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INDIAN JOURNAL OF APPLIED RESEARCH X 1
Volume : 3 | Issue : 10 | Oct 2013 | ISSN - 2249-555X
ReseaRch PaPeR
Medical Science
Vitamin A and Oral Health: A Review
Dr. Manu Rathee Dr. Mohneesh Bhoria Dr. Renu Kundu
Senior Professor and Head,
Department of Prosthodontics,
Post Graduate Institute of
Dental Sciences, Pt. B.D Sharma
University of Health Sciences
Rohtak, Haryana, India.
Demonstrator, Department of
Prosthodontics, Post Graduate
Institute of Dental Sciences, Pt.
B.D Sharma University of Health
Sciences Rohtak, Haryana, India.
Post Graduate Student,
Department of Prosthodontics,
Post Graduate Institute of
Dental Sciences, Pt. B.D Sharma
University of Health Sciences
Rohtak, Haryana, India.
Keywords
enamel hypoplasia, vitamin A, xerostomia
ABSTRACT The word vitamin means vital amine. Vitamin A is one of the earliest vitamins discovered and is an essential
part of the nutrients. Deficiency of Vitamin A causes night blindness, xerophthalmia, keratoconjunctivitis,
enamel hypoplasia, xerostomia, gingivitis, periodontitis and irregular dentinal tubular formation. Excess intake of Vitamin
A results in angular cheilitis. Evidence is generating regarding the use of this vital nutrient in acute promyelocytic leukemia,
oral leukoplakia and oral submucous fibrosis. This essential component must be routinely supplemented in the diet.
Introduction
The good nutritional health promotes good oral health (en-
compassing gingival tissue status, the well-being of teeth
and jaws, salivary quantity and quality and pain). On the oth-
er hand, poor nutritional status is associated with poor oral
health and vice versa. Poor oral health can affect nutritional
quality and intake in a manner that potentially increases the
risk of several systemic diseases.[1] Tooth loss can result in
chewing difficulties. Reduced chewing ability affects food se-
lection which in turn can influence the nutritional status. Pain
resulting from caries, advanced periodontal disease, soft tis-
sue lesions or poorly fitting prosthesis may affect the nutri-
tional status. Most studies relating tooth loss and nutrition
suggest that nutrient intake deteriorates in quality with fewer
teeth.[2] Research indicates that loss of natural teeth causes’
reduced masticatory efficiency even after replacement with
dentures. Among community-dwelling older adults, com-
plete tooth loss may contribute to weight loss as chewing dif-
ficulty or discomfort due to poorly fitting dentures can lead
to diminished nutrient intake. It has also been reported that
denture-wearing individuals consume more refined carbohy-
drates and dietary cholesterol than individuals with natural
dentition. Such detrimental changes in food choices may, in
turn, increase the risk of certain systemic disorders. Factors
affecting nutritional intake include the general health status
of the individual, use of alcohol, drugs and medications and
adverse habits like smoking. Ample evidence has been pre-
sented here to show that nutrition affects oral well-being and
vice versa.
Vitamin is an organic substance that occurs in food in small
amounts and is necessary for the normal metabolic function-
ing of the body. Vitamin A is the first fat soluble vitamin rec-
ognized. The precursor of Vitamin A is beta carotene which is
basically derived from plants.
Absorption and Bioavailability
Seventy to ninety percent of vitamin A from the diet is ab-
sorbed in the intestine. The efficiency of absorption for vi-
tamin A continues to be high (60-80%) as intake continues
to increase. Greater than 90% of the retinol store within the
body enters as retinyl esters that are subsequently found
within the lipid portion of the chylomicron.[3] The maximum
absorption of Vitamin A occurs two to six hours after diges-
tion. Within the intestinal lumen the vitamin is incorporated
into a micelle and absorbed across the brush border into the
intestinal luminal cells. Within the cells, precursors of vita-
min A i.e. beta carotene and other carotenoids are converted
from inactive form to its to active form. These active products
and additional precursors are then packaged into chylomi-
crons and readied for transport throughout the body.
Transport
After leaving the intestinal luminal cells, chylomicrons, which
carry retinyl esters, carotenoids and unesterified retinol along
with triglycerides, are carried first through the lymphatic sys-
tem and then through the general circulation. Upon reach-
ing extra-hepatic tissues, chylomicrons release triglycerides;
however Vitamin A is retained within the chylomicrons which
become chylomicron remnants after releasing triglycerides.
The chylomicron remnant then travels back to the liver where
it is taken up and further stored or metabolized. Whenever
required, retinol is transported from the liver and requires
the use of a carrier for transport through the blood. Retinol-
binding protein (RBP) is the specific carrier used to transport
all-trans retinol in the plasma. This specific carrier is manu-
factured and secreted by the parenchymal cells of the liver.
Each molecule of retinol released binds equivocally with RBP
to form holo-RBP. This compound is then attached to a mol-
ecule of transthyretin (TTR), formerly known as prealbumin.
This newly formed retinol-RBP-TTR complex is not filtered
by the kidney, but instead it freely circulates throughout the
plasma. Retinol is taken up by the tissues via cellular retinoid-
binding protein. Retinoic acid is believed to be manufactured
by the cells as per the requirements of the body. Hence, the
transport of retinoic acid is not substantial but instead, the
cells possess intra-cellular proteins that regulate the amount
of retinoic acid produced.
Storage
Approximately 50 to 85% of the total body retinol is stored in
the liver when vitamin A status is adequate. Retinol returning
to the liver is re-esterified before storage. Because of this,
over 90% of the retinol is stored as retinyl esters. The reti-
nol is stored in star shaped hepatic cells along with droplets
of lipid. Thus constitutes the fat-soluble property of vitamin
A.[4] With increase in retinol levels, the size of hepatic cells
increases. When threshold level is reached, the hepatic cells
get saturated with retinol and hypervitaminosis results. The
precursor to vitamin A, beta-carotene, can be stored in fat
cells of the body. The side effect of excess beta-carotene is
the yellowing of the skin. Serum levels of beta-carotene gives
an indication of recent intake and not body stores.
2 X INDIAN JOURNAL OF APPLIED RESEARCH
Volume : 3 | Issue : 10 | Oct 2013 | ISSN - 2249-555X
ReseaRch PaPeR
The kidneys are the main paths of RBP and retinol excretion
manly via renal catabolism and glomerular filtration. Those
persons suffering from renal disease often experience ele-
vated serum levels of RBP and retinol and therefore must be
more aware of vitamin A toxicity.
Vitamin A Deficiency
The major etiological factors for Vitamin A deficiency include
inadequate intake, disorders of digestion, defective absorp-
tion and alteration in metabolism and increased metabolic
demands. Vitamin A deficiency results in night blindness,
epithelial proliferation and maturation defects, hyperkeratot-
ic white patches, xerostomia, gingivitis, periodontitis, tooth
morphogenesis defects, decreased odontoblast differen-
tiation, enamel hypoplasia.[5] Retinol deficiency can reduce
mucin production which leads to compromised salivary flow
leading to weakened tooth integrity and marked increase in
risk for caries. Vitamin A deficiency also leads to irregular tu-
bular dentin formation and decreased taste sensitivity.
Vitamin A deficiency is diagnosed mainly clinically, by check-
ing blood Vitamin A levels and by seeing the response to
replacement therapy. The intake of retinol palmitate, 30 mg
peroral for two days andtreatment should encompass treat-
ment of associated malnutrition and super added infections.
Role of Vitamin A
Vitamin A plays an important role in vision, immune defens-
es, maintenance of body linings and skin, bone growth, nor-
mal cell development, reproduction, keeps mucous forming
cells from becoming keratinized, allows for differentiation
of cells, stimulates osteoclasts. Vitamin A toxicity results in
angular cheilitis, hair loss, joint pain, stunted growth, bone
and muscle soreness, nausea, diarrhea, rashes, enlargement
of liver and spleen, appetite loss, growth failure and itching
of the skin.
Safety and effectiveness have not always been proven. So,
these conditions must be evaluated by a qualified health care
provider. In acute promyelocytic leukemia, the prescription
drugs all trans- retinoic acid is a Vitamin A derivative that is
an established treatment for acute promyelocytic leukemia
and it improves median survival in this condition. Strict medi-
cal supervision is advised for these cases. Vitamin A should
not be supplemented with all trans- retinoic acid due to risk
of increased toxicity. In anemia, Vitamin A deficiency leads
to lack of mobilization of iron, impair red blood cell forma-
tion and increase susceptibility to infection. There is evidence
that Vitamin A has been shown to raise haemoglobin lev-
els and serum iron concentration particularly in children and
pregnant women. There is evidence that Vitamin A enhances
the efficacy of iron supplementation in patients with Vitamin
A deficiency and iron deficiency anaemia. Retinol is terato-
genic; the incidence of birth defects in infants is high with
vitamin A.
Vitamin A in Oral Health
Vitamin A plays an important role in measles, oral leukopla-
kia, oral submucous fibrosis, growth promotion and wound
healing in oral cavity. It is also important for immune defens-
es, maintenance of oral cavity linings, bone growth, normal
cell development, keeps mucous forming cells from becom-
ing keratinized, allows for differentiation of cells, stimulates
osteoclasts and permits normal tooth spacing.[6] Teeth are
made from protein matrix that is mineralized with collagen,
calcium and phosphorus (requires Vitamin A and D). Synthe-
sis of glycoproteins such as mucin is also a function of Vita-
min A.
Current Dietary Reference Intakes (DRI)
The Recommended Dietary Allowance (RDA) established in
1980 for vitamin A was set at 800 ug retinol equivalent (RE)
for adult women and 1000 ug (1mg) retinol equivalent (RE)
for adult men. It should be noted that 1 RE of vitamin A is
equal to 3.33 IU of the vitamin. The levels (RDA) were not
changed in 1989 when the RDAs were revised. The RDA has
also been based on the amount needed to raise the plasma
vitamin A levels to normal in depleted subjects.[7] Dietary
Reference Intakes (DRI) was developed to replace the RDA
in 2000. For vitamins, the DRI was not established. The ab-
sence of a safe upper limit plus the numerous carotenoids
has led the National Academy of Sciences to not establish
a DRI at this time. The RDA is the current dietary guideline
being used in place of the DRI. For men the RDA is 1000 mg
of retinol equivalents (RE) and for women the RDA is 800mg
of retinol equivalents.
Conclusion
Vitamin A is required for the oral health and the general
health of the body in totality and be provided in the diet.
Regular monitoring for the deficiency symptoms must be
done. Vitamin A supplements are to be included in the diet
in case the need arises.
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between specific measure of adult oral health and nutrition outcomes. Crit Rev Oral Bio Med 2002;13(3):291-300. | 2. Burt B.A. Sugar
consumption and caries risk: A systematic review. J Dent Educ 2003:65(10):1017-23. | 3. Chatterjea’s Textbook of Medical Biochemistry 8th Edition; Jaypee Brothers
Medical Publishers (P) Ltd. 2012. | 4. Groff J.L., Gropper S.S. and Hunt S.M. The fat soluble vitamin in advanced nutrition and human metabolism. J Dent Educ
1995;267-284. | 5. Shafer’s Textbook of Oral Pathology; 5th Edition; Elsevier health sciences 2005:874-9. | 6. Enwonwu C.O., Phillips R.S., Falker W.A. Jr. Nutrition
and oral infectious diseases: state of the science. Compend Cont Edu Dent 2002;23(5):431-4. | 7. Park’s Textbook of Preventive and Social Medicine 21st Edition;
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