CONTENTS
• Introduction
• History
• Classification
• Individual vitamins
• Public health importance
• Conclusion
• Other relavent publications
• References
Intoduction
• “vitamins have been defined as organic
compounds which are required in minute
amounts to maintain normal health of
organisms’.
A Short History of Vitamins
o From about 1500 BC it
was known that various
diseases could be treated
with specific foods.
o In 1880 Christian Eijkman
produced vitamin-deficiency
conditions in animals on an
experimental basis and then
reversed the condition with
an appropriate feeding
regimen.
VITAMINS
Fat Soluble Water Soluble
B-Complex Non B-ComplexVitamin A
Vitamin D
Vitamin E
Vitamin K
Thiamine (B1)
Riboflavin (B2)
Niacin (B3)
Pyridoxine(B6)
Biotin (B7)
Pantothenic acid(B5)
Energy-releasing Hematopoitic
Folic acid (B9)
Vitamin B12
(cyanocobalamin)
Vitamin C
Vitamin-A
VITAMIN - A :- Is widely distributed in animal
and plant foods
animals –pre-formed – Retinol.
plants – pro-formed - carotene
Vitamin-A……
Dietary sources of vitamin A
7
PRE-FORM VITAMIN A :
meat, liver & dairy products
PRO-FORM VITAMIN A :
Yellow, red and green vegetables
and fruits
Vitamin-A……
Recommended dietary allowance :
Men and women – 600 mcg. Per day
Pregnancy and lactation – 950 mcg. Per day
Infants – 350 mcg. Per day
Children – 600 mcg. Per day
Vitamin-A……
Absorption and storage:
The liver has enoromous capacity
to store – in the form of retinol
palmitate.
under normal conditions a well-fed
person has sufficient Vitamin A
reserves to meet his need for 6 to 9
months or more.
Free retinol is highly active but
toxic & therefore transported in
blood stream in combination with
retinol binding protein (liver)
The signs of vitamin A deficiency
Ocular
Night blindness.
Conjunctival xerosis
Bitot’s spot
Corneal xerosis
keratomalacia
Extra ocular
Retarded growth
Skin disorders
Effect on reproductive
organs.
Effect on bone
14
Hyper Vitaminosis A
If the daily dose > 30,000 mcg
toxic symptoms:-
painful joint
thickening of long bones.
anorexia
low grade fever
rashes
irregular menstruation
fatigue.
loss of hair
15
ORAL MANIFESTATION OF VITAMIN A
DEFICIENCY
Teeth – vitamin A deficiency leads to defective
formation of enamel.
Hypoplasia of teeth – since enamel forming cells
are disturbed.
Dentin – lacks the normal tubular structure.
Caries – there is increased risk for caries
Eruption – delayed in prolonged deficiency.
16
Alveolar bone – retarted in its rate of formation.
Gingiva – gingival epithelium becomes hyperplastic, in
prolonged deficiency it shows keratinization.
Periodontal disease – tissue is easily invaded by
bacteria that may cause periodontal disease.
Salivary gland – undergo typical keratinizing metaplasia
17
TREATMENT
vitamin deficiency should be treated urgently .
depending upon deficiency symptoms it is given in the
dose of 7,500 to 15,000 mcg per day for one month
nearly all of the early stages of xerophthalmia can be
reversed by administration of a massive dose – 2,00000
IU or 110mg orally on two successive days.
If Hypervitaminosis restriction of diet
Prevalence
• World bank (2007) : Prevalence of vitamin A
deficiency (VAD) Prevalence of clinical and sub
clinical vitamin A deficiency in India is among
the highest in the world. Though prevalence of
clinical vitamin A deficiency is less than 1% in
India, biochemical subclinical deficiency is quite
high.
Massive dose vitamin A programme in India
The National Prophylaxis Programme against
Nutritional Blindness due to Vitamin A
Deficiency (NPPNB ) was initiated in 1970 with
the specific aim of preventing nutritional
blindness due to keratomalacia
• In 1994, under the National Child Survival and Safe
Motherhood (CSSM) Programme, the NPPNB due to
VAD was modified keeping in view of the vulnerability
of VA deficiency in young children. The age group of
eligible children for coverage was restricted to 9 to 36
months of age
• In 2006, the age group of eligible children was revised
as 6-59 months. This was done after reconsidering the
recommendations of WHO, UNICEF and Ministry of
Women and Child Development.
VITAMIN - D
It is also called SUNSHINE VITAMIN.
It is available in 2 forms
D3 – cholecalciferol
D2 - calciferol
24
Dietary Sources of Vitamin D
Good sources of vitamin
D include fatty fish, fish
liver oils, egg yolk etc.,
In a natural way ,
exposure of skin to
sunlight synthesizes
vitamin D
25
Chemical origins of vitamin D
Precursors of vitamin D are found in both yeast and animal
tissues. In yeast, a sterol precursor (ergosterol) is converted to
vitamin D2 (ergocalciferol). Ergocalciferol is the compound
most commonly found as the additive to fortify milk.
In the dermal tissue of animals, the precursor is 7-
dehydrocholesterol which is converted first to a pre-vitamin D3,
then to vitamin D3 (cholecalciferol).
Vitamin D2 and vitamin D3 are both converted to similar active
compounds (calcidiol and calcitriol) in the liver and kidney. D2
and D3 are sometimes referred to as vitamers.
26
Recommended dietary allowance of
Vitamin D:
The daily requirement of vitamin-D is 400
International Units of cholecalciferol. In countries
with good sunlight(like India), RDA for vitamin D Is
200 international units per day
27
Absorption and Storage of vitamin- D
This depends upon the source of the vitamin D.
Vitamin D that is taken into the gut (vitamin D-
containing foods or nutritional supplements) are
absorbed by intestinal mucosal cells in the duodenum
and jejunum and packaged into lipoproteins called
chylomicrons (CM). The CM carry the vitamin to the
liver or adipose for storage and eventual use.
Vitamin D synthesized in skin through the action of
sunlight is bound to a blood protein called (vitamin) D
binding protein (DBP), which transports it to the liver.
Biochemical functions of vitamin-D
• It regulates the plasma levels of calcium and
phosphate . Calcitrol acts at 3 different levels to
maintain plasma calcium(normal 9-11mg/dl)
Action of calcitriol on intestine
Action of calcitriol on bone
Action of calcitriol on kidney
30
Vitamin D - Deficiency
RICKETS Children's
OSTEOMALACIA Adults
Increase the risk of Osteoporosis
31
Rickets
The term is derived from the old
English word for "twist," or "wrick,“
Rickets is caused by a deficiency in
vitamin D. During growth, human
bone is made and maintained by the
interaction of calcium,
phosphorus, and vitamin D.
Calcium is deposited in immature
bone (osteoid) in a process called
calcification, which transforms
immature bone into its mature and
familiar form.
Osteomalacia
it is also known as adult rickets and flat bones and
diaphysis of long bones are affected
it is most commonly seen in post menopause female
with history of low dietary calcium intake.
The majority of patient have bone pain & muscle
weakness..
32
33
VitaminD…..
Oral manifestation
Teeth – developmental abnormalities of dentine &
enamel.
Caries – higher risk of caries
Enamel – there may be hypoplasia of enamel, may be
mottled, yellow gray in color
Pulp – high pulp horns, large pulp chamber, delayed
closure of root apices
34
MANAGEMENT
Dietary enrichment of vitamin D in the form of
milk
Curative treatment includes 2000 to 4000 IU of
calcium daily for 6 to 12 weeks.
Patient with osteomalacia due to intestinal
malabsorption require larger dose of vitamin D
& calcium i.e. 40,000 to 1,00,000 IU of vitamin
D &15 to 20 gms of calcium lactate.
Prevalence
• Vitamin D Status of Ostensibly Healthy Indians
Countrywide studies (2014) have reported
vitamin D deficiency in as high as 70%–100%
of ostensibly healthy individuals. All over India,
vitamin D deficiency was highly prevalent in
pregnant women and lactating mothers.
Subjects from rural and urban areas presented a
similar picture. Evidently, countrywide
prevalence of vitamin D deficiency is
undeniable.
Vitamin D Supplements Available in India
• Supplements commonly available are—D3
(cholecalciferol), 1,25(OH)2D3 and 1 alpha
hydroxy vitamin D3 (alfacalcidol). Some
formulations have calcium too. Multivitamin
formulations are also available and contain
about 400 IU of D3. D3 supplement of 60,000
IU is the highest selling one.
Need for Vitamin D Fortified Food Products
• In India Vitamin D sufficiency via sun exposure
is untenable for most Indians. Most Indians are
vegetarians. Fortification of widely consumed
staple foods with vitamin D is the only viable
solution towards attaining vitamin D deficiency
in India. Unlike supplementation strategies,
fortification of food with vitamin D poses a
negligible risk of toxicity
VITAMIN- E
• Vitamin E is a naturally occurring antioxidant. It
is essential for normal reproduction in many
animals, hence known as anti sterility vitamin.
Dietary sources of Vitamin-E
Many vegetable oils are
rich sources of vitamin
E. Wheat germ oil,
cotton seed oil, peanut
oil, corn oil, sunflower
oil.
It also present in meat,
milk, butter and eggs
Recommended dietary allowance of vitamin E
A daily consumption of
For men- 10 mg
For women- 8 mg
Vitamin E supplemented diet is advised for
pregnant and lactating women.
Biochemical functions of vitamin E
Vitamin E is essential for the
membrane structure and integrity
of the cell, hence it is regarded as
membrane antioxidant.
It prevents the peroxidation of
polyunsaturated fatty acids in
various tissues and membranes. It
protects RBC from hemolysis by
oxidizing agents.
It preserves and maintains
germinal epithelium of gonads for
proper reproductive funtion and
prevents sterility.
It protects liver from being
damaged by toxic
compounds such as carbon
tetrachloride.
It works in association with
vitamins A, C and beta
carotene, to delay the onset
of cataract.
It is believed that it prevents
the oxidation of LDL, which
have been implicated to
promote heart diseases.
Deficiency of vitamin E
Sterility
Degenerative changes in muscle
Megaloblastic anaemia
Changes in central nervous system
Oral manifestations
loss of pigmentation ,
atrophic degenerative changes in enamel
Vitamin - K
It is available in 2 forms
K1 – it is the form occurs in plant origin.
K2 - is synthesized by intestinal bacteria.
44
Dietary sources of vitamin K
SPINACH
CABBAGE
CAULIFLOWER
SOYA BEAN
WHEAT GERM
CARROTS
POTATOES
TOMATOES
MILK
MEAT
FISH
Biochemical functions of vitamin K
it is essential for the hepatic synthesis of
coagulation factor II, V, VII, IX, X.
CLOTTING – it prevents hemorrhage only in
cases when there is defective production of
prothrombin
OXIDATIVE PHOSPHORYLATION – it acts
as a co- factor in oxidative phosphorylation
associated with lipid
47
DEFICIENCY OF VITAMIN K
Causes
Increase clotting time
Prolong bleeding
Hemorrhagic
conditions
After antibacterial
therapy,
Surgical operations-
Cholecystectomy
Conditions like
Malabsorption
Obstructive
jaundice
Vitamin - C
It is also called ascorbic acid and antibiotic
vitamin.
it is the most active reducing agent.
it is powerful antioxidant
Dietary sources of vitamin C
• Citrus fruits, gooseberry,
guava, green vegetables,
tomatoes, potatoes are
rich in ascorbic acid.
• High content of vitamin
C is found in adrenal
gland and gonads.
• Milk is poor source of
ascorbic acid
Recommended daily allowance of vitamin C
• Adults : 60-70 mg per day
• Additional intake (20-40 % increase) are
recommended for women during pregnancy and
lactation
Biosynthesis and metabolism of vitamin C
Men cannot synthesize ascorbic acid due to the
deficiency of single enzyme namely L-
gulonolactone oxidase
Biochemical functions of vitamin C
1. Collagen formation
2. Bone formation
3. Iron and hemoglobin metabolism
4. Tryptophan metabolism
5. Tyrosine metabolism
6. Folic acid metabolism
7. Synthesis of corticosteriod harmones
8. Sparing action of other vitamins
9. Immunological function
10. Preventive action on chronic diseases
Vitamin C deficiency
SCURVEY : this disease is characteized by
Spongy and sore gums
Loose teeth
Anemia
Swollen joints
Decreased immunocompetence
Delayed wound healing
Haemorrhage
Osteoporosis
Prevalence
• Ravindran Rd et al (2011). The age, sex and
season standardized prevalence of vitamin
C deficiency was 73.9 in 2668 people in north
India and 45.7% in 2970 from south India.
Only 10.8% in the north and 25.9% in the south
met the criteria for adequate levels. Vitamin
C deficiency was more prevalent in men, with
increasing age, users of tobacco, poor
nutition and with lower intakes of
dietary vitamin C
B complex vitamins
Most B complex occurs in nature in the bound
form within the cells of vegetables or animal
tissues.
The digestion for the liberation of vitamins and its
absorption is a result of breakdown of cellular
structures in the gut.
Excretion of vitamins occurs in the kidney.
THIAMINE (VIT B1)
It is also called Anti Beri-Beri factor, Anti
Neuritic factor, and also Aneurin.
It has a specific coenzyme, thiamine
pyrophosphate(TTP) which is mostly associated
with carbohydrate metalolism
It is colorless basic organic compound
composed of a sulfated pyramiding ring.
57
Dietary source of thiamine
• cereals, Pulses, oil seeds,
nuts, yeast. Polishing of rice
removes about 80% of
thiamine
• Animal: pork, liver, heart,
kidney, milk
58
Recommended dietary allowance of vitamin B1
Men – 1.3 mg per day
women – 1.0 mg per day
Pregnancy and lactation-2
mg .per day
Children – 1.1mg.per day
Biochemical functions of vitamin B1
• The coenzyme, thiamin pyrophosphate or
cocarboxylase is intimately connected with the
energy releasing reactions in the carbohydrate
metabolism.
• TPP plays an important role in the transmission
of nerve impulse. It is believed that TPP is
required for acetylcholine synthesis and the ion
translocation of neural tissue
60
Deficiency of vitamin B1
Nervous disorders – when cells cannot metabolize
glucose, it affects the nervous system first, since it
depends entirely on glucose for its energy requirement.
& There is mental depression.
Digestive symptoms- it occurs due to defective
hydrochloric acid production in the stomach patient
complains of loss of appetite, poor digestion, loss of
weight.
Deficiency of vitamin B1
BERI BERI
a) DRY BERI BERI
b) WET BERI BERI..
c ) INFANTILE BERI BERI
Other diseases which can be associated with it are
wernickes encephalopathy
peripheral neuritis
korsakoff’s psychosis.
62
VitaminB1….
Management
Complete rest
Thiamine 50 mg IM for 3 days then 10 mg 3 times daily
by oral route.
Infantile beriberi is treated via mothers milk. The
mother should receive 10,000 mcg twice daily, in
addition infant should be given thiamine in doses of
10,000 to 20,000 mcg IM once in a day for 3 days
VitaminB1….
Oral manifestations
There is hypersensitivity of oral mucosa
Pain in tongue, teeth, jaw, and face
Thiamine antagonists:
Pyrithiamine and oxythiamine are the two
important antimetabolites of thiamine
Riboflavin (Vit B2)
• Riboflavin through its coenzymes takes part in a
variety of cellular oxidation reduction reactions.
• Coenzymes of riboflavin
• Flavin mononucleotide (FMN) and flavin
adenine dinucleotide (FAD) are the two
coenzyme forms of riboflavin
Dietary sources of vitamin B2
• Milk and milk
products, meat, eggs,
liver, kidney are rich
sources. Cereals,
fruits, vegetables and
fish are moderate
sources
Recommended dietary allowance of vitamin B2
• Adults: 1.2-1.7 mg/day
• Higher intakes (0.2-0.5 mg/day) are advised for
pregnant and lactating women.
Biochemical functions of vitamin B2
• The flavin coenzymes participate in many redox
reactions responsible for energy production
• The coenzymes, FAD and FMN are associated
with several enzymes involved in carbohydrate,
lipid, protein, and purin metabolism
68
CHEILOSIS
• Chapping & fissuring
of lips
GLOSSITIS
• Inflammmed
• Red beefy tongue
Deficiency of vitamin B2
Niacin ( Vit B3)
• Niacin or nicotinic acid is also known as Pellagra
preventive(p.p) factor of Goldberg.
• The coenzymes of niacin (NAD and NADP)
can be synthesized by the essential amino acid,
tryptophan.
Dietary sources of Niacin
Rich natural souces:
Liver
Yeast
Whole grain
Cereals
Pulses
Moderate sources:
milk
Fish
Eggs
vegetables
Biochemical functions of Niacin
The coenzymes NAD and NADP are involved
in a variety of oxidation reduction reactions.
A large number of enzymes belonging to the
class oxidoreductases are dependent on NAD or
NADP.
73
Deficiency of Niacin
its deficiency results in pellagra.
it is called disease of 3 ds
DERMATITIS
DIARRHOEA
DEMENTIA
skin - in acute cases, skin lesions may
produce vesiculation, cracking,
exudation, crusting with ulceration &
secondary infection
Chronic cases – dermatitis occurs as
roughening & thickening of skin .
If not treated may rarely lead to 4th
D - death
74
VitaminB3….
Oral manifestation
Oral mucosa – becomes fiery red & painful & salivation is
profuse.
Tongue – epithelium of entire tongue is desquamated.
The tongue becomes red swollen & beefy
In advanced cases, the tongue loses all the papillae & reddening
becomes intense.
pyridoxine (Vit B6)
Vitamin B6 is used to collectively represent
the three compounds namely pryidoxine,
pyridoxol and pyridoxamine
Recommended dietary allowance of vitamin B6
Adults : 2.2 mg / day
During pregnancy, lactation and old age an
intake of 2.5 mg / day recommended
Isoniazide , deoxypyridoxine and methoxy
pyridoxine are the antagonists of vitamin B6
Biochemical functions of pyridoxine
Pyridoxal phosphate, the coenzyme of vitamin
B6 is found attached to the e- amino group of
lysine in the enzyme.
Pyridoxal phosphate participates in reactions like
transamination, decarboxylation, deamination,
transsulfuration, condensation
Deficiency of vitamin B6
Neurological symptoms such as:
Depression, irritability, nervousness and mental
confusion
Convulsions and peripheral neuropathy are
observed in severe deficiency
These symptoms are related to the decreased
synthesis of biogenic amines (GABA, seratonin,
epinephrine, norepinephrine)
Demyelination of neurons
Biotin ( Vit B7)
• Biotin ( formerly known as anti egg white injury
factor, vitamin B7 or vitamin H) is a sulfur
containing B- complex vitamin. It directly
participates as a coenzyme in the carboxylation
reactions.
Dietary sources of biotin
• The rich sources are liver, kidney, eggyolk, milk,
tomatoes, grains.
Recommended dietary allowance of biotin
Men – women – 100- 300 mcg/day
Children – 50-200 mcg./day
Infant – 35 mcg/day
Biochemical functions of Biotin
• Biotin serves as a carrier of CO2 in
carboxylation reactions.
• As a coenzyme , biotin is involved in various
metabolic reactions
Gluconeogenesis and citric acid cycle
Fatty acid synthesis
Deficiency of Biotin
Anemia
Loss of appetite
Nausea
Dermatitis
Glossitis
Biotin deficiency is uncommon as it is well
distributed In foods and also supplied by the
intestinal bacteria
Pantothenic acid (vit B5)
• Pantothenic acid (Greek: pantos- everywhere),
formely known as chick anti dermatitis factor.
Its metabolic role as coenzyme A is also
widespread
Recommended dietary allowance of vitB5
Adults : 5-10 mg
Dietary sources of pantothenic acid
• It is one of the most widely distributed vitamins
found in plants and animals.
• The rich sources are egg, liver, meat, yeast, milk
Biochemical functions of Vit B5
The function of pantothenic acid are exerted
through coenzyme A or CoA ( A for
acetylation).
Co enzyme A serves as a carrier of activated
acetyl or acyl groups. This is comparable with
ATP which is a carrier of activated phosphoryl
groups.
Deficiency of Vit B5
Burning feet syndrome: pain and numbness in
toes, sleeplessness, fatigue
Folic acid (Vit B9)
• Folic acid or folacin (latin: folium-leaf) is
abundantly found in green leafy vegetables.
• It is required for synthesis of certain
aminoacids, purins and pyrimidine- thymine.
Dietary sources of Vit B9
• Rich sources are green leafy vegetables, whole
grains, cereals, liver, kidney, yeast and eggs.
• Milk is rather a poor source of folic acid
Recommended dietary allowance of folic acid
Adults : 200 mcg
Higher intakes are recommended during
pregnancy and lactation: 400 mcg
Biochemical functions of folic acid
Tetra hydrofolate, the coenzyme of folic acid is
actively involved in the one carbon metabolism
Aminopterin and methopterin are structural
analogues of folic acid. They competetively
inhibit dihydrofolate reductase and block
formation of THF.
Aminpterin and methotrexate are used in
treatment of many cancers
Deficiency of folic acid
Macrocytic anemia
Folic acid deficiency in pregnant women may
cause neural defects in the fetus. Hence, high
doses of folic acid are recommended during
pregnancy to prevent birth defects
Formiminoglutamate (FIGLU) , in urine is used
to assess folic acid deficiency
Cyanocobalamine ( Vit B12)
• Most of the therapeutic preparations contain
cyanocobalamine. It is sensitive to light. It is
heat liable.
Dietary sources of Vit B12
• It is mainly present in animal sources. Liver,
kidney, brain, meat, fish and eggs are good
souces.
• Milk and milk products are fair sources. curd is
better source than milk.
• Since, it Is absent in plant foods, vegetarians are
likely to develop Vit B12 deficiency
Recommended dietary allowance of Vit B12
• Adults : 3 mcg per day
• Children : 0.5-1.5 mcg per day
• During pregnancy and lactation : 4 mcg per day
Biochemical functions of Vit B12
• Vitamin B12 acts as the prosthetic group or
coenzyme. Vitamin B12 enzymes are called
cobamide enzymes.
• About ten enzymes requiring Vit B12 have been
identified, most of them are found in bacteria.
• Synthesis of methionine from homocystein
• Isomerization of methymalonyl Co A
Deficiency of Vit B12
• Perinicious anemia: it is characterized by low
hemoglobin levels, decreased number of
erythrocytes and neurological manifestations.
• The excretion of methylmalonic acid in urine
and estimation of serum B12 level are used to
assess B12 deficiency.
Vitamin B12…..
oral manifestations
• Vitamin B deficiencies are one of the most
common deficiencies that can affect your teeth
and your mouth. Common oral effects of
vitamin B deficiency are burning sensations in
the mouth and on the tongue, trouble
swallowing, swollen tongue, and pale tissues in
the inner cheeks that could break apart easily
and come off
Prevalence
• Bhawna singh et al(2011): A total of 422 patients
screened for serum vitamin B12 levels were enrolled.
B12 deficiency was observed in 19.4% men and 23.7%
women in the present study suggesting that risk of
developing B12 deficiency is affected by gender
• Among the vegetarian group, 59 out of 107 (55%) had
vitamin B12 level less than 200 pg/ml where as only 16
of 77 non vegetarians (20.8%) had B12 deficiency
• Vegetarian dietary habit was found to be a substantial risk
factor for B12 deficiency in our population
Public healthimportance
• Vitamin deficiency conditions are widespread
among people in developing and in developed
countries. This silent epidemic affect people of
all genders and ages, as well as certain risk
groups. They not only cause specific diseases,
but they act as exacerbating factors in infectious
and chronic diseases, greatly impacting
morbidity, mortality, and quality of life.
• most effective way to meet community health
needs safely is by population based approaches
involving food fortification. These
complementary methods, along with food
security, education, and monitoring, are
challenges for public health and for clinical
medicine.
• Understanding the pathophysiology and
epidemiology of vitamin deficiencies, and
implementing successful methods of
prevention, both play a key part in the New
Public Health
Conclusion
• Living a healthy life means making sure that your body
is receiving all the proper vitamins and minerals it needs
to function correctly. It’s also important to make sure
that you’re maintaining a healthy mouth, since that poor
oral health may be a link to certain health issues,
including heart disease, obesity, stroke and even cancer.
• A daily multivitamin is a great nutrition insurance
policy. Some extra vitamin D may add an extra
health boost.
J Appl Oral Sci. 2013 Nov-Dec;21(6):601-6.
Dental manifestations of patient with vitamin D-resistant
rickets.
Souza AP, Kobayashi TY, Lourenço Neto N, Silva SM, Machado MA, Oliveira TM.
Abstract
Patients with Vitamin D-resistant rickets have abnormal tooth morphology such as
thin globular dentin and enlarged pulp horns that extend into the dentino-enamel
junction. Invasion of the pulp by microorganisms and toxins is inevitable. The
increased fibrotic content of the pulp, together with a reduced number of
odontoblasts, decreases the response to pulp infection. The most
important oral findings are characterized by spontaneous gingival and dental
abscesses occuring without history of trauma or caries. Radiographic examinations
revealed large pulp chambers, short roots, poorly defined lamina dura and
hypoplastic alveolar ridge. These dental abscesses are common and therefore the
extraction and pulpectomy are the treatment of choice. The purpose of this article
is to report a case of Vitamin D-resistant rickets in a 5 year-old boy, describing the
dental findings and the treatment to be performed in these cases.
J Tenn Dent Assoc. 2011 Spring;91(2):30-3; quiz 34-5.
Vitamin D and its impact on oral health--an update.
Stein SH1, Tipton DA.
Abstract
Vitamin D has been shown to regulate musculoskeletal health by mediating calcium
absorption and mineral homeostasis. Evidence has demonstrated that vitamin D
deficiency may place subjects at risk for not only low mineral bone
density/osteoporosis and osteopenia but also infectious and chronic inflammatory
diseases. Studies have shown an association between alveolar bone density,
osteoporosis and tooth loss and suggest that low bone mass may be a risk
factor for periodontal disease. Several recent reports demonstrate a significant
association between periodontal health and the intake of vitamin D. An emerging
hypothesis is that vitamin D may be beneficial for oral health, not only for its direct
effect on bone metabolism but also due to its ability to function as an anti-
inflammatory agent and stimulate the production of anti-microbial peptides.
Nutr Rev. 2013 Feb;71(2):88-97.
Vitamin D and dental caries in controlled clinical trials:
systematic review and meta-analysis.
Hujoel PP. Abstract
Vitamin D has been used to prevent and treat dental caries. The objective of this
study was to conduct a systematic review of controlled clinical trials (CCTs) assessing
the impact of vitamin D on dental caries prevention. Random-effects and meta-
regression models were used to evaluate overall and subgroup-specific relative-rate
estimates. Twenty-four CCTs encompassing 2,827 children met the inclusion criteria.
Twenty-two of the 24 CCTs predated modern clinical trial design, some of which
nonetheless reported characteristics such as pseudo-randomization (n = 2), blinding
(n = 4), or use of placebos (n = 8). The relative-rate estimates of the 24 CCTs
exhibited significant heterogeneity (P < 0.0001), and there was evidence of significant
publication bias (P < 0.001). The pooled relative-rate estimate of
supplemental vitamin D was 0.53 (95% CI, 0.43-0.65). No robust differences were
identified between the caries-preventive effects of vitamin D(2) , vitamin D(3) , and
ultraviolet radiation (Prob > F = 0.22). The analysis of CCT data
identified vitamin D as a promising caries-preventive agent, leading to a low-
certainty conclusion that vitamin D may reduce the incidence of caries.
J Oral Sci. 2009 Mar;51(1):11-20.
Vitamin D and periodontal disease.
Amano Y, Komiyama K, Makishima M.
Abstract
1,25-Dihydroxyvitamin D(3) [1,25(OH)(2)D(3); 1,25-dihydroxycholecalciferol or
calcitriol] is the active form of vitamin D(3), a lipid-soluble vitamin that plays a role in
calcium and bone metabolism. Recently, vitamin D(3) has been shown to function in
cancer prevention, immunity and cardiovascular regulation. 1,25(OH)(2)D(3) exhibits
physiological and pharmacological effects by activating the vitamin D receptor
(VDR), a transcription factor of the nuclear receptor superfamily. 1,25(OH)(2)D(3)
plays a role in maintaining oral health through its effects on bone and mineral
metabolism and innate immunity, and several VDR gene polymorphisms have
been reported to be associated with periodontal disease. VDR ligands should
prove to be useful in the treatment and prevention of periodontal disease.
J Periodontol. 2009 Apr;80(4):603-8.
Association between vitamin D receptor gene polymorphisms and
severe chronic periodontitis in a Chinese population. Wang C, Zhao
H, Xiao L, Xie C, Fan W, Sun S, Xie B, Zhang J.
Abstract
BACKGROUND:
Chronic periodontitis (CP) exhibits inflammation and alveolar bone loss, and severe
forms of periodontitis are suggested to have a genetic basis. Vitamin D receptor
(VDR) regulates bone metabolism and inflammation-related genes, and single
nucleotide polymorphisms (SNPs) in the VDR gene may affect the functional activity
of the VDR protein in CP. Therefore, the aim of this study was to investigate the
association between VDR SNPs and severe CP in a Chinese population.
METHODS:
DNA was obtained from 107 patients with severe CP and 121 control subjects. The
BsmI, TaqI, ApaI, and FokI SNPs of VDR genes were investigated by restriction
fragment length polymorphism of polymerase chain reaction (PCR) products. The
digested PCR products were electrophoresed on an 8% polyacrylamide gel and
developed by the DNA silver staining method.
CONCLUSION:
TaqI SNP of VDR gene might be associated with severe CP in Chinese patients.
Community Dent Oral Epidemiol. 2003 Jun;31(3):213-20.
Caries and micronutrient intake among urban South African childr
en: a cohort study.MacKeown JM1, Cleaton-Jones PE, Fatti P.
Abstract
OBJECTIVE:
To report on associations between caries and micronutrient intake among a
'true cohort' group of 5-year-old urban black South Africanchildren.
METHODS:
The study sample was a true cohort that had nutrition as well as dental information for
1991 and 1995 (n = 259). Micronutrient intake and dental caries associations were
examined with SAS using the linear logistic analysis and a critical level of statistical
significance of P < 0.05.
RESULTS:
Of the 21 micronutrients investigated, vitamin B12, riboflavin, magnesium and biotin
were individually significantly associated with cariesincidence, but taken together only
magnesium was significant.
CONCLUSIONS:
The association of micronutrient intake with caries was weak, isolated and not
clinically relevant. Micronutrient intake was not an indicator of the presence or
absence of caries among the children studied.
Community Dent Oral Epidemiol. 2010 Feb;38(1):43-9.
Tooth loss and intakes of nutrients and foods: a nationwide survey of Japanese dentists.
Wakai K, Naito M, Naito T, Kojima M, Nakagaki H, Umemura O, Yokota M, Hanada N, Kawamura T.
Abstract
OBJECTIVES:
To clarify the association of tooth loss with dietary intakes among dentists, for whom sufficient dental
care is available.
METHODS:
We analyzed the data from 20 366 Japanese dentists (mean age +/- SD, 52.2 +/- 12.1 years; women
8.0%) who participated in anationwide cohort study from 2001 to 2006. The baseline questionnaire
included a validated food-frequency questionnaire to estimate intakes of foodsand nutrients. We
computed the geometric means of daily intakes by the number of teeth, adjusting for age, sex, smoking,
physical activity, and history of diabetes.
RESULTS:
The mean intakes of some key nutrients and food groups, such as carotene, vitamins A and C, milk and
dairy products, and vegetables including green-yellow vegetables, decreased with the increasing
number of teeth lost (P for trend <0.05). On the contrary, mean intakes of carbohydrate, rice, and
confectioneries were increased among those with fewer teeth (P for trend <0.05). The difference in the
geometric mean (%) between totally edentulous subjects and those with > or =25 teeth, that is
[(Geometric mean for > or =25 teeth) - (Geometric mean for 0 teeth)]/(Geometric mean for > or =25
teeth) x 100, was 14.3%, 8.6%, 6.1%, and -6.1% for carotene, vitamin C, vitamin A, and carbohydrate,
respectively. For food groups, it was 26.3%, 11.9%, 5.6%, -9.5%, and -29.6% for milk and dairy products,
green-yellow vegetables, total vegetables, rice, and confectioneries, respectively.
CONCLUSIONS:
Tooth loss was linked with poorer nutrition even among dentists.
Community Dent Oral Epidemiol. 2005 Jun;33(3):167-73.
The association between tooth loss and the self-reported intake of selected CVD
related nutrients and foodsamong US women. Hung HC, Colditz G, Joshipura KJ.
Abstract
OBJECTIVES:
Many studies have reported associations between oral health and cardiovascular diseases; poor
nutritional status due to impaired dentition status has been suggested as a mediator. Our objective is to
evaluate the associations between tooth loss and the self-reportedconsumption of fruits and vegetables
and selected CVD-related nutrients.
METHODS:
A total of 83,104 US women who completed a food frequency questionnaire (FFQ) in 1990 and 1994
and reported number of natural teeth in 1992, were included in a cross-sectional analysis relating
dietary intake to number of natural teeth. A longitudinal analysis was also conducted to evaluate
whether tooth loss in 1990-1992 was associated with change in diet between 1990 and 1994.
RESULTS:
After adjusting for age, total calorie intake, smoking and physical activity, edentulous women appeared
to have dietary intake associated with increased risk for CVD, including significantly higher intake of
saturated fat, trans fat, cholesterol and vitamin B12, and lower intake of polyunsaturated fat, fiber,
carotene, vitamin C, vitamin E, vitamin B6, folate, potassium, vegetables, fruits, and fruits excluding
juices compared withwomen with 25-32 teeth. In the longitudinal analyses, women who lost more
teeth were more likely to change their diet in ways that would potentially increase risk for development
of CVD. They also tended to avoid hard foods, such as raw carrot, fresh apple or pear.
CONCLUSIONS:
Women with fewer teeth have unhealthier diets such as decreased intake of fruits and vegetables,
which could increase CVD risk. Diet may partially explain associations between oral health and
cardiovascular disease.
Community Dent Oral Epidemiol. 2000 Dec;28(6):407-13.
Nutritional variables related to gingival health in adolescent girls.
Petti S1, Cairella G, Tarsitani G.
Abstract
In order to study the nutritional variables associated with gingival health, a case-
control study was designed to control strong variables whose effect
on gingival status may obscure the potential effect of weaker ones, such as
nutrition. Two groups of 27 gingivitis-affected and -unaffected female adolescents
were selected. All were aged 17-19 years, with mean age of the two groups
statistically not different. All were non-smokers, all reported daily toothbrushing
frequency of twice/day or more, and none had clinical signs of hyponutrition.
Mean DMFT of the two groups was statistically not different. The effect
of nutritional variables, obtained by a three-day food record and by assessing
the nutritional status of the girls, on presence/absence of gingivitis was evaluated
by a variety of stepwise logistic regression analyses. Age (positive correlation),
riboflavin, calcium and frequency of fibre intake (negative correlations)
significantly explained the risk for gingivitis. Strong intercorrelation between
riboflavin and calcium was also found, due to the high quantity of milk consumed
by the girls, since this food provided the main source of riboflavin and calcium. The
data suggest that some dietary measures may be useful for the maintenance of
healthy gingival status.
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