vitamins notes for dental students

1. VITAMINS
PRESENTED BY – DR.ANUKRATI DONERIA
1ST YEAR M.D.S
DEPARTMENT OF PAEDIATRIC AND
PREVENTIVE DENTISTRY
NEW HORIZON DENTAL COLLEGE AND
RESEARCH INSTITUTE

2. TABLE OF CONTENT :
• INTRODUCTION
• DEFINATIONS
• HISTORY
• CLASSIFICATION
• VITAMIN-B COMPLEX
• VITAMIN-C
• VITAMIN- A
• VITAMIN-D
• VITAMIN-E
• VITAMIN-K
• REFRENCES

3. INTRODUCTION
• Name ‘vitamine’ was proposed by polish chemist CASIMIR
FUNK in 1911 in rice polishing and later in yeast.
• VITAMIN = VITAL + AMINE
• Earlier it was believed that all the vitamins are amines, Later it
was found that not all the vitamins are amines , the term
vitamin has been adopted universally.
• Since their chemical nature were unknown later designations
were applied for their nomenclature e.g. vitamin A, B, C .
• Doesn’t provide energy, mainly acts as catalysts for energy
releasing reactions from carbohydrates, lipids and proteins.

4. DEFINATION –
Vitamins are organic nutrients that are required in small quantities for a
variety of biochemical functions for normal maintenance of optimum
growth and health of the organism , also which cannot be generally
synthesized by the body and must therefore be supplied in the diet.
• The most prominent function of the vitamins is to serve as coenzymes
for enzymatic reactions.
• They can be used for medicinal purposes as a non-specific tools in
high doses for:
a. diabetes mellitus -B1, B2, B6
b. Cold and infectious disease – vitamin C

5. History
• Hopkins coined the term accessory factors to the unknown
and essential nutrients present in natural foods.
• Term vitamin has been applied to a group of biologically
essential compounds that includes 14 compounds that
can’t be synthesized in the body of human beings.
• Uses of vitamin A, B and C was introduced in 1915 by
McCollum and Davis.

6. CLASSIFICATION -
VITAMINS
WATER SOLUBLE FAT SOLUBLE
VITAMIN-A
VITAMIN-D
VITAMIN-E
VITAMIN-K
B COMPLEX NON B COMPLEX
VITAMIN-C

7. B COMPLEX
ENERGY RELEASING HEMOPOETIC
Thiamine (B1)
Riboflavin (B2)
Niacin (B3)
Pyridoxine(B6)
Biotin (B7)
Pantothenic acid(B5)
Folic acid (B9)
Vitamin B12
(cyanocobalamin)

8. WATER SOLUBLE VS FAT SOLUBLE
• Fat-soluble vitamins are soluble in fats.
• They are absorbed by fat globules that travel through the
small intestines and into the general blood circulation within
the body.
• Unlike water-soluble vitamins, fat-soluble vitamins are
stored in the body when they are not in use. Typically, they
are stored in the liver and fat tissues.

9. • Water-soluble vitamins dissolve in water, which means
these vitamins and nutrients dissolve quickly in the
body.
• Unlike fat-soluble vitamins, water-soluble vitamins are
carried to the body’s tissues, but the body cannot store
them.
• Any excess amounts of water-soluble vitamins simply
pass through the body.
• Vitamin A in its Beta-Carotene form is water-soluble.

10. B COMPLEX VITAMINS-
• Most B complex vitamins that occurs in nature are in the bound form,
within the cells of plants or animal tissues.
• Excretion of vitamins occurs in the kidney. Vitamin B complex is
composed of eight B vitamins:
B-1 (thiamine)
B-2 (riboflavin)
B-3 (niacin)
B-5 (pantothenic acid)
B-6 (pyridoxine)
B-7 (biotin)
B-9 (folic acid)
B-12 (Cobalamine)

11. THIAMINE (VIT B1)
• It is also called Anti Beriberi factor, Anti Neurotic factor.
• It is colorless, basic organic compound containing pyrimidine
ring with thiazole group held by methylene bridge.
• Chemical formula C12H17N4OS

12. • It has an active coenzyme form , thiamine
pyrophosphate(TTP) which is mostly associated with
carbohydrate metabolism.
• Alcohol group of thiamine is esterified with
phosphates in presence of ATP to form co-enzyme
TPP.

13. History
• In 1884, Takaki Kanehiro , hypothesized that the disease beri-beri
was due to insufficiencies of thiamine in the diet.
• Switching diets on a navy ship, he discovered that replacing a diet
of white rice only with one also containing barley, meat, milk,
bread, and vegetables, nearly eliminated beriberi on a nine-month
sea voyage.
• Gerrit Grijns in 1901, correctly interpreted the connection
between excessive consumption of polished rice and beriberi .
• He concluded that rice contains an essential nutrient in the outer
layers of the grain that is removed by polishing.

14. Sources :
• Unrefined cereals,
• Meat
• Nuts
• Green vegetables
• Eggs etc.

15. Functions :
• The coenzyme, thiamin pyrophosphate(TPP) is connected with
the energy releasing reactions in the carbohydrate
metabolism.
• Conversion of pyruvate to acetyl Co-A , along with pyruvate
dehydrogenase. Acetyl Co-A plays an important role in
transmission of nerve impulse.
• Plays role as a co-enzyme in citric acid cycle in conversion of
alfa-ketogluterate into succinyl Co-A with alfa-ketogluterate
dehydrogenase
PYRUVATE ACETYL CO-A

17. Nutritional requirements
Nutritional research council recommends :
• 1.0 to 1.5 mg of thiamine – for adults
• Men – 1.3 mg per day
• women – 1.0 mg per day
• Pregnancy and lactation-1.4 mg per day
• Children – 1.1mg.per day
• can be increased with increased muscular activity

18. Deficiency manifestations
• Deficiency causes BERI-BERI
• Mostly occurs in population consuming polished rice
• Thiamin deficiency leads to 3 types of beri-beri –
Dry beri-beri :
- when diet chronically contains slightly less than daily
requirements.
- Primary peripheral neuritis, severe muscular weakness and
fatigue.
- Dry skin, poor appetite, mental confusion.

19. 2. Wet beri-beri :
• Also known as cardiac beri-beri
• When deficiency is more severe, Cardiovascular system is
affected along with neurological disturbances.
• Edema of extremities, heart enlargement, cardiac insufficiency,
tachycardia, bradycardia, and palpitation.
3. Infantile beri-beri :
• In breast feed newborns with thiamine deficiency in mothers.
• Cardiac dilation, tachycardia, convulsions, edema, GI
disturbances. Infant may die in acute condition.

21. Wernicke-Korsakoff's Syndrome
• Chronic alcoholics.
• The body needs of thiamine increases
• Insufficient intake or impaired
intestinal absorption of thiamine will
lead to this syndrome
• Korsakoff’s psychosis : confusion, loss
of recent memory
• Wernicke’s encephalopathy:
nystagmus and extra ocular palsy

22. Oral Manifestations
• Hypersensitivity of dentin
• Minute vesicles on the buccal mucosa, under the tongue, or
on the palate described by Weisberger in 1941.
• Erosion of the oral mucosa, Pain in tongue, teeth, jaw, and
face.
Antimetabolites
• Thiaminase – destroys thiamine
• Present in raw fish and sea food

23. Diagnosis
• response to treatment with thiamine
• Whole blood erythrocyte transketolase is thiamine assay
Management
• 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 of thiamine 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.

24. VITAMIN B-2 (RIBOFLAVIN)
• Warburg and Christian (1932) identified a
yellow enzyme which contained riboflavin.
• Consists isoalloxazine ring with a D- Ribitol
side chain.
• Heat stable but decomposes in visible
light.
• Active forms are : Flavin Mono
Nucleotide(FMN) and Flavin adenine
dinucleotide (FAD)

25. History
• The British chemist Alexander W. Blyth in 1879 isolated a water-
soluble, yellow fluorescent compound from milk whey that he
called lactochrome.
• The importance of lactochrome was not fully realized until later
investigational studies by McCollum and Kennedy (1916), Emmett
and Luros, and Smith and Hendricks that showed it’s preventive
capabilities against beriberi, pellagra, and pellagra-like dermatitis.
• These water-soluble B fractions were later termed vitamin B2.

26. Sources
• Yeast
• Germinating seeds
• Green leafy vegetables
• Milk and milk products
• Egg
• Liver
• meat

27. Functions
• Riboflavin FMN, FAD
• FMN, FAD – required for several oxidation
reduction reaction in metabolism.
• Carbohydrates, protein, lipid, nucleic acid
metabolism and electron transport chain.
• FAD is required to convert tryptophan to
niacin (vitamin B3).
• FAD is required to convert retinol(vitamin A)
to retinoic acid.

28. Daily nutritional requirements
• Adults: 1.2-1.7 mg/day
• Higher intakes (0.2-0.5 mg/day) are advised for pregnant
and lactating women.
Deficiency manifestations
• Seen in chronic alcoholics.
• Cheilosis, glossitis, dermatitis, vascularization of cornea .

29. • Mild to moderate cases : dorsum →
magenta, patchy atrophy of the filiform
papillae and engorged fungiform
papilla (pebble-like elevations).
• Severe deficiency : dorsum is flat, with
a dry and fissured surface.
• Angular cheilitis begins as an
inflammation of the commissure of the
lips erosion, ulceration and
fissuring.

30. • Candidiasis may develop in the commissures
of debilitated persons perleche

31. NIACIN (VITAMIN-B3)
• Also known as nicotinic acid and nicotinamide. Formula
C6H5NO2 .
• Belongs to a group of pyridine carboxylic acid
• Also known as “Pellagra preventive factor of Goldberg.”
• Active forms :
Nicotinamide adenine
dinucleotide
(NAD+)
Nicotinamide adenine
dinucleotide phosphate
(NADP+)

32. History
• Niacin was first described by chemist Hugo Weidel in 1873 in his
studies of nicotine.
• For the first time, niacin was extracted by Casimir Funk, but he
thought that it was thiamine due to amine group.
• Niacin was extracted from livers by biochemist Conrad Elvehjem
in 1937, who later identified the active ingredient, then referred
to as the "pellagra-preventing factor" and the "anti-black
tongue factor”.

33. Sources
• Yeast
• Liver
• Legumes
• Meat
• Tryptophan metabolism –
60mg tryptophan = 1 mg niacin
generated.

34. Nutritional requirement
• Adults : 15-20 mg/day
• Children: 10-15 mg/day
• 1 mg niacin= 60 mg tryptophan
Functions
• Niacin NAD, NADP
• NAD – in citric acid cycle and glycolysis
• NADP – synthesis of cholesterol, fatty acid, pentose
phosphate pathways

35. Deficiency manifestations
• Pellagra – involves skin, GIT, CNS
• Characterized by 3-D’s :
a. Dermatitis (severe sunburn-
butterfly like pattern)
b. Diarrhea
c. Dementia and
• if not treated, 4th D - death

36. • Pellagra was initially described by the physician Gaspar Casal
in 1735, while he was looking for a cure of a skin disease
named “mal de la rosa”.
• soon after the maize was introduced into Europe.
• The name of the disease was established in 1771 by an
Italian physician Francesco Frapolli.
• In 1915, Goldberger conducted a series of experiments on 11
healthy prisoners in a Mississippi jail and found that he could
induce pellagra by altering their diets.
• He concluded that the disease was caused by the absence of
some factor that was lacking in corn, but that could be found
in meat and milk. He named it the P-P (for pellagra-
preventative) factor.

37. • Niacin deficiency= diet poor in both niacin and tryptophan
• Hartnup disease : a condition caused by the body's
inability to absorb certain (amino acids) from the diet. As
a result there is impaired production of other substances
such as vitamins and proteins.
• malignant carcinoid syndrome : functioning tumour cells
indirectly depress endogenous niacin production by
diverting tryptophan metabolism towards serotonin and
away from niacin. Anorexia and diarrhoea, frequently
present in the carcinoid syndrome.

38.  Oral manifestation’s –
• Glossitis and stomatitis - Tongue is “beefy
red”, glossodynia and glossopyrosis
• Profuse salivation.
• The most common finding is NUG usually
in areas of local irritation.
• Necrosis of gingiva and leukopenia-
terminal features

39. Vitamin B-5 (Pantothenic acid)
• Pantothenic acid (Greek: pantos- everywhere)
• Its metabolic role in synthesis of coenzyme A is also
widespread.
• Discovered by Roger J. Williams in 1933.

40. Chemistry
• It is an amide of β-alanine and dihydroxy dimethyl butyric acid
(Pantoic acid)
• It is stable to heat but unstable to alkali or acid

41. Absorption
• Intestinal phosphatases release pantothenic acid from dietary sources.
• Free pantothenate or its salts are freely absorbed in the intestine via sodium
dependent active transport system and reach various tissues through
circulation.
Co-A hydrolysis 4’phosphatepantetheine
dephosphorylation
pantethienepantetheinaseFree pantothenic acid

42. Nutritional requirements
Adults- 5-10mg
Sources
• Egg
• Liver
• Yeast
• Milk
• Cabbage
• Avocado

43. Functions
• Only the dextrorotatory (D) isomer of pantothenic acid
possesses biologic activity
• Pantothenic acid is used in the synthesis of coenzyme A
(CoA). Coenzyme A carry acyl group to form acetyl Co-A.
• Coenzyme (CoA) participates in several enzymatic
reactions of carbohydrate, lipid and amino acid
metabolism.
Pantothenic acid Coenzyme-A

44. Deficiency
• Rarely occurs since it is found in everything.
• It cause burning feet, abdominal cramps, restlessness and
fatigue in humans.
• Acetylcholine synthesis is also impaired; therefore,
neurological symptoms can also appear in deficiency.
• In an experiment done by D.E.ZISKIN, M.KAEHAN , G.STEIN
AND D.A.DKAGIFF in 1949 on rats, the diet deficient in
pantothenic acid showed ulcers of the tongue in various
sizes characterized by agranular type of necrosis.

45. VITAMIN B-6 (pyridoxine)
Chemistry
• Vitamin B-6 is a mixture of three closely related pyridine
derivatives :
a. Pyridoxine
b. pyridoxal
c. pyridoxamine.
• Pyridoxine is stable to heat and sensitive to light and alkali.
• Pyridoxal phosphate(PLP) is active form. It is formed from
phosphorylation of all 3 forms of vitamin b-6.

46. Absorption and Transport
• Pyridoxine is easily absorbed and reaches various tissues
through circulation.
• In the tissues pyridoxine is converted to pyridoxal and
pyridoxamine.
Recommended dietary allowance of
vitamin B6
• Adults : 1.6 to 2.2 mg / day
• During pregnancy, lactation and old age an intake of 2.5
mg / day recommended

47. Sources
• Wheat
• Corn
• Cabbage
• Egg yolk
• Fish
• Milk
• Meat

48. Functions
• Pyridoxal phosphate acts as a co-enzyme in reactions
of amino acid metabolism :
a. Transamination
b. Decarboxylation
c. Non- oxidative deamination
d. Transsulfuration
e. Condensation reactions of amino acids
• Transamination reaction : PLP acts as a co-enzyme
for converting amino acids into keto acids.

49. • Decarboxylation reactions : acts as co-enzyme in
decarboxylation of amino acids and forms
various biogenic amines . E.g. – GABA, Serotonin,
histamines, catecholamine's production
• Non-oxidative deamination of hydroxyl group
containing amino acids also requires PLP.
• PLP is also required for condensation reactions
of L-glycine and succinyl CoA to form δ- amino
levulinic acid , a precursor of heme.
• PLP is required for production of sphignosine, a
component of sphignomyelin.

50. Pyridoxine Deficiency
• It is rare in human adults.
• Neurological disorders like depression, nervousness
and irritability .
• In children vitamin B6 deficiency causes epileptic form
convulsions (seizures) due to decreased formation of
neuro transmitters like GABA, serotonin and
catecholamine's.
• Hypochromic microcytic anemia .

51. Oral manifestations
Glossitis
Cheilitis
Therapeutic uses
Pyridoxine is used for treatment of :
a. Seizures
b. Down syndrome
c. Autism
d. Premenstrual tension syndrome

52. Vitamin b7(Biotin)
• Formally known as vitamin H
• The human body cannot synthesize biotin. Only bacteria,
molds, yeasts, algae, and certain plants can make it, so the
diet needs to supply it.
• Unused biotin is eliminated in urine
Chemistry
• Imidazole derivative .
• Consists tetrahydrothiophene ring bound to an imidazole
ring with a valeric acid side chain

53. Sources
• Banana
• Egg yolk
• Raspberries
• Liver
• Mushrooms
• Cauliflowers

54. Active form
• Biocytin
Functions
• It is a co-enzyme of carboxylase reactions, it is a carrier of
CO2 in these reactions. Some reactions requiring biotin as
co-enzymes are :
a. Conversion of acetyl –Co-A to malonyl Co-A in fatty acid
synthesis.
b. Gluconeogenesis

55. Nutritional requirements
• It is synthesized by intestinal microorganisms in large amount,
so dietary intake is not necessarily required.
• However a daily intake of 150-300 ųg is recommended for
adults .
Deficiency manifestation
• Deficiency doesn’t occurs in humans in most of cases.
• Deficiency of biotin occurs in :
a. people consuming large amount of uncooked eggs .
b. People on prolonged antibiotics.

56. Vitamin B12 (cyanocobalamin)
• Anti-pernicious anemia vitamin.
Chemistry
• Cobalamine exists in 3 forms that differ in the nature of
chemical groups attached to cobalt.
• Cyanocobalamin is commercial available form of vitamin B-
12.
Active forms
a. Methylcobalamin
b. Deoxyladenosylcobalamin

57. Sources
Absent in plant foods.
Present in small amount in intestinal flora
Animal sources are :
egg, meat, milk, fish, poultry and diary
products .

58. Absorption, transport and storage
• Intestinal absorption of vitamin b-12 requires Intrinsic factor (IF)
• IF + vitamin B-12 – in stomach –> vitamin B-12 Intrinsic factor
complex which binds to specific receptors on surface of mucosal
cells of ileum.
• After binding, vitamin B12 is released from vitamin b12 intrinsic
factor complex.
• Vitamin b-12 is converted into Methylcobalamin and then
transported by vitamin b12 binding protein known as
transcobalamin(TC-1, TC-2)

59. • Excess Methylcobalamin is taken up by liver and stored in
deoxyladenosyl B12 form.
• It is the only water soluble vitamin that can be stored in
significant amount in liver.
Nutritional requirement
• Adults : 3 mcg per day
• Children : 0.5-1.5 mcg per day
• During pregnancy and lactation : 4 mcg per day

60. Functions
Only 2 enzyme system requires vitamin B12 as coenzyme:
a. Isomerization of methylmalonyl Co-A to succinyl Co-A
b. conversion of homocysteine to methionine.
Deficiency manifestations
Due to decreased absorption or dietary intake. Deficiency
leads to :
a. Pernicious anemia – due to deficiency of intrinsic factors
b. Megaloblastic anemia – due to functional folate
deficiency
c. Methylmalonic aciduria
d. Neuropathy

61. Oral Manifestations
• Glossitis:50-60% (Moeller’s glossitis or Hunter’s
glossitis)
• stomatitis and mucosal ulcerations.
• Epithelial cell abnormalities- More susceptible to
epithelial dysplasia or malignant transformation
Treatment
Vitamin B12 (100-1000µg)-IM

62. Vitamin-B9 (Folic acid)
• Lucy Wills in 1931 identified folate as the nutrient needed to
prevent anemia during pregnancy.
• Derived from Latin word Folium-leaf
Structure
• Consists of 3 components :
a. Pteridine ring
b. P-amino benzoic acid (PABA)
c. L- glutamic acid

63. Active form
Tetrahydrofolate (THF) .
Sources
Green leafy vegetables, liver, yeast
Nutritional requirements
• Adults : 200 mcg
• Higher intakes are recommended
during pregnancy and lactation:
400 mcg

64. Functions
• THF acts as a carrier of one carbon units like methyl,
methylene, methenyl, formyl , formimino.
• 5 major reactions in which THF is involved are :
a. Conversion of serine to glycine
b. Synthesis of thymidylate .
c. Catabolism of histidine
d. Synthesis of purine
e. Synthesis of methionine from homocysteine

65. Deficiency manifestation
• Deficiency Frequently occurs in pregnant women and alcoholics.
• Clinical symptoms of folic acid deficiency includes :
a. Megaloblastic or macrocytic anemia
b. Neural tube defects in fetus during pregnancy.
c. Hyperhomocysteinemia
• Oral symptoms includes :
a. Glossitis – swelling of lateral borders and tip of the tongue.
b. Generalized stomatitis
c. Cheilitis

67. Vitamin c ( ascorbic acid )
• First vitamin to be artificially synthesized in 1935.
• humans doesn’t produce ascorbic acid due to
deficiency of L- gluconolactone oxidase.
• Ascorbic acid - active form .
• Most powerful antioxidant.
• Ascorbic acid is a weak sugar acid.
• In biological systems, ascorbic acid can be found only
at low pH, but in solutions with PH above 5 it is found
in the ionized form, ascorbate.

68. History
• In 1769 William stark conducted an experiment on himself
when he restricted his diet up to meat and starch but it was
devoid of fresh fruits and vegetables, after consuming his diet
for 31 days he recorded that his gums were red and swollen and
bleeds easily to touch, 7 months later he died possibly from
scurvy.
• In 1907 , experimentally scurvy was produced by the Norwegian
physicians Alex Holst and Theodor Frolic in guinea pigs through
diet restricted to grains and flour only and shown to be
prevented by feeding of fresh fruits and vegetables.
• Vitamin C was isolated in 1928 and synthesized in 1935 by
Albert Szent Gyorgyi, making it the first vitamin to be
synthesized artificially.

69. Sources
• Leafy vegetables
• Fruits
• Citrus fruits
• Tomatoes
• Spinach
• Potatoes
• Animals and diary products are
very poor sources .

70. • The biological role of ascorbic acid is :
• participate in hydroxylation of many
structures e.g. hydroxylation of proline
• Collagen formation.
• Works in association of vitamin A and E.
• tissue regeneration
• building steroid hormones
• converting folic acid into tetra folic acid.
• One of the very important role of
vitamin C is its antioxidant activity.
Functions
- serves as
cofactor
and an
electron
donor in
various
reactions.

71. Absorption and transport
• Ascorbic acid is absorbed in the body by both active transport and simple
diffusion.
• The two transporter proteins required for active absorption:
a. Sodium- ascorbate Co-Transporters and
b. Hexose transporters
• Sodium- ascorbate Co-Transporters import the reduced form of ascorbate
across plasma membranes.
• Hexose transporters are glucose transporters, and transfer only the
dehydroascorbic acid (DHA) form of vitamin C.
• Excretion can be in the form of ascorbic acid, via urine.

72. Deficiency manifestation
SCURVEY : this disease is
characterized by
• Anaemia
• Swollen joints
• Ecchymosis
• Decreased immunity
• Increased blood cell fragility
• Delayed wound healing
• Haemorrhage
• Osteoporosis
• Corkscrew hairs
• Barlow’s syndrome

73. Oral manifestations
• The effects of vitamin C deficiency in periodontal tissues were
first studied by Glickman (1948) in guinea pigs.
• There is bleeding, osteoporosis and resorption of alveolar bone,
rupture of periodontal ligament fibers, widening of periodontal
ligament space and increased tooth mobility. Topping and Fraser
1939; Turseky and Glickman 1954; Dunphy et al 1956;
Waerhaug 1958.
• Boyle (1937,1938) believed that the deficiency produced
atrophic changes in the gingiva and underlying bone in guinea
pigs .
• Spongy gums, loose teeth.

74. • Oral scurvy is
characterized by
intense red, painful
swollen gingiva that
bleeds spontaneously
on slightest
provocation, resulting
in hemorrhages/
purpuras /bruising.
• The general
discoloration that
results from bleeding
and blood cells
breakdown is called
scurvy siderosis.

75. • Associated periodontal syndrome called “scorbutic gingivitis”–
1. Ulcerative gingivitis
2. Rapid periodontal pocket development
3. Tooth exfoliation
Diagnosis
• Most of the times, scurvy is misdiagnosed as vasculitis , blood
dyscrasias, ulcerative gingivitis.
• However, a thorough general physical examination, past
medical history, diet history along with blood examination and
histopathological examination can aid in formulating a proper
diagnosis.

76. Nutritional requirement
• Adults : 60-70 mg per day
• Additional intake(20-40%increase) are
recommended for women during pregnancy and
lactation
Treatment
• 250 mg of vitamin C, 4 times a day for 1 week aids in
achieving recovery.

77. Vitamin A (retinol)
• Consists of single 6 membered ring, a side chain of 11 carbons is
attached to it.
• An alcohol (retinol), can be converted into an aldehyde (retinal) or
an acid (retinoic acid)
• There are two types of vitamin A that are found in the diet:
a. Preformed vitamin A is found in animal products such as meat,
fish, poultry, and dairy foods in 3 forms : Retinol, retinal and
retinoic acid.
b. Provitamin A is found in plant-based foods in form of beta-
carotene

78. • Retinal is converted in to retinol by the action of enzyme
retinal aldehyde reductase, retinoic acid is formed by
oxidation of retinal.

79. History
• It is recorded in history that HIPPOCRATES cured night blindness(about
500 B.C) He prescribed to the patients Ox liver(in honey)which is now
known to contain high quantity of vitamin A.
• By 1917, Elmer McCollum et al discovered few accessory factors. These
"accessory factors" were termed "fat soluble" in 1918 and later
"vitamin A" in 1920.
• In 1931, Swiss chemist Paul Karrer described the chemical structure of
vitamin A.
• Vitamin A was first synthesized in 1947 by two Dutch chemists, David
Adriaan van Dorp and Josef Ferdinand Arens.

80. Absorption, transport and storage
ß- carotene
All trans Retinal
Retinol
Retinaldehyde reductase
• Retinol is then esterified and delivered to the liver for storage.
Beta-carotene dehydrogenase

81. • Transported by specific proteins- serum
retinal binding protein and cystolic
retinol binding proteins
Sources
• Richest sources are fish liver oil, animal
liver.
• Milk
• Dairy products
• Green leafy vegetables
• Red and yellow coloured fruits and
vegetables

82. Functions
• Vision- retinol and retinal
• Cell differentiation and growth
• Mucus secretion
• Epithelial cells maintenance
• antioxidant function – beta carotene – traps peroxy
free radicals in tissues and may account for
anticancer activity.

83. Rod cells
rhodopsin
11-cis-
retinal+
opsin
11-cis-
retinol
Role of vitamin A in vision :

84. Nutritional requirements
• Men and women – 600 mcg. Per day
• Pregnancy and lactation – 950 mcg. Per day
• Infants – 350 mcg. Per day
• Children – 600 mcg. Per day

85. Deficiency manifestation
• Night blindness
• Xeropthalmia
• Keratosis - rough and dry skin
• Bitot’s spot
• Retarded growth
• Abnormalities of reproductive
system

86. 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 – atypical dentin, lacks the
normal tubular structure.
• Caries – there is increased risk for caries
• Eruption – delayed in prolonged
deficiency.

87. • Alveolar bone – retardation 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

88. Hypervitaminosis A
• Symptoms : nausea, vomiting, diarrhea, bone and joint pain,
enlargement of liver, weight loss etc.
• In pregnant women Hypervitaminosis may cause congenital
malformation in growing fetus.
Therapeutic uses
• In treatment of psoriasis , and several skin diseases related
to involvement of epithelial cell differentiation and integrity.
• Precancerous lesion treatment with carotenoids.

89. 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 dose of 110
mg orally on two successive days.
• If Hypervitaminosis, restriction of diet

90. Vitamin D (cholecalciferol)
• It is also called SUNSHINE VITAMIN.
• It is thought of a hormone rather than a
vitamin because :
a. It can be synthesized in body
b. Released in circulation
c. Action is similar to steroid hormones.
d. Has distinct target organs

91. Structure
In 2 forms –
a. D3 or cholecalciferol : from animal or made in skin by
action of sunlight on 7-dehydrocholestrol.
b. D2 or ergocalciferol : by irradiation of sunlight on plants
sterol named ergosterol
Absorption, transport and activation
• Dietary vitamin D is absorbed in duodenum along with
lipids
• Transported to liver through chylomicrons

92. Active form :
Cholecalciferol is inactive form, it
metabolizes to produce active form of
vitamin D 1,25 dihydroxycholecalciferol
or calcitriol.
Sources
• Cod liver oil
• fish oils
• Egg yolk
• Sunlight
• Milk
• cheese

93. Functions
• Regulation of calcium and phosphorus metabolism to maintain their
normal plasma levels.
• Action of on intestine :
Increases calcium and phosphorus absorption from intestine by
enhancing synthesis of calcium binding protein “calbidins”.
• Action on kidney :
Calcitriol stimulates resorption of calcium and phosphorus from kidney
and decrease their excretion.

94. • Action of calcitriol on bone :
Promotes bone mineralization by depositing calcium and
phosphorus.
Promotes synthesis of calcium binding protein osteocalcin
Nutritional requirement
• The daily requirement of vitamin-D is 400 IU of
cholecalciferol.
• In countries with good sunlight(like India), RDA for vitamin
D Is 200 IU per day.

95. Deficiency manifestations
Rickets in growing children –
• characterized by formation of soft and
pliable bone, bent and deformed bones.
• Large and protruded forehead, pigeon
chest, bow heads, knock knees, kyphosis.
• Low plasma levels of calcium and
phosphorus, high alkaline phosphate
activity.

96. Osteomalacia in adults-
• Demineralization of previously formed
bones, bone fractures.
Renal rickets –
• In chronic renal failure
• Hypocalcemia and hyperphosphatemia
occurs
Oral manifestation
• Teeth - delayed formation of teeth
• Caries – higher risk of caries

97. • Enamel – there may be
hypoplasia of enamel, may be
mottled, yellow grey in colour
• Pulp – high pulp horns, large
pulp chamber, delayed closure
of root apices.
• Tendency of alveolar bone to
resorb.
• Tooth loss at young age
• Malocclusion

98. In a healthy individual, that pulp takes the form of an arch topped by two
"horns." In someone with a vitamin D deficiency, however, the shape of the
pulp is asymmetrical and constricted, looking more like a side view of a hard-
backed chair.

99. Hypervitaminosis D
• Vitamin D is mostly stored in liver and slowly metabolized.
• Most toxic in overdoses (10-100 times RDA).
• Characterized by : Renal calculi, Loss of appetite, nausea,
increased thirst and loss of weight.
• Hypervitaminosis will lead to increased calcium absorption and
bone resorption.
• Metastatic calcium deposition.

100. 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.

101. Vitamin E (Tocopherol )
• 1922 Herbert Evans and Katherine Scott Bishop found an
“anti sterility factor-x” in rats .
• Rats fed a purified diet of casein , cornstarch , butterfat salts ,
adequate Vitamin-A (as cod liver oil), Vitamin-B (as yeast),
and Vitamin-C (as orange juice) lost their ability to reproduce
.
• In 1936, Evans first published the chemical formula of
Vitamin-E in the Journal of Biological Chemistry
Active form :
• alfa-tocopherol

102. Sources
• Germ oil
• Fish oil
• Eggs
• Corn oil
• lettuce

103. Absorption, transport and storage
• Absorption : Vitamin E is absorbed from the intestines
packaged in chylomicrons.
• Transport : to the tissues via chylomicron and then
transported to the liver .
• The liver can export vitamin E in VLDLs.
• Due to its lipophilic nature, vitamin E accumulates in cellular
membranes, fat deposits and other circulating lipoproteins.
• Storage : adipose tissue.

104. Functions
• act as a natural antioxidant by scavenging free radicals and
molecular oxygen.
• Prevents peroxidation of polyunsaturated fatty acids in membrane
in cell membrane.
• Prevention of RBC from hemolysis
• Protection against athreomatous coronary heart disease.
• Prevents sterility .
Nutritional requirements
• For men-10mg
• For women-8 mg

105. ROLE OF VITAMIN E IN PREVENTION OF
ORAL CANCER
• Chandra Mouli PE et al. recommended use of Vitamin-
E as an antioxidant in oral lesions.
• Recent studies by Balwant Rai et al. have proved that
antioxidants such as Vitamin-C and Vitamin-E may be
utilized in oral Lichen planus patients to counteract
free radical mediated cell disturbances.
• T.N. Uma Maheswari highlighted the role of Vitamin-E
in the treatment of leukoplakia

106. Deficiency manifestations
• Sterility
• Degenerative changes in muscle
• Megaloblastic anaemia
• Changes in central nervous system
• Erythrocyte membrane fragility
• Depressed immunity.
• In premature Infants – haemolytic anaemia, thrombocytosis
and edema.

107. Oral manifestation
• loss of pigmentation ,atrophic degenerative changes in enamel
Vitamin E and periodontal tissues:
• Goodson and Bowles(1973) used vitamin E to treat 14 patients
with periodontal disease and found a reduction in inflammation
after 21 days.
• Cerna et al showed that long term (12 weeks) administration of
300 mg of Vitamin E significantly reduced inflammation of the
periodontal tissues.

108. Diagnosis
• A low alpha- tocopherol level or low ratio of serum alpha-
tocopherol to serum lipids measurement is the main way of
diagnosis.
Treatment
• Finding the underlying cause of the deficiency (fat
malabsorption, fat metabolism disorders, among others) and
then provide oral vitamin E supplementation.
• Modification in diet.

109. VITAMIN K
• Anti-hemorrhagic factor
• 1929, H Dam gave the name koagulation vitamin.
Chemistry :
• Available in 2 active natural forms :
a. vitamin K1 or phylloquinone – from plants
b. Vitamin k2 or menaquinones – from microorganisms
• Synthetic form : vitamin K3 – alkylated form of vitamin K2

110. Sources
• Cabbage,
• cauliflower,
• spinach,
• green vegetables
• Cheese,
• Dairy products ,
• Meat,
• egg yolk
• Synthesized by microorganisms
in intestinal tract

111. Absorption, transport and storage
• Absorbed only in presence of bile salts .
• Transported to liver in form of chylomicrons
• Stored in liver.
• Menadoine - synthetic vitamin K3 – water soluble, doesn’t require
bile salts for absorption.
Functions
• Blood coagulation by activation of blood clotting factors.

112. • OXIDATIVE PHOSPHORYLATION – it acts as a co-factor in oxidative
phosphorylation associated with lipid.
Nutritional requirements
men and women – 70 – 140 mcg Per day
children – 35 – 75 mcg per day
Deficiency manifestations - Deficiency occurs in patients
with
- liver disease
- In new born infants
- Following antibiotic therapy
• Increased clotting time

113. Oral manifestations
• excessive gingival bleeding after tooth-
brushing or spontaneously.
• Petechiae, ecchymosis and hematoma
may occur in the oral mucosa.
• In severe case, a slow constant, mild
hemorrhage occurs from the gum.
• Post extraction hemorrhage

114. Prothrombin level
• < 35% - bleeding on brushing.
• < 20% - spontaneous bleeding occurs
Diagnosis :
Elevated prothrombin levels or reduced clotting factors.
Management
parenteral dose of 10 mg
Antagonists to Vitamin K-
a. Warfarin
b. dicumoral

116. References
• Richard A. Harvey, Pamela C. Champe Book of Biochemistry
• John W. Baynes , Barek H. Dominiczak Book of medical Biochemistry
• Sharana basappa R. Japatti, Anuradha Bhatsange, Manjunath Reddy,
Y.S. Chidambaram, Satish Patil and Priyanka Vhanmane in Scurvy-
scorbutic siderosis of gingiva: A diagnostic challenge - A rare case
report.
• Lanska DJ. Historical aspects of the major neurological vitamin
deficiency disorders: the water-soluble B vitamins. In: Finger S, Boller
F, Tyler Kl, editors. Handbook of Clinical Neurology, Vol. 95 (3rd series)
- History of Neurology. Elsevier B.V., 2009; pp. 445-479.