients.  This becomes of particular concern when we consider that RNI’s are not optimum levels of nutrients, but rather levels that prevent overt deficiency. These figures to some degree may also be reflected in our patients.

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Whatever our feelings on supplementation, if we take the DoH guidelines as our yardstick we are left with the conclusion that “the well balanced healthy diet” is simply not being achieved. The relevance of this to us as dental professionals becomes apparent on consideration of the biochemical and physiological importance of specific micronutrients in the regulation of cellular and humoral response indicated in the defence against bacterial colonisation, and the endocrine system in its regulation of Ca+ homeostasis. Can we therefore provide our patients with more specific dietary advice than “the well balanced healthy diet”? We are only too aware of the role diet plays in dental caries and enamel erosion, but are we fully aware of the possible dietary implications in the progression of periodontal disease and alveolar bone loss?

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Nutrition and Periodontal Disease

Periodontal disease is not a nutritional deficiency disease. For the majority of our patients variations in plaque levels provide the most significant determinant of the disease. Inadequate nutrition, however, could either predispose the host to the disease, or modify the progression of a pre-existing disease.
Targets for nutritional deficiencies could include the epithelial barrier and attachment, gingival connective tissue, alveolar bone and the periodontal ligament. All these, together with the rapid rate of protein synthesis required for cells with a rapid turnover, are potential targets of nutritional deficiencies (2).

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Carbohydrates

Of the macro nutrients, evidence of the effect of refined carbohydrates in the progression of periodontal disease is mixed. There is very little evidence showing a direct effect of carbohydrates per se on the periodontal ligament. More recent trials suggest refined sugar may hasten the development of gingivitis, however, sugar avoidance fails to protect against the development of the disease (3).

From a general health point of view, and certainly as regards caries , refined carbohydrates still pose a significant risk. Whatever the out come, the fact remains that refined carbohydrates are denatured, nutrient poor foods. The recommendation therefore, to avoid refined, denatured foods in favour of complex, nutrient rich carbohydrate sources, provides valid guidance.
 
Protein

Protein can often be a two edged sword. One of the principal consequences of protein deficiency is an increased susceptibility to infection. In addition depressed immunoglobulin A (IgA) in saliva, complement protein, phagocytic function, interleukin-1 secretion from monocytes and T-cell mediated responses all may facilitate oral infection, peridontitis and alveolar bone loss.

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On the other side of the coin excess protein can have a deleterious effect on calcium homeostasis in bone.
The World Health Organisation recommends that only 0.5 grams per kilo of body weight is needed. Therefore an 11 stone person needs about 35g of protein per day. The average western diet contains between 60 and 150g of protein per day. Excess protein is catabolised and the waste products are excreted in the urine. The renal excretion of protein waste products namely nitrogen compounds, increases the urinary excretion of calcium. Recent study has suggested that excess protein reduces bone density and is associated with increased fracture risk in women who consume more than 95g per day . (4,5) The recommendation therefore is to ensure adequate protein for repair and maintenance but to avoid excess. Varying choices of protein with more vegetarian sources is also recommended , as this appears to have less effect on bone mineral density.(6)

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Fats and Prostaglandins

When is a fat not a fat? When it’s an essential fatty acid (EFA). Most 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. Growing animals who are totally deprived of essential fatty acids (EFA’s), show a range of symptoms(7). Amongst the main ones are:

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1) Poor wound healing due to failure of connective tissue.
2) Loss of membrane integrity, in particular the skin.
3) Impaired immune function and increased host susceptibility.

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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 knownmediators 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 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 metabolites of AA are released into gingival tissue in esponse to tissue damage, which in the progression of periodontal disease is caused by bacterial plaque.

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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. (8,9) Whilst it is by no means certain that EFA’s may help prevent periodontal disease, it is easy to see how a deficiency may modify the host’s response to bacterial plaque.

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Recommended food sources include nuts, seeds, oily fish, avocados.  EFA deficiency symptoms may include: Dry, cracked lips, dry skin and poor wound healing,

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Calcium Metabolism and Bone.

The effect of calcium in bone density is well documented. Adequate calcium intake is important to attain peak bone mass and oppose age related bone loss. Magnesium is an important co-factor involved in the enzyme regulated process ofCa+ absorption into hydroxyapitite crystals. The ideal Ca:Mg ratio is 2:1. Calcium rich foods, therefore may not always the best choice. Milk for example has a Ca:Mg ratio of 8:1. The best Ca:Mg ratio appears to be found in whole grains, dark green vegetables, nuts and seeds. Sea plants are also rich in calcium and magnesium.

The other important part of the equation is of course vitamin D, recommended food sources are found in oily fish, milk, butter and egg yolks.

Calcium and magnesium deficiency symptoms may include: Muscle cramps or spasms, high blood pressure and irregular heart beat.

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Phosphorus.

Phosphorous is the second most prevalent mineral in bones. Phosphate is an important part of cellular membranes and plays a role in membrane permeability and integrity. The parathyroid gland regulates plasma phosphate levels and the rate of phosphate excretion from the kidneys. In bone formation phosphorus to calcium ratios are important. Calcium and phosphates initially combine as tricalcium phosphate which is converted to crystalline hydroxyapatite.

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[Ca3(Po4)2,Ca(OH)2.] If phosphorous is high, relative to calcium, osteoclasts increase in size number and activity in response to PTH, leading to enhanced osteoclast activity and increased bone resorption. Although adequate phosphorous is needed to maintain healthy bone, an excess relative to calcium can lead to bone loss. . Phosphorous deficiency in the diet is rare, particularly in western diets, it is also well absorbed at 70%. The largest probable source of phosphates in the western diet are carbonated drinks which often have phosphate buffers. The average intake of soft drinks in the West has risen from 8-12 cans per week, with women and children being the main consumers. As a rule the western diet contains more phosphorous than the ideal calcium to phosphorous ratio of 1.5:1.

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It is recommended that carbonated drinks, including carbonated water and especially colas which also contain caffeine are avoided. Bear in mind too that many smoked, spiced and processed meats, fish and poultry may also contain phosphorous.

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Micronutrients.

Vitamin A.

Vitamin A is important in the synthesis of connective tissue and the collagen matrix of cartilage and bone . It is normally produced intracellularly by metabolism of betacarotene. Vitamin A acts on cells which have both a rapid turnover and potential to differentiate in more than one direction (10). It is, therefore, particularly indicated in the maintenance and integrity of mucus membrane. The importance of vitamin A as retinol in oral health is its involvement in the synthesis of proteoglycans, the expression of fibronectin and Type I procollagen and epithelial tissue differentiation. A deficiency, therefore can affect epithelial tissue and bone formation and maintenance. Lack of vitamin A can also cause decreased salivary flow and hyperplasia of the gingival epithelium. Deficiency symptoms may include: Apthous ulceration, Acne and dry, flaky skin.

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Vitamin C

Vitamin C contributes to the integrity of fibroblasts, osteoblasts (11), chondroblasts, and odontoblasts (12). It plays a key role as a reducing substance in the synthesis of collagen, which is the main organic component of extracellular matrices of many tissues, and bone. Without vitamin C for collagen synthesis , connective tissue formation and maintenance, wound healing, and scar tissue formation would all be adversely affected. Because collagen is the essential organic matrix necessary for the deposition of calcium phosphate crystals during bone formation, a deficiency in vitamin C will also affect bone formation.

Vitamin C is also involved in the immune response, it is involved in phagocytosis and can increase the resistance of tissues to infection. It is of importance therefore to monitor the vitamin C status of those at risk( smokers, diabetics) in view of the clinical evidence that now exists that vitamin C improves host defence mechanisms.(13) Deficiency symptoms may include: Easy bruising, frequent colds or infections, nose bleeds and slow wound healing.

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Zinc.

Zinc is an essential trace element of significant biological importance inclusive of cell membrane integrity, epithelial cell turnover ,connective tissue and immune system regulation(14). Studies show Zinc (Zn) deficiency leads to T-cell depletion, phagocytic activity is lowered, and sulcular epithelial permeability is increased(15). It has been concluded that Zn deficiency may cause oxidative damage to membranes.

Polenik et al (16) has shown significantly depressed levels of serum Zn in patients with periodontal disease, and a positive therapeutic effect of orally administered zinc sulphate in patients with periodontitis.
Deficiency symptoms may include : White marks on more than two finger nails, Acne and /or pale skin. Poor sense of taste or smell. 

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The MAFF survey highlights that one third of the adult population in the UK do not receive adequate vitamin A. It is also of concern that over ¼ of adult men and 34% of women do not receive adequate vitamin C from their diet. The MAFF survey also found that calcium intakes were generally insufficient with 48% of women consuming inadequate levels. That 71% of female teenagers (16-18yrs) (17) fail to consume adequate calcium from the diet is of particular concern, as peak bone mass is determined during adolescence. That magnesium intake has declined during the past few decades is borne out by the finding that 72% adult women and 42% of men receive inadequate amounts. An alarming 89% of UK female teenagers (16-19yrs) (17) do not receive the RNI for this dietary constituent.

In encouraging our patients to adopt a “well balanced healthy diet”, therefore, it is clear that specific food choices are needed to facilitate more efficient absorption and utilisation of the micro-nutrients implicated in bone density and immune function. Nutritional medicine is being hailed by many as the medicine of the future. We as healthcare professionals are in a position to dispense valuable nutritional advice. So next time our patients ask us for nutritional advice, let’s not just resort to “the well balanced healthy diet”.

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References

1. MAFF National Food Survey: Annual report on food expenditure, consumption and nutrient intakes. HMSO. London . UK . 1995.
2. Speirs, R.L., Beeley,J.A.,: Food and Oral Health:2. Periodontium and Oral Mucosa. Dental Update pg 161-167. May 1992.
3. Gaengler,P. et al. The effecte of carbohydrate reduced diet on development of gingivitis. Clin.Preven. Dent. 8(6):17-23. 1986
4. Anderson ,J.J., Ronano,P., Holmes,A: Roles of Diet and Physical Activity in the Prevention of Osteoporosis. Sand. J.Rheum.Suppl. 103:65-74. 1996
5. Protein Consumption and Bone Fractures in Women. Am.J.Epidemiol. 143(5):472-9. 1996.
6. Allolio,B: Osteoporosis and Nutrition. Artzl. Fortbild. ( Jena ) 90:(1):19-24. Feb. 1996.
7. Horrobin, D.F.: Prostaglandins: physiology,pharmacology, and clinical significance. Montreal ; Eden Press. 1978
8. Goodson,J.M., Dewhirst,F.C., Brunetti,A: Prostagandin E2 Levels and human periodontal disease. Prostaglandins 6:81-85. 1974.
9. El-Attar,T.M.A., Lin,H.S: Prostaglandins in gingivae of patients with periodontal disease. J.Periodontol. 52:16-19. 1981.
10. Zile, M.H., Cullum , M.E. : The function of Vitamin A; current concepts. Proc. Soc. Exp. Biol. Med. 172:139-152. 1983.
11. Dixon., S.J., Wilson , J.X.: Adaptive regulation of ascorbate transport in osteoblast cells. J. Bone Miner. Res. 7(6) :675-681. 1992.
12. Pollack, R.L., Kravitz,E.: Nutrition in oral health and disease. Philadelphia , Lea& Ferbiger , pp 141-142, 174-175, 207, 407. 1985.
13. Rubinoff, A.B., Latner, P.A., Pasut, L.A. ,: Vitamin C and Oral Health. J.Can. Dent. Assoc. 55(9): 705-7. 1989
14. Allen,J.L.,Perri,R.T.,McClain,C.J.,Kay, N.E: Alterations in human natural killer activity and monocyte cytotoxicity induced by zinc deficiency. J.Lab.Clin.Med. 102: 577. 1983.
15. Speirs, R.L., Beeley, J.A: Food and Oral Health:2. Periodontium and Oral Mucosa. Preven.Dent. Dent Update. 161-167. May 1992.
16. Polenik.,P. : Zinc in the aetiology of periodontal disease. Medical Hypotheses 40: 182-185. 1993.
17. MAFF: The dietary and nutritional survey of British Adults – further analysis. HMSO London UK