What Role Does Nutrition Play in Dentistry?
Foods make various contributions to many areas of oral problems and growth development.
In dental caries, the frequency and consistency (and nature of) the carbohydrate taken in affects the kind of bacteria present. The more adherent the food is and the greater the fermentable carbohydrate, the greater is the opportunity to form decay.
Our diet directly affects the formation of tooth-adhering plaque, the substance produced by certain bacteria when they break carbohydrates down to polysaccharides. These by-products are not water-soluble and must be mechanically removed daily by flossing and brushing. You cannot get decay without food as tube-fed experimental animals formed no cavities even with plaque present.
In the past, attention was centered on sugar as the cause of caries. We now know that many forms of starches (e.g. potato chips) can also be a substrate for decay. In essence, a nutritionally induced predisposition to decay can be caused based on the kind of diet and the type of saliva present. In addition, the diet pre-eruptively establishes what kind of bacteria will survive as well as the size and eruption pattern of teeth, their composition and alignment, quality and amount of saliva flow. Growth occurs at different rates and phases. Proper nutrition must be present when DNA replicates itself and RNA attaches to it to form a protein. The free amino acid pool necessary for this must be derived from the protein in our diet otherwise the developing area may be smaller in size or form congenital anomalies. Experimentally in rats, a 100% incidence of cleft palates can be caused by a folic acid deficiency (not elimination) between the tenth to thirteenth days of development in utero. Protein deficiency can cause hypovitaminosis, resulting in enamel hypocalcification. Iron deficiency can result in the absence of pigment in the part of the tooth being formed, reduced or altered saliva, and increased decay susceptibility.
The oral tissues have rapid cell turnover (metabolism) and many nutritional illnesses have symptoms or are visible in the mouth. These include angular cheilosis (cracking at the corner of the lips), tongue lesions, aberrations of taste and wound healing.
These are comments I often hear when people learn that they have periodontal problems:
Is this an expected process of aging? Its onset is usually 30-35 years of age and the progress is not rapid. It is essentially a bacterial infection. Over 150 species have been isolated in the mouth of which only a small number are the causative agents. Bacteria and their by-products adhere to the tooth above and below the gingiva and harden to form calculus. This accumulation irritates and leads to gingivitis, the beginning of periodontal disease. As the disease progresses, it involves the destruction of the bone supporting the teeth. Having gingivitis doesnít mean you go on to periodontal disease. The scaling and cleaning at the dentist's not only cleans off bacteria from the teeth but also prevents the level of micro-organisms from building up once again for six weeks. This explains the success of the 2-6 month recalls, which always keeps the bacteria level off balance.
Calcium and phosphorus in the diet are related to the necessary bone support. Studies giving a minimum of 600 milligrams of calcium and 400 units of Vitamin D, showed retardation of bone loss. Magnesium is generally given with calcium. Excessive meat consumption (meat has 50 parts of phosphorus to one part calcium); processed foods and soft drinks (both of which have no calcium), contribute to low calcium/magnesium. Other nutrient factors that contribute to resisting infection are zinc, folic acid, and Vitamin C, although all nutrients are important so that you donít have to lose your teeth to periodontal disease.
Article from NOHA NEWS, Vol. XI, No. 2, Spring 1986, page 2.