Essential Vitamins for Oral Health

CONTENTS
• INTRODUCTION
• NUTRITION
• VITAMIN A
• VITAMIN D
• VITAMIN E
• VITAMIN K
• VITAMIN C
• VITAMIN B COMPLEX
• CONCLUSION

INTRODUCTION
• Vitamins are organic nutrients that are
essential for life. Each of the vitamins and
minerals known today has specific
functions in the body, which makes them
unique and irreplaceable. A variety of
foods is therefore vital to meet the body’s
vitamin and mineral requirements.

NUTRITION
W.H.O:- nutrition is the science of food and its
relationship to health. It is concerned primarily
with the part played by the nutrient in body
growth, development & maintenance.
NIZEL 1989:- the science which deals with
the study of nutrients and foods and their effects
on the nature & function of organism under
different condition of age, health & disease.

NUTRIENTS
•
1. Macronutrients: These are
proteins, fats, and
carbohydrates, which are often
called ‘proximate principles’
2. Micronutrients: These are
vitamins and minerals. They
are called micronutrients
because they are required in
small amounts

ROLE OF NUTRITION IN
PERIODONTAL DISEASE
• Research studies have shown increased levels of bleeding
on probing when participants were fed with a diet high in
carbohydrates when compared to those on a low sugar
diet.
• As would be expected plaque levels increased
significantly and classic periodontal pathogens emerged
within the biofilm, but unexpectedly gingival bleeding
significantly reduced from 35% to 13%.
• These studies support a role for nutrition in controlling
periodontal inflammation.

VITAMINS
• Vitamins may be defined as organic
compounds occurring in small quantities in
different natural foods and necessary for
growth and maintenance of good health in
human beings and in experimental animals. “A
vitamin is a substance that makes you ill if you
don’t eat it” (Albert Zsent-Gyorgyi, Nobel Prize
winner, 1937).

HISTORYAND NOMENCLATURE OF
VITAMINS.
• Hopkins coined the term accessory factors
• Funk (1913) isolated an active principle (an amine) from
rice polishings. He coined the term vitamine
(Greek:vita-life) to the accessory factors.
• The usage of A, B and C to vitamins was introduced in
1915 by McCollum and Davis

CLASSIFICATION OF VITAMINS
• The vitamins are mainly classified into two:
1. The fat soluble vitamins are A, D, E and K
2. Water soluble vitamins are named as B
complex and C.

• McCollum,
Simmonds and
Kennedy isolated
vitamin A in 1913.
• Richard Kuhn (Nobel
prize, 1938)
identified carotenes.
• Paul Karrer in 1931
elucidated the
structure of vitamin
A1 (Nobel prize,
1937).

CHEMISTRY
Vitamin A is fat soluble. The active form is present only in
animal tissues.
• All the compounds with vitamin A activity are referred
to as retinoids
• retinol (vitamin A alcohol),
• retinal (vitamin A aldehyde) and
• retinoic acid (vitamin A acid)
• The pro-vitamin, beta-carotene is present in plant
tissues.

BIOCHEMICAL ROLE OF VITAMIN A
1. Wald’s Visual Cycle

OTHER BIOCHEMICAL FUNCTIONS
OF VITAMIN A
• 1. Retinoic acid has a role in the regulation of
gene expression and differentiation of tissues.
• 2. Retinol is necessary for the reproductive
system. Retinol acts like a steroid hormone in
controlling the expression of certain genes.

DEFICIENCY MANIFESTATIONS OF
VITAMIN A
1. Night Blindness or Nyctalopia
• Visual acuity is diminished in dim light. The dark
adaptation time is increased.

2. Xerophthalmia - The conjunctiva becomes keratinized, dry, thick
and wrinkled.
3. Bitots Spots- These are seen as greyish-white triangular plaques
firmly adherent to the conjunctiva on either side of the cornea.

4. Keratomalacia
There is degeneration of corneal epithelium which may get
vascularized. Later, corneal opacities develop. Bacterial
infection leads to corneal ulceration, perforation of cornea
and total blindness.

6. Skin and Mucous Membrane Lesions
• Follicular hyperkeratosis results from
hyperkeratinization.
• The alterations in skin may cause increased
occurrence of generalized infections. Therefore
in old literature, vitamin A is referred to as
anti-inflammatory vitamin.

Other General Manifestations
• In vitamin A deficiency, growth retardation,
• decreased protein synthesis,
• lowered glycoprotein content of cell and
• reduced immunity against infections.

Daily Requirement of Vitamin A
The recommended daily allowance (RDA) for
i. Children = 400-600 microg/day.
ii. Men = 750-1000 microg/day
iii. Women = 750 microg/day
iv. Pregnancy = 1000 microg/day

HYPERVITAMINOSIS
• Excessive consumption of vitamin A leads to
toxicity. The symptoms include
• Dermatitis, raised intracranial tension,
• enlargement of liver, skeletal decalcification,
• tenderness of long bones, joint pains etc.
Elderly people are more susceptible to vitamin
A toxicity.

• Periodontitis is defined as “an inflammatory disease of
the supportive tissues of the teeth caused by specific
microorganisms or groups of specific microorganisms,
resulting in progressive destruction of the periodontal
ligament and alveolar bone with increased probing
depth formation, recession, or both”.

VITAMIN A AND PERIODONTIUM
• VITAMIN A deficiency influences the
development of periodontal disease by
affecting
(1) the gingival epithelium and its cuticular
attachment to the tooth surface;
(2) the collagen fiber apparatus by which the
tooth is suspended from the alveolar bone ; or
(3) the calcified tissues, bone and cementum, in
which the collagenous fibers are imbedded.

• According to a review done by Paul E.
Boyle.(1947). He concludes that there is
considerable evidence from investigations
with laboratory animals that changes in the
oral mucosa and alveolar bone occur which
predispose to the development of
periodontal disease.
• However The relation of vitamin A
deficiency to periodontal disease in human
beings awaits investigation.

• Angus and coworkers isolated
vitamin D in 1931 and named
it as calciferol, later identified
as vitamin D3.
• The structural elucidation was
done by Otto Diels and Kurt
Adlerin 1950.
• Hess (1924) reported that
irradiation with ultraviolet
light induced antirachitic
activity in some foods.

Structure of vitamin D3 and D2
• Ergocalciferol (vitamin D2) is formed from
ergosterol and is present in plants .
• Cholecalciferol (vitamin D3) is found in
animals.
Both the sterols are similar in structure except
that ergocalciferol has an additional methyl
group and a double bond.
Ergocalciferol and cholecalciferol are sources
for vitamin D activity and are referred to as
provitamins.

The calcitriol
thus formed is
the active form
of vitamin; it
acts as a
hormone.
- De LUCA

Biochemical Effects of Vitamin D
The sites of action are
(a) intestinal villi cells,
(b) bone osteoblasts and
(c) kidney distal tubular cells

Vitamin D and Intestinal Absorption of
Calcium:

• Effect of Vitamin D in Bone:
Mineralisation of the bone is increased by
increasing the activity of osteoblasts. Calcitriol
coordinates the remodelling action of
osteoclasts and osteoblasts.
• Effect of Vitamin D in Renal Tubules:
• Calcitriol increases the reabsorption of
calcium and phosphorus by renal tubules,
therefore both minerals are conserved.

Deficiency Manifestations of Vitamin D
• The deficiency diseases are Rickets in children
and Osteomalacia in adults.
Hence vitamin D is known as antirachitic
vitamin.

RICKETS
Rickets is seen in children. There is
insufficient mineralisation of bone. Bones
become soft and pliable.

CLINICAL FEATURES
• Enlarged ends of long bones.
• bow legs
• knock-knee
• rickety rosary
• bossing of frontal bones and
• pigeon chest.
• Harrison’s sulcus

Types of Rickets
1. The classical vitamin D deficiency rickets
2. The hypophosphatemic rickets - defective renal tubular reabsorption
of phosphate.
3. Vitamin D resistant rickets is found to be associated with Fanconi
syndrome.
4. Renal rickets: calcitriol is not synthesised.
5. End organ refractoriness to 1, 25-DHCC will also lead to rickets.

Osteomalacia
Manifests as softened bones due to insufficient
mineralization. Bone aches and pains are
common.
Prolonged use of phenobarbitone may be
manifested as osteomalacia.

HYPERVITAMINOSIS D
• Doses above 1500 units per day for very long
periods may cause toxicity.
• Hypervitaminosis results from the
consumption of excessive supplements and
not from the consumption of usual diets.
• It is primarily due to increased intestinal
absorption of calcium along with resorption
of bone.

VITAMIN D AND PERIODONTIUM
• The local effects of vitamin D supplementation
on periodontal tissues are more apparent
than systemic administration.
• Furthermore, intraperitoneal injections of
vitamin D3 accelerates orthodontic tooth
movement in patients undergoing
bisphosphonate therapy.

• Clinical studies have suggested that a
deficiency of dietary vitamin D leads to
periodontal inflammation and a delay in post-
surgical periodontal healing.
• However, other clinical trials have found no
significant link between serum vitamin D
levels and periodontal health and more
studies are required to investigate its role.

• Evans and his associates
(1936) isolated the
compounds of vitamin E
activity was isolated from
wheat germ oil & named
them as tocopherols
• ANTI- FERTILITY VITAMIN

Chemical Nature
The structure of vitamin E was elucidated by Paul
Karrer, who was awarded Nobel Prize in 1937.

Metabolism of Vitamin E:
• Normal blood level of tocopherol is 0.5-1
mg/dl.
• It is absorbed along with other fats and needs
the help of bile salts.
• Tocopherol is absorbed and transported as
chylomicrons. It is stored in adipose tissue.

Biochemical Role of Vitamin E:

• Vitamin E is the most powerful natural anti-
oxidant. It protects RBC from hemolysis. By
preventing the peroxidation, it keeps the
structural and functional integrity of all cells.

• Vitamin E also boosts immune response; acts
as an antimutagen; and slows progression in
Alzheimer’s disease.
• It is closely associated with reproductive
functions and prevents sterility. Vitamin E
preserves and maintains germinal epithelium
of gonads for proper reproductive function.

• It increases the synthesis of heme by
enhancing the activity of enzymes
aminolevulinic acid (ALA) synthase and ALA
dehydratase.

• It is required for cellular respiration– through
electron transport chain (believed to stabilize
coenzyme Q).
• Vitamin E prevents the oxidation of vitamin A
and carotenes. It works in association with
vitamins A, C and carotene, to delay the onset
of cataract.
• It is involved in proper synthesis of nucleic
acids.

• Vitamin E protects liver from being damaged
by toxic compounds such as carbon
tetrachloride.
Interrelationship with Selenium
• Selenium is present in glutathione peroxidase;
an important enzyme that oxidises and
destroys the free radicals. Selenium has been
found to decrease the requirement of vitamin
E and vice versa.

Deficiency Manifestations of Vitamin E

• SOURCES OF VITAMIN E
Requirement:.
• Males 10 mg
• Females 8 mg
• Pregnancy 10 mg
• Lactation 12 mg per day

Hypervitaminosis E:
• At doses above 1000 IU per day, it may cause
tendency to hemorrhage.
• Because it is a mild anticoagulant, those who
have bleeding disorders should take
precautions before taking vitamin.

VITAMIN E AND PERIODONTIUM
• Few studies reported favorable effects of
vitamin E in maintaining periodontal health
and controlling inflammation.
• However No relationship has been
demonstrated between deficiencies in vitamin
E and oral disease, but systemic vitamin E
appears to accelerate gingival wound healing
in the rat.

• It is the abbreviation of the
German word “koagulation
vitamin”.
• Henrik Dam first reported its
existence in 1929.
• In 1939, Edward Doisy isolated
a factor with similar properties
but different in structure from
fish meal and it was named as
vitamin K2.

Chemistry of Vitamin K:
They are naphthoquinone derivatives
• Vitamin K exists in different forms.
• Vitamin K1 (phylloquinone) is present in
plants.
• Vitamin K2 (menaquinone) is produced by the
intestinal bacteria and also found in animals.
• Vitamin K3 (menadione) Menadione is water
soluble synthetic vitamin, widely used in
clinical practice.

Absorption and Storage:
• Absorption of vitamin K occurs in the intestine
along with chylomicrons.
• The vitamin K may be derived from the diet or
intestinal bacterial synthesis. It is stored in the
liver and transported in plasma along with
beta lipoproteins.

Biochemical Role of Vitamin K:
1. Vitamin K is necessary for coagulation. Factors
dependent on vitamin K are factors
• II (prothrombin),
• VII (SPCA)
• IX (Christmas factor) and
• X (Stuart Prower factor).

2. All these factors are synthesised by the liver
as inactive zymogens. They undergo post-
translational modification.

• The gamma carboxy glutamic acid (GCG)
synthesis requires vitamin K as a co-factor.

• Vitamin K dependent gamma carboxylation is
also necessary for the functional activity of C-
reactive protein, osteocalcin and structural
proteins of kidney, lung and spleen.

• Vitamin K Dependent Carboxylase: It is
microsomal enzyme. It requires oxygen, C02,
NADPH and reduced vitamin K.

Deficiency of Vitamin K
• In normal adults dietary deficiency seldom
occurs.
• Prolonged antibiotic therapy and
gastrointestinal infections with diarrhoea will
destroy the bacterial flora and can also lead
to vitamin K deficiency.

Clinical Manifestations:
• Hemorrhagic disease of the newborn is
attributed to vitamin K deficiency. The
newborns, especially the premature infants
have relative vitamin K deficiency. This is due
to
• lack of hepatic stores,
• limited oral intake and
• absence of intestinal bacterial flora.

• In children and adults, vitamin K deficiency
may be manifested as bruising tendency,
echymotic patches, mucous membrane
hemorrhage, post-traumatic bleeding and
internal bleeding. Prolongation of
prothrombin time and delayed clotting time
are characteristic of
vitamin K deficiency.

• Warfarin and dicoumarol will competitively
inhibt the gamma carboxylation system due to
structural similarity with vitamin K. Hence
they are widely used as anticoagulants for
therapeutic purposes.

• Treatment of pregnant women with
warfarin can lead to fetal bone
abnormalities (fetal warfarin syndrome).

Recommended daily allowance is 50-100
Ug/day. Usually, this amount is available in a
normal diet.

Hypervitaminosis K:
• Administration of large quantities of
menadione may result in toxicity. In
hypervitaminosis K,
• hemolysis,
• hyperbilirubinemia,
• kernicterus and
• brain damage may be noticed.
This should be kept in mind in treating
premature babies.

VITAMIN K AND PERIODONTIUM
• Vitamin K is a group of vitamins required for
the synthesis of proteins that are precursors
of the formation of blood coagulation factors
hence if antibiotics are to be made part of
periodontal therapy for a long period of time,
thus coagulopathies might be observed.

• Research has indicated that vitamin K also
plays a role in the formation of proteins
required for bone metabolism such as
osteocalcin and periostin.
• If periodontal therapy is to be administered to
patients with kidney failure, vitamin K can be
used to treat any bleeding incidents, as it
reverses the pharmacological action of
warfarin.

• Although vitamin K deficiency may lead to
gingival bleeding, a recent study by Aral et al.
has found that vitamin K supplementation was
not able to reduce pro-inflammatory factors
in the periodontium.

• James Lind published
‘Treatise on Scurvy’, in
1753.
• Zilva et al, in 1928, showed
that the antiscorbutic factor.
• The factor was isolated in
1930 and named as
“Hexuronic acid” by Albert
Szent-Gyorgi (Nobel prize,
1937).
• In 1933, Haworth
established the molecular
structure. He renamed it as
ascorbic acid (Nobel prize,
1937).

STRUCTURE OF VITAMIN C
• Vitamin C is water soluble and is easily destroyed by
heat, alkali and storage.
• Cooking destroyed about 70% of vitamin C.

BIOSYNTHESIS OF VITAMIN C
• Man cannot synthesize ascorbic acid (block in
gulonolactone oxidase step). They lack the genes
responsible for the synthesis of this enzyme.

Biochemical functions of vitamin C:
• The main property of vitamin C is the reversible
oxidation-reduction reaction between ascorbic acid
and dehydroascorbic acid.

• Collagen formation : Vitamin C plays the role of a
coenzyme in hydroxylation of
proline and lysine while
protocollagen is converted
to collagen .

• Vitamin C or ascorbic acid is essential for the formation of
collagen and intercellular material, bone and teeth, and for
the healing of wounds. It helps maintain elasticity of the skin,
aids the absorption of iron, and improves resistance to
infection (Mazzotta 1994).

• 2. Bone formation : Bone tissues possess an organic
matrix, collagen and the inorganic calcium,
phosphate etc. Vitamin C is required for bone
formation.

• Iron and hemoglobin metabolism : Ascorbic acid
enhances iron absorption by keeping it in the ferrous
form. This is due to the reducing property of vitamin C.
Vitamin C is useful in the reconversion of
methemoglobin to
hemoglobin.

• Ascorbic acid deficiency increases the
permeability of the oral mucosa to endotoxin,
inulin, and of normal human crevicular
epithelium to dextran.
• An optimal level of ascorbic acid is apparently
required to maintain the integrity of the
periodontal microvasculature.

• Depletion of vitamin C may interfere with the
ecologic equilibrium of bacteria in plaque and
thus increase its pathogenicity. However, no
evidence demonstrates this effect.

• Tyrosine metabolism : Ascorbic acid is required
for the oxidation of p-hydroxy phenylpyruvate
(enzyme hydroxylase) to homogentisic acid in
tyrosine metabolism.

• Tryptophan metabolism : Vitamin C is
essential for the hydroxylation of tryptophan
(enzyme-hydroxylase) to hydroxytryptophan
in the synthesis of serotonin.

• Folic acid metabolism : Vitamin C is needed for
the formation of FH4 (enzyme-folic acid
reductase). Further, in association with FH4,
ascorbic acid is involved in the maturation of
erythrocytes.

• Peptide hormone synthesis : Hydroxylation of glycine is
carried out by peptidylglycine hydroxylase which
requires vitamin C.
• Synthesis of corticosteroid hormones : Adrenal gland
possesses high levels of ascorbic acid, particularly in
periods of stress.

• Sparing action of other vitamins : Ascorbic acid is a
strong antioxidant. It spares vitamin A, vitamin E,
and some B-complex vitamins from oxidation.

• Immunological function : Vitamin C enhances the
synthesis of immunoglobulins (antibodies) and
increases the phagocytic action of leucocytes.

• Preventive action on cataract : Vitamin C reduces the
risk of cataract formation.
• Preventive action on chronic diseases : As an
antioxidant, vitamin C reduces the risk of cancer,
cataract, and coronary heart diseases.

Deficiency of vitamin C
• Scurvy.
• The chief feature of the disease is that the limbs
become painful and tender from
the hemorrhages beneath the
periosteum.

• Scurvy is diagnosed by its symptoms, including
ecchymosis of the skin, loose attachment of the
periosteum, subperiosteal hemathomas, bleeding into
the joint spaces, gingivitis, hemorrhages,
opportunistic bacterial infections, and impaired
wound healing (Vaxman et al.)

Infantile Scurvy (Barlow’s Disease)
• In infants between 6 to 12 months of age, (period in
which weaning from breast milk)
Hemorrhagic Tendency
• In ascorbic acid deficiency, collagen is abnormal and
the intercellular cement substance is brittle. So
capillaries are fragile, leading to the tendency to
bleed even under minor pressure.

Internal Hemorrhage
• In severe cases, hemorrhage may occur in the
conjunctiva and retina. Internal bleeding may be
seen as epistaxis, hematuria or melena.
Oral Cavity
• In severe cases of scurvy, the gum becomes painful,
swollen, and spongy. The pulp is separated from the
dentine and finally teeth are
lost. Wound healing may be
delayed.

Bones
• In the bones, the deficiency results in the failure of
the osteoblasts to form the intercellular substance,
osteoid. Without the normal ground substance, the
deposition of bone is arrested.

Anemia
• In vitamin C deficiency, microcytic, hypochromic
anemia is seen. Poikilocytosis and anisocytosis are
also common in anemia due to deficiency of
vitamin C.

VITAMIN C AND PERIODONTIUM
• However, the majority of workers who have looked
into ascorbic acid–periodontal relationships in
humans estimated the dietary intake of vitamin C.
(Ismail et al. 1983, Nishida et al. 2000)
• It has been established that ascorbic acid plays a
major role in the synthesis of collagen especially the
hydroxylation process, helix formation and cross-
linking of collagen molecules
(Alfano et al. 1975, Berg et al. 1983).

• There are several lines of evidence to suggest that
vitamin C affects chemotaxis as well as phagocytosis
of polymorphonuclear leucocytes and thereby
influences the hostimmune reactions.
(Alfano et al. 1975, Boxer et al. 1979, Dallegri et
al. 1980, Patrone et al. 1982).
• Vitamin C indirectly affects the histamine breakdown
and this in turn would retard gingival inflammation
(Nakamoto et al. 1984)

• The deficiency in vitamin C levels could be linked to
increased permeability of gingival mucosa, which
allows easy passage of microbial and other noxious
products into the periodontium.
(Alfano et al. 1975, Alvares and Siegel 1981)
• It has also been shown that ascorbic acid
demonstrates antioxidant properties.
(Nishida et al. 2000).

• Tobacco, especially, cigarette smoke contains
various oxidants that cause tissue damage and
consequently smokers do require a higher serum
concentration of vitamin C.
(Kallner et al. 1981, Nishida et al. 2000).

WATER – SOLUBLE VITAMINS
B COMPLEX GROUP OF VITAMINS
• The vitamin B-complex refers to all of both the known
essential water- soluble vitamins except for vitamin C.

• The important members of vitamin B complex
group are:
(1) Thiamine
(2) Riboflavin
(3) Niacin
(4) Pyridoxine
(5) Pantothenic acid
(6) Biotin
(7) Folic acid, and
(8) Vitamin B12.

• Christian Eijkman
(1900) produced
beriberi in chicken by
feeding polished rice.
• It is designated as
Aneurine (it can relieve
neuritis) or antiberiberi
factor.

Structure of Thiamine:
The vitamin is converted to its active coenzyme form
by addition of two phosphate groups, with the help of
ATP, catalyzed by thiamine pyrophosphotransferase.

Physiological Role of Thiamine

• The coenzyme form is thiamine pyrophosphate
(TPP). It is used in oxidative decarboxylation of alpha
keto acids.

• α-Ketoglutarate dehydrogenase is an
enzyme of the citric acid cycle.

• Transketolase is dependent on TPP. This is an enzyme
of the hexose monophosphate shunt (HMP shunt).

• The branched chain α-keto acid dehydrogenase
(decarboxylase) catalyses the oxidative
decarboxylation of branched chain amino acids
(valine, leucine and isoleucine) to the respective
keto acids.
• 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.

CLASSIFICATION OF BERI-BERI
• DRY BERI-BERI
• WET BERI-BERI
• INFANTILE BERI-BERI
• WERNICKE
KORSAKOFF

Deficiency Manifestations of Thiamine
Deficiency of thiamine leads to beriberi. The early
symptoms are anorexia, dyspepsia, heaviness and
weakness.
• Wet Beriberi: Cardiovascular manifestations are
prominent. Death occurs due to heart failure.

• Dry Beriberi: In this condition, CNS manifestations
are the major features. Peripheral neuritis with
sensory disturbance leads to complete paralysis.

• Infantile beriberi: It occurs in infants born to
mothers suffering from thiamine deficiency.

• Wernicke-Korsakoff Syndrome: It is also called
as cerebral beriberi. Clinical features are those
of encephalopathy plus psychosis.

• Alcoholic Polyneuritis:
Polyneuritis with motor
and sensory defects is
seen in chronic alcoholics.
Alcohol utilization needs
large doses of thiamine.

RDA OF B1
SOURCES OF VITAMIN
B1

• Riboflavin was the
first B complex
component to be
isolated in a pure
state.

Structure of Riboflavin:
• Riboflavin is converted to its active coenzyme
forms (FMN and FAD) with the help of ATP. The
solution when exposed to LJV light emits a
strong greenish-yellow fluorescence. It is heat
stable.

Coenzyme Activity of Riboflavin:
• Riboflavin exists in tissues tightly bound with
enzymes. Enzymes containing riboflavin are
called flavoproteins. The two coenzymes are
• FMN (flavin mono nucleotide) and
• FAD (flavin adenine dinucleotide).
• The enzyme complex contains molybdenum and
iron also, called metalloflavoproteins.

FUNCTIONS OF RIBOFLAVIN :
• Converted into enzymes necessary for tissue
respiration
• Needed for normal respiratory function.

• Required for the activation of B6. (pyridoxine).

• Maintains erythrocyte integrity

Riboflavin Deficiency:
• Riboflavin deficiency usually accompanies other
deficiency diseases such as beriberi, pellagra and
kwashiorkor.
• Phototherapy for neonatal jaundice causes transient
riboflavin deficiency. Symptoms are confined to skin
and mucous membranes.
• Glossitis, magenta colored tongue, atrophy of lingual
papillae, fissures of tongue,

• seborrhic dermatitis,
• cheilosis (Greek, cheilos = lip), inflammation at
the corners of mouth (angular stomatits),
• Proliferation of the bulbar conjunctival capillaries
is the earliest sign of riboflavin deficiency.

RDA OF VITAMIN B2
• Adults on sedentary work
require about 1.5 mg per
day.
• During pregnancy and
lactation, additional 0.2 to
0.4 mg is required.
• People aged above 60
years, also need
supplementation.
SOURCES OF VITAMIN B2

• It is also called as
Pellagra preventing
Factor of Goldberger.
• Niacin and niacinamide
are active forms of the
vitamin.
• Niacinamide is the form
present in tissues.

Chemistry of Niacin:
• Niacin is pyridine-3-carboxylic acid. Niacinamide
is the acid amide.
• Warburg in 1931 & Todd in 1937 compiled the
structure of niacin.

Co-enzyme forms of Niacin:
• Niacin is converted into its con-enzyme NAD +
and NADP + .

These co-enzymes play an important role in
• electron transport chain

• hexose shunt pathway
• conversion of met-hemoglobin to normal
hemoglobin.

• Two hereditary disorders involve niacin deficiency
• Schizophrenia
• Hartnup’s disease
• Certain drug therapies (e.g. isoniazid) can lead to
niacin deficiency (Carpenter 1983).

Toxicity of Niacin
• Nicotinic acid when given orally or parenterally
produces a transient vasodilatation of the
cutaneous vessels and histamine release. The
reaction is accompanied by itching, burning and
tingling

• The Greek word
“pantos” means
everywhere.
• It is widely distributed
in nature. Lipmann
discovered the CoA in
1946 (Nobel prize in
1953).

COENZYMES OF B5
The important CoA derivatives are:
• a. Acetyl CoA
• b. Succinyl CoA
• c. HMG CoA
• d. Acyl CoA.

DEFICIENCY OF PANTOTHENIC ACID
• Gopalan’s Burning Foot Syndrome is manifested
as paresthesia (burning, lightning pain) in lower
extremities, staggering gait due to impaired
coordination and sleep disturbances.

• In experimental animals, deficiency has resulted in
• anemia (due to reduced heme synthesis from succinyl CoA),
• reduced steroidogenesis (due to lack of acetyl CoA),
• dermatitis,
• fatty liver and
• adrenal necrosis.

• PAUL GẎORGI (1934)
showed that the
factor which cured
rat acrodynia was
VITAMIN B6.
• RICHARD KUHN et al
showed that B6 was
a pyridine derivative.

COENZYME OF PYRIDOXINE
• The active form of vitamin B6 is the coenzyme
pyridoxal phosphate (PLP).

BIOCHEMICAL FUNCTIONS OF PYRIDOXINE
• Pyridoxal phosphate (PLP), is closely associated with
Heme synthesis.

• The synthesis of certain
specialized products
such as serotonin,
histamine.

• Niacin coenzymes
from the amino acids
is dependent on
pyridoxine.

• Pyridoxal phosphate participates in reactions like
• Transamination,
• Decarboxylation,
• Deamination,
• Transsulfuration,
• Condensation etc.

Deficiency of pyridoxine
• Affects the neuro-muscular systems.
• Convulsions due to decreased GABA
availability,
• peripheral neuritis, synovitis. Etc.
• Glossitis
• As it is required for tryptophan synthesis,
deficiency of pyridoxine, can also contribute to
pellagra.

• Biotin was known as
anti-egg white injury
factor.
• Biotin was isolated in
1942 by Vincent du
Vigneaud, who was
awarded Nobel Prize in
1955.
• Avidin, is anti vitamin

STRUCTURE OF BIOTIN
• The structure is formed by fusion of imidazole
and thiophene rings with a valeric acid side
chain.
• Biocytin may be regarded as the coenzyme of
biotin.

FUNCTIONS OF BIOTIN
As a coenzyme, biotin is involved in various metabolic
reactions.
1. Gluconeogenesis and citric acid cycle :
• Biotin serves as a carrier of CO2 in carboxylation
reactions. The conversion of
pyruvate to oxaloacetate by
biotin dependent pyruvate
carboxylase is essential for the
synthesis of glucose from
many non-carbohydrate
sources.

2. Fatty acid synthesis : Acetyl CoA is the starting
material for the synthesis of fatty acids.
• The very first step in fatty acid synthesis is a
carboxylation reaction.
• Propionyl CoA is produced in the metabolism of
certain amino acids and degradation of odd chain
fatty acids. Its further metabolism is dependent on
biotin.

• In the metabolism of leucine, the following reaction
is dependent on biotin

Deficiency of Biotin
• i. Prolonged use of antibacterial drugs
• ii. Biotin deficiency symptoms include dermatitis,
atrophic glossitis, alopecia, hyperesthesia,
muscle pain, anorexia and hallucinations.

RDA OF B7
• About 200-300 mg
will meet the daily
requirements.
SOURCES OF B7

• Vitamin B9/folic acid
was discovered in 1941
by Henry Mitchell

• Folic acid is abundant in vegetables. It is soluble
in water and is rapidly destroyed on exposed to
light.
• Folic acid is readily absorbed by the upper part
of the jejunum. It is transported in blood by two
beta globulins.
• It is taken up by the liver where the coenzyme
forms are produced. It is not stored in any
tissues.

Deficiency of Vitamin B9:
• Folic acid deficiency is common in India. It is seen
in various physiological and pathological states
such as
• pregnancy,
• defective absorptive states,
• drugs such as phenytoin inhibit absoption, in
hemolytic anemias.

Macrocytic anemia:
• Most characteristic feature of folate deficiency.
In the normal process of erythropoesis, folate
deficiency lead to slowing of DNA synthesis with
normal protein synthesis.

• The most pronounced effect of folate deficiency
on cellular processes is on DNA synthesis. This is
due to cell cycle arrest in the S-phase of rapidly
proliferating cells, in particular hematopoietic
cells, resulting in megaloblastic anemia.
• Other GIT symptoms of folate deficiency include
vomiting, abdominal pain and diarrhea.

• It is also called
Extrinsic factor of
castle,
• and Anti-pernicious
anemia factor.

STRUCTURE OF VITAMIN B12
• It has 4.35 % cobalt and four pyrrole rings
coordinated with each cobalt atom – “Corrin
ring”.

• Vitamin B 12 combines with the intrinsic factor
of castle secreted from the gastric parietal cells.
The absorption takes place in the ileum.
• Enzymes linked to B 12 are many in bacteria, but
only two in animal tissues.

Vitamin B 12 deficiency:
• Nutritional deficiency is the most common cause
in India. Decresed absorption due to non-
availability of absorptive surface occurs in
gastrectomy,
• resection of ileum,
• malabsorption syndromes, etc.
• pernicious anemia, and
• autoimmune disease is another cause.
• Long standing chronic iron deficiency anemia
leads to erosion of mucosal surfaces and causes B
12 deficiency.

Clinical manifestations:
• Include megaloblastic anemia.
• Pernicious anemia is a megaloblastic anemia
resulting from vitamin B12 deficiency that develops
as a result of a lack of intrinsic factor in the stomach
leading to malabsorption of the vitamin.

B COMPLEX AND PERIODONTIUM
• In addition to anemia, a deficiency of vitamin B12
may lead to gingival bleeding. A recent study by Zong
et al. found an inverse association between serum
vitamin B12 levels and the severity of periodontitis.
• Additionally, reduced serum vitamin B9 levels have
been observed in smokers, which may lead to
periodontitis.
• However, the mechanism of this association is not
clear.

Vitamins as Antioxidants
• Vitamins A, C, and E have all been observed to
modulate the anti‐oxidant defense system.
• Vitamins A, C, and E has been observed to decrease
the severity of periodontitis in non‐smokers.
• Similarly, supplementation with vitamin E has been
observed to simultaneously reduce levels of serum
superoxide dismutase and improve the outcomes of
scaling and root‐planing.

CONCLUSION
• Vitamins play an essential role for constant
regenerative processes for coping with oxidative
stress and to maintain adequate immune
response. In oral health, deficiency of certain
vitamins can lead to defects of hard tissue, oral
mucosa and Periodontium.

Essential Vitamins for Oral Health

Recommended

Recommended

More Related Content

What's hot

What's hot (20)

Similar to Essential Vitamins for Oral Health

Similar to Essential Vitamins for Oral Health (20)

Recently uploaded

Recently uploaded (20)

Essential Vitamins for Oral Health