Vitamin c and oral health pdf

Ascorbic acid is found in all living tissues but it must be consumed; it is not absorbed through the environment. The human body does not manufacture vitamin C. Important sources are fresh fruits and vegetables Table 1. Foods containing vitamin C should also be stored in airtight containers to prevent their early oxidation.

In humans, the absorption intake via the oral route is 3 g. Ascorbic acid is widely distributed throughout the tissues with the highest amounts found in the adrenal and pituitary glands.

Other organs, such as the liver, spleen, and brain, also contain slightly lower concentrations Table 2. The body has a saturation level of approximately 20 mg per kilogram of body weight. Thus, increasing the intake of vitamin C may be helpful during these times.

Lack of ascorbic acid results in reduced stability of connective tissue and capillary integrity. Research shows that skin, bone, and tendons are sensitive to vitamin C deficiencies.

In addition, studies have demonstrated that daily doses of 1 g to 4 g are beneficial to people who have pressure sores, ulcers, or Ehlers-Danlos syndrome type VI. A higher rate of complete or partial healing has been observed leading to improved wound healing, corneal growth, less bleeding time, muscle strength, and greater pulmonary volume. A lack of vitamin C in the diet has significant systemic and oral health effects.

Tables 3 and 4 provide lists of the most common systemic and gingival signs of vitamin C deficiency. Oral side effects can be detected as early as 60 days to 90 days on a vitamin C-deficient diet. In addition, petechiae, follicular hyperkeratosis, dryness of the mouth, loss of teeth, periodontal diseases, and disintegrating restorations are frequently noted. In periodontium and scorbutic gingivitis, adequate ascorbic acid intensively regulates the health of the periodontal ligament because of its direct relationship to collagen and its presence in the sulcular epithelial basement membrane.

Thus, the necessary amounts of vitamin C for a healthy gingiva may be greater than the recommended daily allowance. Collagen is also a significant factor when considering healthy tissue fibers in the gingival and periodontal ligament and is a major contributor to alveolar bone health.

Histological studies have also deter- mined that fibroblasts, osteoblasts, and odontoblasts that form the dentin of teeth are readily affected by a lack of vitamin C. When too little vitamin C is available, these vital cells exhibit a decrease in their orderly arrangement and little or no dentin is formed.

Without it, bone development and fractures are more likely to occur. The good news is that after consuming increased amounts of vitamin C, the body is replenished and the connective tissue begins to maintain itself again.

The recommended daily intake of vitamin C is 60 mg for adults and 45 mg for children. However, caution should be used when chewable vitamin C tablets and syrup are used because they may cause enamel erosion and dentin hypersensitivity. Contributing factors may include drugs steroids, antibiotics, and salicylates , alcohol, and tobacco. This is particularly important because post-surgical collagen is being laid down during the healing phase.

A lingual vitamin C test is available to assist with the treatment planning of patients. It involves the application of a blue dye on the tongue and then timing how long it takes the dye to disappear. The dye is a complex compound dichloroindophenol sodium salt and undergoes discoloration when in contact with vitamin C.

Vitamin C is needed in the normal metabolism of tissue cells, including the fungiform papillae and supporting tissue, which assist in the dental application of this screening test. Dietary assessment and counseling are important facets of treatment planning. In body tissues and fluids, the concentrations of the vitamin C are maintained by interplay between absorption from intestine, cellular transport and excretion. Very small amount of vitamin C is needed to prevent scurvy.

Evidence has shown that oxidative damage is a root cause of or at least associated with many diseases, the clinical role of vitamin C becomes very important.

Although clinical trials have not confirmed this, but still vitamin C may prove to be effective in people with certain diseases or conditions.

However, the evidence that ascorbic acid acts as an important antioxidant in many body tissues is convincing. In healthy individuals, amounts taken greater than the RDA are not helpful. Introduction tective action on enzymes such as p-hydroxyphenylpyruvic Vitamin C or L-ascorbic acid, or simply ascorbate the anion acid oxidase. Vitamin C consists of At the tissue structural level vitamin C is involved with the a number of vitamers that have vitamin C activity in animals synthesis of intercellular substances and the collagen fibres including ascorbic acid and its salts and many oxidized forms of various forms of the connective tissues in which collagen of the molecule like dehydro-ascorbic acid.

In at least eight enzymatic reactions, Vita- lar system, including capillaries. When these synthetic reactions become dysfunctional, In a normal adult man of 70 kg mass and with a vitamin C they cause the most severe symptoms of scurvy1.

This can be caused Ascorbate may also act as an antioxidant agent. The enanti- by a reduction of 45 mg vitamin C per day for 60 days on a vi- omer D-Ascorbate, which is not found in nature, has identical tamin C-free diet. Scurvy is an avitaminosis resulting from lack antioxidant activity to L-Ascorbate but very less vitamin activ- of vitamin C, because without this vitamin, the synthesized ity.

Ascorbic acid is a weak sugar acid which is structurally collagen is very unstable to perform its normal function. The spots are more abundant on thighs and legs; the person looks pale, feels depressed and is partially Biological significance immobilized. In advanced stages of scurvy, there are open, The biological role of ascorbate is to act as a reducing agent suppurating wounds, loss of teeth and eventually, death.

Gingivitis is not caused by vitamin C deficiency per se, Thus, the presence of glutathione in cells and extracellular but if the gingivitis exists in a scorbutic patient it seems to be fluids helps maintain ascorbate in a reduced state. The legendary association of severe gingival disease with scurvy led to the incorrect presumption Vitamin C and oral health that vitamin C deficiency is a primary factor in the causation Vitamin C has diverse functions in the body at a chemical of gingivitis and periodontal disease.

It is now believed that and structural level. For example, a major function of ascor- blood ascorbic acid levels bear no relationship to the inci- bic acid is its involvement in the synthesis of collagen fibres dence or severity of gingivitis or periodontal disease in non- from proline via hydroxyproline. Other metabolic reactions scorbutic patients. Furthermore, vitamin C deficiency does for which vitamin C is required are the hydroxylation of lysine not cause periodontal pockets; local irritating factors are re- into hydroxylysine in collagen, the conversion of folic acid to quired for pocket formation to occur.

The intake of citrus fruits such as grape- weakness with lack of connective tissue support of the capil- fruit leads to an increase in plasma levels of vitamin C and im- lary walls. This vascular fragility leads to a bleeding tendency proved scores for sulcus bleeding index. However, long term which produces petechiae and ecchymoses and is confirmed studies are required to determine whether other periodontal by a positive Hess test.

Haematuria, epistaxis, subperiosteal bleeding, haemarthrosis and bleeding into muscles and deeper tissues also occur. Vitamin C is also an important physiological antioxidant [ 3 ] and has been shown to regenerate other antioxidants within the body, including alpha-tocopherol vitamin E [ 4 ]. Ongoing research is examining whether vitamin C, by limiting the damaging effects of free radicals through its antioxidant activity, might help prevent or delay the development of certain cancers, cardiovascular disease, and other diseases in which oxidative stress plays a causal role.

In addition to its biosynthetic and antioxidant functions, vitamin C plays an important role in immune function [ 4 ] and improves the absorption of nonheme iron [ 5 ], the form of iron present in plant-based foods. Insufficient vitamin C intake causes scurvy, which is characterized by fatigue or lassitude, widespread connective tissue weakness, and capillary fragility [ 1 , 2 , 4 , ].

The intestinal absorption of vitamin C is regulated by at least one specific dose-dependent, active transporter [ 4 ]. Cells accumulate vitamin C via a second specific transport protein. In vitro studies have found that oxidized vitamin C, or dehydroascorbic acid, enters cells via some facilitated glucose transporters and is then reduced internally to ascorbic acid. The physiologic importance of dehydroascorbic acid uptake and its contribution to overall vitamin C economy is unknown.

Oral vitamin C produces tissue and plasma concentrations that the body tightly controls. Results from pharmacokinetic studies indicate that oral doses of 1. The total body content of vitamin C ranges from mg at near scurvy to about 2 g [ 4 ]. High levels of vitamin C millimolar concentrations are maintained in cells and tissues, and are highest in leukocytes white blood cells , eyes, adrenal glands, pituitary gland, and brain.

Relatively low levels of vitamin C micromolar concentrations are found in extracellular fluids, such as plasma, red blood cells, and saliva [ 4 ]. DRI is the general term for a set of reference values used for planning and assessing nutrient intakes of healthy people. These values, which vary by age and gender [ 8 ], include:.

Table 1 lists the current RDAs for vitamin C [ 8 ]. The RDAs for vitamin C are based on its known physiological and antioxidant functions in white blood cells and are much higher than the amount required for protection from deficiency [ 4 , 8 , 11 ]. For infants from birth to 12 months, the FNB established an AI for vitamin C that is equivalent to the mean intake of vitamin C in healthy, breastfed infants.

Fruits and vegetables are the best sources of vitamin C see Table 2 [ 12 ]. Citrus fruits, tomatoes and tomato juice, and potatoes are major contributors of vitamin C to the American diet [ 8 ].

Other good food sources include red and green peppers, kiwifruit, broccoli, strawberries, Brussels sprouts, and cantaloupe see Table 2 [ 8 , 12 ]. Although vitamin C is not naturally present in grains, it is added to some fortified breakfast cereals. The vitamin C content of food may be reduced by prolonged storage and by cooking because ascorbic acid is water soluble and is destroyed by heat [ 6 , 8 ]. Steaming or microwaving may lessen cooking losses.

Fortunately, many of the best food sources of vitamin C, such as fruits and vegetables, are usually consumed raw. Consuming five varied servings of fruits and vegetables a day can provide more than mg of vitamin C. The U. Food and Drug Administration FDA developed DVs to help consumers compare the nutrient contents of foods and dietary supplements within the context of a total diet. The DV for vitamin C is 90 mg for adults and children age 4 years and older [ 13 ].

FDA does not require food labels to list vitamin C content unless vitamin C has been added to the food. Department of Agriculture's USDA's FoodData Central lists the nutrient content of many foods and provides a comprehensive list of foods containing vitamin C arranged by nutrient content and by food name.

Supplements typically contain vitamin C in the form of ascorbic acid, which has equivalent bioavailability to that of naturally occurring ascorbic acid in foods, such as orange juice and broccoli [ ]. A few studies in humans have examined whether bioavailability differs among the various forms of vitamin C. These findings, coupled with the relatively low cost of ascorbic acid, led the authors to conclude that simple ascorbic acid is the preferred source of supplemental vitamin C [ 17 ].

Mean intakes for children and adolescents aged years range from Although the — NHANES analysis did not include data for breastfed infants and toddlers, breastmilk is considered an adequate source of vitamin C [ 8 , 14 ]. Use of vitamin C-containing supplements is also relatively common, adding to the total vitamin C intake from food and beverages. Vitamin C status is typically assessed by measuring plasma vitamin C levels [ 4 , 14 ]. Other measures, such as leukocyte vitamin C concentration, could be more accurate indicators of tissue vitamin C levels, but they are more difficult to assess and the results are not always reliable [ 4 , 9 , 14 ].

Acute vitamin C deficiency leads to scurvy [ 7 , 8 , 11 ]. Initial symptoms can include fatigue probably the result of impaired carnitine biosynthesis , malaise, and inflammation of the gums [ 4 , 11 ].

As vitamin C deficiency progresses, collagen synthesis becomes impaired and connective tissues become weakened, causing petechiae, ecchymoses, purpura, joint pain, poor wound healing, hyperkeratosis, and corkscrew hairs [ 1 , 2 , 4 , ]. Additional signs of scurvy include depression as well as swollen, bleeding gums and loosening or loss of teeth due to tissue and capillary fragility [ 6 , 8 , 9 ].

Iron deficiency anemia can also occur due to increased bleeding and decreased nonheme iron absorption secondary to low vitamin C intake [ 6 , 11 ]. In children, bone disease can be present [ 6 ]. Left untreated, scurvy is fatal [ 6 , 9 ]. Until the end of the 18 th century, many sailors who ventured on long ocean voyages, with little or no vitamin C intake, contracted or died from scurvy.

During the mids, Sir James Lind, a British Navy surgeon, conducted experiments and determined that eating citrus fruits or juices could cure scurvy, although scientists did not prove that ascorbic acid was the active component until [ ].

Today, vitamin C deficiency and scurvy are rare in developed countries [ 8 ]. Vitamin C deficiency is uncommon in developed countries but can still occur in people with limited food variety. The following groups are more likely than others to be at risk of obtaining insufficient amounts of vitamin C. Studies consistently show that smokers have lower plasma and leukocyte vitamin C levels than nonsmokers, due in part to increased oxidative stress [ 8 ].

For this reason, the IOM concluded that smokers need 35 mg more vitamin C per day than nonsmokers [ 8 ]. Exposure to secondhand smoke also decreases vitamin C levels.

Although the IOM was unable to establish a specific vitamin C requirement for nonsmokers who are regularly exposed to secondhand smoke, these individuals should ensure that they meet the RDA for vitamin C [ 4 , 8 ].

For many reasons, feeding infants evaporated or boiled cow's milk is not recommended. This practice can cause vitamin C deficiency because cow's milk naturally has very little vitamin C and heat can destroy vitamin C [ 6 , 12 ]. Although fruits and vegetables are the best sources of vitamin C, many other foods have small amounts of this nutrient. Thus, through a varied diet, most people should be able to meet the vitamin C RDA or at least obtain enough to prevent scurvy.

People who have limited food variety—including some elderly, indigent individuals who prepare their own food; people who abuse alcohol or drugs; food faddists; people with mental illness; and, occasionally, children—might not obtain sufficient vitamin C [ 4 , , 11 ].

People with severe intestinal malabsorption or cachexia and some cancer patients might be at increased risk of vitamin C inadequacy [ 27 ]. Low vitamin C concentrations can also occur in patients with end-stage renal disease on chronic hemodialysis [ 28 ].

This section focuses on four diseases and disorders in which vitamin C might play a role: cancer including prevention and treatment , cardiovascular disease, age-related macular degeneration AMD and cataracts, and the common cold.

Epidemiologic evidence suggests that higher consumption of fruits and vegetables is associated with lower risk of most types of cancer, perhaps, in part, due to their high vitamin C content [ 1 , 2 ].

Vitamin C can limit the formation of carcinogens, such as nitrosamines [ 2 , 29 ], in vivo; modulate immune response [ 2 , 4 ]; and, through its antioxidant function, possibly attenuate oxidative damage that can lead to cancer [ 1 ]. Most case-control studies have found an inverse association between dietary vitamin C intake and cancers of the lung, breast, colon or rectum, stomach, oral cavity, larynx or pharynx, and esophagus [ 2 , 4 ].

Plasma concentrations of vitamin C are also lower in people with cancer than controls [ 2 ]. However, evidence from prospective cohort studies is inconsistent, possibly due to varying intakes of vitamin C among studies.

Evidence from most randomized clinical trials suggests that vitamin C supplementation, usually in combination with other micronutrients, does not affect cancer risk.

MAX study, a randomized, double-blind, placebo-controlled clinical trial,13, healthy French adults received antioxidant supplementation with mg ascorbic acid, 30 mg vitamin E, 6 mg beta-carotene, mcg selenium, and 20 mg zinc, or placebo [ 33 ].

After a median follow-up time of 7. In addition, baseline antioxidant status was related to cancer risk in men, but not in women [ 34 ].

Similar findings were reported in women participating in the Women's Antioxidant Cardiovascular Study [ 36 ].

In a large intervention trial conducted in Linxian, China, daily supplements of vitamin C mg plus molybdenum 30 mcg for 5—6 years did not significantly affect the risk of developing esophageal or gastric cancer [ 37 ]. Moreover, during 10 years of follow-up, this supplementation regimen failed to significantly affect total morbidity or mortality from esophageal, gastric, or other cancers [ 38 ]. A review of vitamin C and other antioxidant supplements for the prevention of gastrointestinal cancers found no convincing evidence that vitamin C or beta-carotene, vitamin A, or vitamin E prevents gastrointestinal cancers [ 39 ].

A similar review by Coulter and colleagues found that vitamin C supplementation, in combination with vitamin E, had no significant effect on death risk due to cancer in healthy individuals [ 40 ]. At this time, the evidence is inconsistent on whether dietary vitamin C intake affects cancer risk.

Results from most clinical trials suggest that modest vitamin C supplementation alone or with other nutrients offers no benefit in the prevention of cancer. A substantial limitation in interpreting many of these studies is that investigators did not measure vitamin C concentrations before or after supplementation. Plasma and tissue concentrations of vitamin C are tightly controlled in humans.

At daily intakes of mg or higher, cells appear to be saturated and at intakes of at least mg, plasma concentrations increase only marginally [ 2 , 10 , 22 , 31 , 37 ]. If subjects' vitamin C levels were already close to saturation at study entry, supplementation would be expected to have made little or no difference on measured outcomes [ 22 , 23 , 41 , 42 ].

During the s, studies by Cameron, Campbell, and Pauling suggested that high-dose vitamin C has beneficial effects on quality of life and survival time in patients with terminal cancer [ 43 , 44 ]. However, some subsequent studies—including a randomized, double-blind, placebo-controlled clinical trial by Moertel and colleagues at the Mayo Clinic [ 45 ]—did not support these findings. The authors of a review assessing the effects of vitamin C in patients with advanced cancer concluded that vitamin C confers no significant mortality benefit [ 40 ].

Emerging research suggests that the route of vitamin C administration intravenous vs. Most intervention trials, including the one conducted by Moertel and colleagues, used only oral administration, whereas Cameron and colleagues used a combination of oral and intravenous IV administration. Concentrations of this magnitude are selectively cytotoxic to tumor cells in vitro [ 1 , 67 ]. Research in mice suggests that pharmacologic doses of IV vitamin C might show promise in treating otherwise difficult-to-treat tumors [ 49 ].

A high concentration of vitamin C may act as a pro-oxidant and generate hydrogen peroxide that has selective toxicity toward cancer cells [ ]. Based on these findings and a few case reports of patients with advanced cancers who had remarkably long survival times following administration of high-dose IV vitamin C, some researchers support reassessment of the use of high-dose IV vitamin C as a drug to treat cancer [ 3 , 47 , 49 , 52 ].

Therefore, individuals undergoing these procedures should consult with their oncologist prior to taking vitamin C or other antioxidant supplements, especially in high doses [ 54 ]. Evidence from many epidemiological studies suggests that high intakes of fruits and vegetables are associated with a reduced risk of cardiovascular disease [ 1 , 55 , 56 ]. This association might be partly attributable to the antioxidant content of these foods because oxidative damage, including oxidative modification of low-density lipoproteins, is a major cause of cardiovascular disease [ 1 , 4 , 56 ].

In addition to its antioxidant properties, vitamin C has been shown to reduce monocyte adherence to the endothelium, improve endothelium-dependent nitric oxide production and vasodilation, and reduce vascular smooth-muscle-cell apoptosis, which prevents plaque instability in atherosclerosis [ 2 , 57 ].

Results from prospective studies examining associations between vitamin C intake and cardiovascular disease risk are conflicting [ 56 ].

In the Nurses' Health Study, a year prospective study involving 85, female nurses, total intake of vitamin C from both dietary and supplemental sources was inversely associated with coronary heart disease risk [ 58 ]. However, intake of vitamin C from diet alone showed no significant associations, suggesting that vitamin C supplement users might be at lower risk of coronary heart disease.

In male physicians participating in the Physicians' Health Study, use of vitamin C supplements for a mean of 5. The authors of a meta-analysis of prospective cohort studies, including 14 studies reporting on vitamin C for a median follow-up of 10 years, concluded that dietary, but not supplemental, intake of vitamin C is inversely associated with coronary heart disease risk [ 55 ].

Results from most clinical intervention trials have failed to show a beneficial effect of vitamin C supplementation on the primary or secondary prevention of cardiovascular disease.

Other clinical trials have generally examined the effects on cardiovascular disease of supplements combining vitamin C with other antioxidants, such as vitamin E and beta-carotene, making it more difficult to isolate the potential contribution of vitamin C. The SU. The authors of a meta-analysis of randomized controlled trials concluded that antioxidant supplements vitamins C and E and beta-carotene or selenium do not affect the progression of atherosclerosis [ 66 ].

Similarly, a systematic review of vitamin C's effects on the prevention and treatment of cardiovascular disease found that vitamin C did not have favorable effects on cardiovascular disease prevention [ 67 ]. Since then, researchers have published follow-up data from the Linxian trial, a population nutrition intervention trial conducted in China [ 38 ]. Although the Linxian trial data suggest a possible benefit, overall, the findings from most intervention trials do not provide convincing evidence that vitamin C supplements provide protection against cardiovascular disease or reduce its morbidity or mortality.