Dr. P. Mounika Dept of Pedodontics and preventive dentistry

1. B Y :
P . M O U N I K A
2 N D Y E A R P G
WATER SOLUBLE VITAMINS
[B – Complex and C]

2. Contents:
1. Introduction
2. Classification
3. Vitamin C
 Dietary sources
 Metabolism
 Metabolic functions
 RDA (Recommended dietary allowance)
 Deficiency symptoms
 Hypervitaminosis
 Dental considerations

3. 4. Vitamin B complex
 Dietary sources
 Metabolism
 Metabolic functions
 RDA (Recommended dietary allowance)
 Deficiency symptoms
 Hypervitaminosis
 Dental considerations
5. Vitamin B-Complex and their co-enzymes
6. Conclusion
7. References

4. INTRODUCTION:
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, except for Vit B12. They are readily excreted
through urine hence toxicity due to overdosage is rare.

5. CLASSIFICATION OF WATER SOLUBLE VITAMINS:
1. Non B- complex 2. B-complex
Vitamin C
A. Energy releasing B. Hemotopoietic
Thiamine (B1)
Riboflavin (B2)
Niacin (B3)
Pantothenic acid (B5)
Pyridoxine (B6)
Biotin (B7)
Folic acid (B9)
Cynacobalamine (B12)

6. VITAMIN C (ASCORBIC ACID):
DIETARY SOURCES:
Vitamin C is widely distributed in both plants and animals, occurring mostly (80–90%) as ascorbic
acid but also as dehydroascorbic acid .

7. METABOLIC FUNCTIONS:
I. ANTIOXIDANT ACTION:
 Ability to react with free radicals
 Can reduce toxic, reactive oxygen species superoxide anion
and hydroxyl radical, as well as organic and nitrogen oxy radicals
 At physiological concentrations - one of the strongest reductants and radical scavengers
Based on this kind of potential,
it shows 2 types of actions in the body
A. Enzyme co-substrate functions
B. Non enzymatic functions

8. A. ENZYME CO-SUBSTRATE FUNCTIONS:
METABOLIC ROLE ENZYME
1. Collagen synthesis Prolyl 4-hydroxylase
Prolyl 3-hydroxylase
Lysine hydroxylase
2. Carnatine synthesis γ-Butyrobetaine2-oxoglutarate4
dioxygenase
Trimethyllysine 2-oxoglutarate dioxygenase
3. Catacholamine synthesis Dopamine β-monooxygenase
4. Peptide hormone synthesis Peptidylglycineα-amidating monooxygenase
5. Tyrosine metabolism 4-Hydroxyphenylpyruvate dioxygenase

9. 5. Drug and steroid metabolism
Microsomal hydroxylation reactions of drug and steroid metabolism—those coupled to the
microsomal electron transport chain.

10. B. NONENZYMATIC FUNCTIONS:
CELLULAR ANTIOXIDATION:
As the most effective aqueous antioxidant in plasma, interstitial fluids, and soluble phases of cells,
ascorbic acid appears to be the first line of defence against reactive oxygen species
 Prevention of lipid peroxidation
 Prevention of protein oxidation
 Prevention of DNA oxidation
 Prevention of NO oxidation

11. II. METAL ION METABOLISM
Ascorbic acid affects the nutritional utilization of iron and other transition elements:
 Promotion of nonheme iron bioavailability:
 Promotion of heme-iron bioavailability
 Interactions with other mineral elements

12. III. HEALTH EFFECTS:
1. Antihistamine reaction
2. Immune function
3. Inflammation
4. Cardiovascular disease
5. Excersice
6. Diabetes
7. Neurological function
8. Pregnancy outcomes
9. Skin health
10. Cataracts
11. Pulmonary function
12. Cancer

13. RECOMMENDED DIETARY ALLOWANCE:
Age Male Female Pregnancy Lactation
0–6 months 40 mg* 40 mg*
7–12 months 50 mg* 50 mg*
1–3 years 15 mg 15 mg
4–8 years 25 mg 25 mg
9–13 years 45 mg 45 mg
14–18 years 75 mg 65 mg 80 mg 115 mg
19+ years 90 mg 75 mg 85 mg 120 mg
[NIH: National Institutes of Health, Office of dietary supplements] *Adequate intake

14. DEFICIENCY SYMPTOMS:
Scurvy is the classical manifestation in human adults after 45–80 days of stopping vitamin C
consumption.
Primary signs in mesenchymal tissues – defect in collagen synthesis:
 Impaired wound healing; oedema; haemorrhage
 Weakening of collagenous structures in bone, cartilage, teeth, and connective tissues.
• Lethargy, fatigue
• Rheumatic pains in the legs
• Muscular atrophy
• Hematomas in the thighs
• Ecchymoses
• Hemorrhages in many organs

15. Moeller–Barlow disease
Seen in non-breastfed infants usually at about 6 months of age.
 Widening of bone–cartilage boundaries, particularly of the rib cage and epiphyseal cartilage of
the extremities
 Severe joint pain
 Anemia and fever
Scorbutic children show
 Inability to walk
 Tenderness of the lower limbs
 Bleeding of the gums
 Petechial hemorrhages.

16. HYPERVITAMINOSIS:
 Ascorbic acid, as such, has not been found to be toxic. But, dehydroascorbic acid (oxidized
form of ascorbic acid) is toxic.
 Oxalate has been implicated in the formation of kidney stones (contraversial)

17. DENTAL CONSIDERATIONS:
1. Avitaminosis
Defect in collagen synthesis
2. SCURVY:
•Failure of wound healing
•Rupture of capillaries
•Petechiae
•Ecchymoses
•Suppuration wounds
•Death
3. GINGIVITIS
PERIODONTITIS
4. Chewable vitamin C tablets --- Severe
erosion of dental enamel
Buffering agents (sodium ascorbate) –
Reduce erosion

18. THIAMINE (B1)
Essential vitamin for carbohydrate metabolism and neural function
DIETARY SOURCES:
Thiamine is mostly concentrated in the outer layer of cereals.
Polishing of rice removes about 80% of thiamine
Thiamine is extracted into the water during cooking process.
Such water should not be discarded.
METABOLISM:
Phosphorylated in the tissues : Thiamin pyrophosphokinase & TTP-ATP phosphoryltransferase
[Thiamin monophosphate (TMP)]
Excretion: Urine ------ Free thiamine, Thiamin monophosphate, Diphosphate ester and other
metabolites.

19. METABOLIC FUNCTIONS
Coenzyme : Thiamine pyrophosphate (TPP)/ Cocarboxylase
Connected with the energy releasing reactions in the carbohydrate metabolism.
Enzymes that are dependent on TPP:
 Pyruvate dehydrogenase ------------------------ Oxidative decarboxylation
 α-Ketoglutarate dehydrogenase ---------------- Citric acid cycle
 Transketolase -------------------------------------- Hexose Monophosphate Shunt (HMP shunt)
 α-ketoThiamine acid dehydrogenase ------------ for conversion of branched chain amino acids -
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.

20. RECOMMENDED DIETARY ALLOWANCE (RDA):
 The daily requirement of thiamine depends on the intake of carbohydrate.
 A dietary supply of 1-1.5 mg/day is recommended for adults
 For children RDA is 0.7-1.2 mg/day.
 The requirement marginally increases in pregnancy and lactation (2 mg/day), old age and
alcoholism.

21. DEFICIENCY SYMPTOMS:
1. BERI – BERI: WET BERI - BERI
DRY BERI - BERI
INFANTILE BERI -
BERI
2. PYRUVATE ACCUMULATION
Pyruvate accumulation in brain
results in disturbed metabolism that
may be responsible for
polyneuritis.
4. Wernicke-Korsakoff syndrome
This is a disorder mostly seen in chronic alcoholics.
The body demands of thiamine increase in alcoholism.
5. Enzyme deficiency due to thiaminase
and pyrithiamine, oxythiamine
3. Impaired nerve impulse

22. HYPERVITAMINOSIS AND DENTAL CONSIDERATIONS:
 Toxic only in the form of thiamin hydrochloride.
 Toxic dose: 100-fold the RDA (Headache, convulsions, weakness, paralysis, cardiac
arrhythmia, and allergic reactions).
Thiamine is a constituent of enzymes that degrade sucrose to organic acids that can ultimately
dissolve tooth enamel.
 Tongue : Flabby, red, and edematous
 Gingiva: “old rose” color
 Fungiform papillae enlarge and become hyperemic

23. RIBOFLAVIN (B2):
DIETARY SOURCES:
Moderate sources:
Cereals, fruits,
vegetables and fish
Bacteria in hindgut
METABOLISM:
SOURCE:
FMN
FAD
Free riboflavin
FAD - pyrophosphatase
FMN-phosphatase
Absorption:
Proximal small intestine
Colon
Excretion:
Urine

24. METABOLIC FUNTIONS:
I. Co-enzymatic functions:
The coenzymes, FAD and FMN are associated with certain enzymes
 Redox reactions – Energy production
 Flavoprotiens & Metalloflavoprotiens
Metabolic process Enzymes
Carbohydrate metabolism Pyruvate dehydrogenase complex
α-Ketoglutarate dehydrogenase complex
Succinate dehydrogenase
Lipid metabolism Acyl CoA dehydrogenase
Protein metabolism Glycine oxidase
D-Amino acid oxidase
Purine metabolism Xanthine oxidase
Electron transport chain L-Amino acid oxidase

25. II. Health Effects:
Oxidative stress:
Flavoenzymes participate in protection of erythrocytes and other cells against oxidative stress.
Vascular disease:
Homocysteine levels leads to increased risks to occlusive vascular disease, stroke, dimentia,
Alzheimer’s disease and chronic heart failure.
Congenital defects in fat metabolism:
As essential coenzymes for acyl-CoA dehydrogenase and NADH dehydrogenase, riboflavin plays
essential roles in lipid metabolism.

26. RECOMMENDED DIETARY ALLOWANCE (RDA):
Age Male Female Pregnancy Lactation
Birth to 6 months 0.3 mg 0.3 mg
7–12 months 0.4 mg 0.4 mg
1–3 years 0.5 mg 0.5 mg
4–8 years 0.6 mg 0.6 mg
9–13 years 0.9 mg 0.9 mg
14–18 years 1.3 mg 1.0 mg 1.4 mg 1.6 mg
19-50 years 1.3 mg 1.1 mg 1.4 mg 1.6 mg
51+ years 1.3 mg 1.1 mg
[NIH: National Institutes of Health, Office of dietary supplements]

27. DEFIECIENCY SYMPTOMS:
 General symptoms : Loss of appetite, impaired growth.
 Specific epithelial lesions and nervous disorders
 Low activities of a variety of flavoenzymes.
 Reduced enteric absorption of dietary iron, resulting in secondary impairments in nutritional
iron.
 The toxicity of riboflavin is very low
 High oral doses of riboflavin are essentially nontoxic
 Somewhat more toxic when administered parenterally.
HYPERVITAMINOSIS:

28. DENTAL CONSIDERATIONS:
Ariboflavinosis : Angular cheilosis, Dermatitis and Anemia.
ANGULAR CHEILOSIS
Lips: Extremely red and smooth.
Tongue: Pebbly or granular appearance.
Fungiform papillae: Swollen and slightly flattened mushroom shaped
Severe conditions:
Papillary atrophy
Irregular denudation of the tongue
Purplish red or Magenta colored
Advanced conditions:
Entire tongue may become atrophic and
smooth

29. NIACIN (B3):
Pellagra Preventive (P.P.) factor of Goldberg
DIETARY SOYRCES:
A substantial amount of niacin can be synthesized from
the indispensable amino acid tryptophan.
METABOLISM:
SOURCE:
NAD(H)
NADP(H),
ABSORPTION:
NAm (Nicotinamide)
Stomach
Small intestine
STORAGE:
NAm (Nicotinamide)
NA (Nicotinamide Adinine)
EXCRETION:
Urine

30. METABOLIC FUNCTIONS:
I. Co-enzyme actions:
 Dietary nicotinamide, niacin and tryptophan ----------- NAD+ & NADP+
 A large number of enzymes (about 40) belonging to the class oxidoreductases are dependent on
NAD+ or NADP+ and NADPH
 E.g: Glyceraldehyde 3-phosphate dehydrogenase, Glutamate dehydrogenase, Isocitrate
dehydrogenase, Glucose 6-phosphate dehydrogenase etc.
II. METABOLIC ROLE:
 Genomic Stability: Play a role in DNA repair and replication, and in cell differentiation and
apoptosis.
 Glucose Tolerance Factor: Enhances the response to insulin.

31. RECOMMENDED DIETARY ALLOWANCE (RDA):
 Adult - 15-20 mg
 Children - 10-15 mg
 1 mg niacin = 60 mg of tryptophan (NE : Niacin Equivalent)
 Pregnancy and lactation in women require addition requirements

32. DEFICIENCY SYMPTOMS:
PELLAGRA (Italian: rough skin)
Skin, GIT & CNS
3D’s – Dermatitis, Diarrhoea, Dementia
Not treated 4th D – Death
Dermatitis :Inflammation of skin exposed to sunlight
Diarrhoea : Loose stools, often with blood and mucus
Dementia (Degeneration of nervous tissue) : Anxiety, irritability, poor memory, insomnia etc
 Seen among people whose staple diet is corn or maize
 Niacin present in maize is in bound form & is unavailable to the body
 Tryptophan content is low in maize

33. THERAPEUTIC USES OF NIACIN:
 Pharmacological doses : 2-4 g/day, 200 times the RDA
 Inhibits lipolysis in the adipose tissue - Circulatory free fatty acids & Triacylglycerol
 The serum levels of LDL, VLDL, triacylglycerol and cholesterol are lowered.
 Treat : Hyperlipoproteinemia type II b (elevation of LDL and VLDL).
 Glycogen and fat reserves of skeletal and cardiac muscle are depleted.
 There is a tendency for the increased levels of glucose and uric acid in the circulation
 Prolonged use of niacin results in elevated serum levels of certain enzymes, suggesting liver damage.
HYPERVITAMINOSIS:

34. DENTAL CONSIDERATIONS:
 Painful stomatitis - Diminished food intake
 Lesions in GIT - Diarrhoea and less vitamin absorption
 Pellagrous glossitis - Swelling of the papillae at
the tip and lateral borders of the tongue.
 Tongue - Painful, scarlet, and edematous.
 Atrophy of filiform and fungiform papillae
 Tongue - Smooth and shiny
 Fissures along the sides of the tongue & become infected rapidly.
 Gingiva – Inflamed
 Corners of the lips - Initially pale; fanlike fissuring occurs,
radiates into the perioral epithelium & may leave permanent scars.

35. PANTOTHENIC ACID (B5):
Chick anti-dermatitis factor or Filtrate factor
DIETARY SOURCES:
It is widely distributed vitamin
found in plants and animals.
METABOLISM:
SOURCE:
CoA
Acyl-carrier protein
Free vitamin
ABSORPTION:
Jejunum
Small intestine
EXCRETION:
Urine
Hydrolytic digestion in
intestinal lumen

36. METABOLIC FUNCTIONS:
I. Co-enzymatic action:
 The functions of pantothenic acid are exerted through coenzyme A or CoA
 CoA is a central molecule involved in all the metabolisms (carbohydrate, lipid and protein)
Eg: Pyruvate dehydrogenase, α-Ketoglutarate dehydrogenase, Thiokinase.
 In few metabolic reactions, group transfer is important which occurs in a bound form coenzyme A
Acetyl CoA + Choline  Acetylcholine + CoA
Acetyl CoA + Oxaloacetate  Citrate + CoA
II. Other functions:
 Pantothenic acid itself is a component of fatty acid synthase complex and is involved in the formation
of fatty acids

37. RECOMMENDED DIETARY ALLOWANCE (RDA):
Age Male Female Pregnancy Lactation
Birth to 6 months 1.7 mg 1.7 mg
7–12 months 1.8 mg 1.8 mg
1–3 years 2 mg 2 mg
4–8 years 3 mg 3 mg
9–13 years 4 mg 4 mg
14–18 years 5 mg 5 mg 6 mg 7 mg
19+ years 5 mg 5 mg 6 mg 7 mg
[NIH: National Institutes of Health, Office of dietary supplements]

38. DEFICIENCY SYMPTOMS:
 Deficiency is very rare due to the widespread distribution of this vitamin
 Dr. Copalan, a world renowned nutritionist from India, linked the burning feet syndrome
with pantothenic acid deficiency
 In experimental animals - Anemia, fatty liver, decreased steroid synthesis etc
HYPERVITAMINOSIS:
 The toxicity of pantothenic acid is negligible. No adverse reactions have been reported in any
species following the ingestion of large doses of the vitamin.

39. PYRIDOXINE (B6):
Vitamin B6 is used to collectively represent the three compounds namely pyridoxine,
pyridoxal and pyridoxamine (the vitamers of B6)
DIETARY SORCES:
METABOLISM:
 The various forms of vitamin B6 are absorbed via passive diffusion primarily in the jejunum
and ileum
 Excretion : Urine

40. METABOLIC FUNCTIONS:
I. Co-enzymatic actions:
 The active form of vitamin B6 is the coenzyme pyridoxal phosphate (PLP)
 Associated with the metabolism of amino acids
 Synthesis of certain specialized products such as serotonin, histamine, niacin coenzymes
from the amino acids is dependent on pyridoxine.
 PLP participates in reactions like transamination, decarboxylation, deamination,
transsulfuration, condensation etc.

41. II. Other actions
 Vascular effects:
Deficiency – Homocyteinemia
Risks of occlusive vascular disease, dementia, Alzheimer’s disease, chronic heart failure
 Neurologic function:
Deficiency - affect the postnatal development of a glutamate receptor in the brain (learning)
 Immune functions:
Vitamin B6 has a role in the support of immune competence
 Cancer:
Studies have demonstrated inverse associations of vitamin B6 intake and colon cancer risk

42. PHARMACOLOGICAL USES:
Vitamin B6 has been used at supranutritional doses for the management of a variety of human
disorders:
 Sideroblastic anemia
 Sickle cell anemia
 Iron storage disease
 Suppression of lactation
 Adverse drug effects of hydrazines,
antibiotics, L-DOPA, ethanol, oral contraceptives.
Schizophrenia
Asthma
Herpes
Carpal tunnel syndrome
Premenstrual syndrome
Morning sickness

43. RECOMMENDED DIETARY ALLOWANCE (RDA):
Age Male Female Pregnancy Lactation
Birth to 6 months 0.1 mg 0.1 mg
7–12 months 0.3 mg 0.3 mg
1–3 years 0.5 mg 0.5 mg
4–8 years 0.6 mg 0.6 mg
9–13 years 1.0 mg 1.0 mg
14–18 years 1.3 mg 1.2 mg 1.9 mg 2.0 mg
19–50 years 1.3 mg 1.3 mg 1.9 mg 2.0 mg
51+ years 1.7 mg 1.5 mg
[NIH: National Institutes of Health, Office of dietary supplements]

44. DEFICIENCY SYMPTOMS:
 Neurological symptoms : Depression, irritabilitv, nervousness and mental confusion
 Convulsions and peripheral neuropathy in severe deficiency (due to decreased synthesis of serotonin, GABA,
norepinephrine and epinephrine)
 Children : Convulsions (epilepsy)
 Hypochromic microcytic anaemia (due to reduced heme production)
 Dietary deficiency is rare but seen in women taking oral contraceptives, alcoholics and infants
DRUG INDUCED B6 DEFICIENCY:
 Administration of drugs namely Isoniazid and Penicillamine should be accompanied by pyridoxine
supplementation to avoid B6 deficiency.

45. HYPERVITAMINOSIS:
Toxicity of vitamin B6 appears to be relatively low
Higher doses : Sensory neuronopathy (changes in gait and peripheral sensation)
DENTAL CONSIDERATIONS:
Glossitis with pain, edema and papillary changes
Initially : Scalded sensation
Later : Reddening and hypertrophy of the filiform papillae at the tip, margins and dorsum.

46. BIOTIN (B7):
Formerly known as anti-egg white injury factor, vitamin B7 or vitamin H
It directly participates as a coenzyme in the carboxylation reactions.
DIETARY SOURCES:
Biotin is widely distributed in both animal and plant foods.
It is also synthesised by the microflora of the proximal colon

47. METABOLISM:
Free biotin is released from the protein bound biotin forms by the action of an intestinal biotin
amide aminohydrolase, biotinidase.
This free biotin is absorbed in proximal part of the small intestine.
Excretion of the vitamin is through urine.

48. METABOLIC FUNCTIONS:
I. Co-enzymatic actions:
 Pyruvate carboxylase enzyme in Gluconeogenesis and citric acid cycle
 Acetyl CoA carboxylase in fatty acid synthesis
 Propionyl CoA carboxylase in case of metabolism of few amino acids.
 β-methylcrotonyl CoA carboxylase enzyme in metabolism of leucine.
II. Other functions:
 Gene expression: Genes, depend on biotin for expression.
 Cell cycle: Biotin has been shown to be necessary for the normal progression of cells through
the cell cycle, with biotin-deficient cells arresting in the G1 phase.

49. RECOMMENDED DIETARY ALLOWANCE (RDA):
Age Male Female Pregnancy Lactation
Birth to 6 months 5 mcg 5 mcg
7–12 months 6 mcg 6 mcg
1–3 years 8 mcg 8 mcg
4–8 years 12 mcg 12 mcg
9–13 years 20 mcg 20 mcg
14–18 years 25 mcg 25 mcg 30 mcg 35 mcg
19+ years 30 mcg 30 mcg 30 mcg 35 mcg
[NIH: National Institutes of Health, Office of dietary supplements]

50. DEFICIENCY SYMPTOMS:
Biotin deficiency is uncommon as it is well distributed in foods & also supplied by the intestinal
bacteria.
1. Destruction of intestinal flora due to prolonged use of drugs such as sulfonamides.
2. High consumption of raw eggs. The raw egg white contains a glycoprotein avidin, which
tightly binds with biotin and blocks its absorption from the intestine
 Anemia, loss of appetite, nausea, dermatitis, glossitis
 Depression, hallucinations, muscle pain

51. HYPERVITAMINOSIS:
 The toxicity of biotin appears to be very low
 Biotin excess appears to provide effective therapy to reduce the diabetic state
DENTAL CONSIDERATIONS:
 Pallor of the tongue and patchy atrophy of the lingual papillae
 Pattern resembles geographic tongue
 Either only on lateral borders or complete dorsum

52. FOLIC ACID (B9):
 Folic acid or folacin (Latin : folium-leaf) is abundantly found in green leafy vegetables.
 Important for one carbon metabolism, for the synthesis of certain amino acids, purines and
the pyrimidine.
DIETARY SORCES:

53. METABOLISM:
 Dietary sources : Polyglutamate
 The enzyme folate conjugase present in duodenum and jejunum splits the glutamate residues into
monoglutamate residues
 This is absorbed from the intestine
 Inside the cells, polyglutamates derivatives are found in the form of tetrahydrofolates(biologically most potent)
 Polyglutamate, folic acid is stored to some extent in the liver, hence body can store 10-12 mg of folic acid
that will usually last for 2-3 months
 In the circulation, N5-methyl tetrahydrofolate is abundantly present.
 Excretion is through urine and bile

54. METABOLIC FUNCTIONS:
I. Co-enzymatic actions:
 Coenzyme : Tetrahydrofolate (THF or FH4)
 Actively involved in the one carbon metabolism to metabolise amino acids and nucleotides.
Many important compounds are synthesized in one carbon metabolism.
1. Purines (carbon 2, 8) which are incorporated into DNA and RNA.
2. Pyrimidine nucleotide-deoxythymidylic acid (dTMP), involved in the synthesis of DNA.
3. Clycine, serine, ethanolamine and choline are produced.
4. N-Formylmethionine, the initiator of protein biosynthesis is formed

55. II. Other functions:
1. Cardiovascular disease
2. Neural tube defects
3. Other pregnancy complications
4. Erythropoiesis
5. DNA methylation
6. Cancer
7. Immune function
Recommended dietary allowance (RDA):
The daily requirement of folic acid is around 200µg. In the women, higher intakes are
recommended during pregnancy (400µg/day) and lactation (300 µ/day).

56. DEFICIENCY SYMPTOMS:
 Most common vitamin deficiency - Primarily in the pregnant women
 The pregnant women, lactating women/ women on oral contraceptives, and alcoholics are also
susceptible to folate deficiency.
 Reasons: Inadequate dietary intake, defective absorption, use of anti-convulsant drugs
(phenobarbitone, dilantin), and increased demand.
 Effects: decreased production of purines ----- Impairs DNA synthesis --- Maturation of erythrocytes
is slowed ------ macrocytic RBC.
 The macrocytic anemia associated with megaloblastic changes in the bone marrow is a
characteristic feature of folate deficiency.
 Pregnant women : Neural defects in the fetus.
 Hence high doses of folic acid are recommended in pregnancy to prevent birth defects

57. HYPERVITAMINOSIS:
Few studies : Increase in the frequency or severity of seizures (reduced anticonvulsant effectiveness)
Others : No such effects.
Folate may form a nonabsorbable complex with zinc, thus antagonizing the utilization of that
essential trace element at high intakes of the vitamin
DENTAL CONSIDERATIONS:
Glossitis : Fiery red tongue & papillae are absent
Chronic periodontitis with loosening of teeth
Impairs immune responses and resistance of the oral mucosa to penetration by pathogenic organisms
such as candida.

58. CYNOCOBALAMIN (B12)
Anti-pernicious anaemia vitamin:
It is a unique vitamin, synthesized by only microorganisms and not by animals and plants.
DIETARY SOURCE:
Curd is a better source than milk, due to the synthesis of B12 by Lactobacillus.

59. METABOLISM:
Diet: Extrinsic factor of castle
(bound form )
Free vitamin
(Cobalamin)
Stomach
Acid hyrolases
IF (produced in stomach) forms a dimer, binds strongly with 1 or 2 moles of vitamin B12. This binding protects
vitamin B12 against its uptake and use by bacteria.
Cobalamin + IF
Gut
Specific receptors on
mucosa cell surface Ca ions
Mucosal cells
B12 is converted to methylcobalamin. It is then transported in the circulation in a bound form to proteins
namely transcobalamins (TC-I, TC-II).
Methylcobalamin which is in excess is taken up by the liver, converted to deoxyadenosyl B12 and stored in this
form.
Excreted via both renal and biliary

60. METABOLOC FUNCTIONS:
I. Co-enzymatic functions:
There are only two reactions in mammals that are dependent on vitamin B12.
Synthesis of methionine from homocysteine :
Coenzyme: methylcobalamin Ezyme : Homocysteine methyltransferase or methionine synthase.
Isomerization of methymalonyl CoA to succinyl CoA:
Enzyme - methylmalonyl CoA mutase
II. Other Effects
Cyanide metabolism
Cobalamins can bind cyanide to produce the nontoxic cyanocobalamin.
Hydroxocobalamin : Canide antidote.
Inactivate low levels of cyanide consumed in many fruits, beans, and nuts.

61. RECOMMENDED DIETARY ALLOWANCE (RDA):
Age Male Female Pregnancy Lactation
0–6 months* 0.4 mcg 0.4 mcg
7–12 months* 0.5 mcg 0.5 mcg
1–3 years 0.9 mcg 0.9 mcg
4–8 years 1.2 mcg 1.2 mcg
9–13 years 1.8 mcg 1.8 mcg
14+ years 2.4 mcg 2.4 mcg 2.6 mcg 2.8 mcg
[NIH: National Institutes of Health, Office of dietary supplements]

62. DEFECIENCY SYMPTOMS:
Pernicious anemia : Decreased number of erythrocytes and neurological manifestations
Reasons:
 Autoimmune destruction of gastric parietal cells that secrete intrinsic factor
 Hereditary malabsorption of vitamin B12.
 Partial or total gastrectomy-these individuals become intrinsic factor deficient.
 Insufficient production of IF and/or gastric HCl, occasionally seen in older people.
 Dietary deficiency of B12, is seen among the strict vegetarians
NEUROLOGICAL SYMPTOMS:
Neuronal degeneration and demyelination of nervous system: Paresthesia of fingers and toes
Accumulation of methylmalonyl CoA that interferes in myelin sheath formation.
Advanced cases : Confusion, loss of memory and even psychosis

63. DENTAL CONSIDERATIONS:
Glossopyrosis
Swelling and pallor with eventual disappearance of the filiform and fungiform papillae.
The tongue may be completely smooth, shinny, and deeply reddened with a loss of taste.
Bright red, diffuse, excruciating painful lesions may occur in the buccal and pharyngeal mucosa and
undersurface of the tongue.
OE: Stomatitis or a pale or yellowish mucosa, xerostomia, cheilosis, hemorrhagic gingiva and bone loss
Vitamin B12 deficiency may cause an increase in prevalence of dental caries and gingival diseases in children.
(Assessment of Vitamin B12 and Its Correlation with Dental Caries and Gingival Diseases
in 10- to 14-year-old Children)

64. VITAMIN B-COMPLEX AND THEIR CO-ENZYMES:
VITAMIN CO-ENZYME
B1 (Thiamine) Thiamine pyrophosphate (TPP)
B2 (Riboflavin) Flavin mononucleotide (FMN) and Flavin adenine dinucleotide
(FAD)
B3 (Niacin) Nicotinamide adenine dinucleotide (NAD+) and Nicotinamide
adenine dinucleotide phosphate (NADP+).
B5 (Pantothenic acid) Co-enzyme A
B6 (Pyridoxine) Pyridoxal phosphate (PLP).
B7 (Biotin) Biotin
B9 (Folic acid) Tetrahydrofolate (THF or FH4)
B12 (Cynacobalamin) Methylcobalamin

65. Vitamin B-Complex supplements:
Syrups:
1. Cobadex Syrup
2. Plexbio Forte Syrup
3. Polybion Lc Syrup
4. Neurobex Syrup
Tablets:
1. Complex B Forte Tablet
2. Beplex Forte Tablet

66. CONCLUSION:
 Although vitamins are required in minute quantities, they are indispensable for maintaining the
integrity and proper functioning of various body systems.
 Diet containing vitamins also play an important role in normal health of the oral structures. As a
dentist, we should have sound knowledge regarding functions of vitamins and oral
manifestations of their deficiencies. This helps us to differentiate clinical features of various
vitamin deficiencies.

67. REFERNCES:
1. Biochemistry - U.Sathyanarayana, U.Chakrapani – 3rd edition
2. The vitamins, Fundamental aspects in nutrition and health – Gerald. F Coombs Jr – 3rd edition.
3. Biochemistry - Jeremy M Berg, John L Tymoczko, and Lubert Stryer – 5th edition.
4. Dr. Manu Rathee Dr. Mohneesh Bhoria Dr. Renu Kundu. Vitamin C and Oral Health: A Review.
Volume : 3 | Issue : 9 | Sept 2013 | ISSN - 2249-555X.
5. M Hugar S, S Dhariwal N, Majeed A, Badakar C, Gokhale N, Mistry L. Assessment of Vitamin B12
and Its Correlation with Dental Caries and Gingival Diseases in 10- to 14-year-old Children: A
Cross-sectional Study.Int J Clin Pediatr Dent. 2017 Apr-Jun;10(2):142-146. doi: 10.5005/jp-
journals-10005-1424. Epub 2017 Jun 1.