vitamins their role on periodontium and general health

1. VITAMINS
PRESENTED BY
K V N VIDYADHAR

2. Contents:
• Introduction
• History of vitamins
• Definition and classification
• Digestion and absorption
• Toxicity or Imbalance
• Vitamin A
• Vitamin D
• Vitamin E
• Vitamin K

3. • B-Complex Vitamins
• Vitamin C
• Role of vitamins in immune system
• Conclusion
• References

4. INTRODUCTION
• Vitamins are a class of organic compounds categorized as essential nutrients.
• Vitamins are calorie-free molecules and are required by the body in very small amounts.
• Vitamins fall in the category of micronutrients.
• Since the body is generally unable to synthesize them (at least in sufficient amounts),
they must be provided by food.
• A well balanced diet supplies the vitamin needs of a healthy person.

5. HISTORY
• Frederick G. Hopkins, a biochemist at Cambridge University, England, and a Nobel
Prize winner, reported in 1906 that there was an unknown something in food essential
for life and health.
• In 1912, he had experimental data that supported this statement.
• Casimir Funk, a Polish chemist, obtained an antiberiberi substance from rice
polishings.
• He believed that the active factor that he found was a protein, i.e., an “amino”. Since
he considered this amino to be the vital element in the food, he called it a “vitamine.”

6. • Later it was found that very few of these “vitamines” were truly protein so the final ‘e’
was dropped.
• As new vitamins were discovered, successive letters of the alphabet were assigned to
them.
• However, in some cases a letter was used because it was the first letter of a word
describing the principle characteristic of the vitamin.
• For example, vitamin K, which is concerned with the coagulation of blood, was
derived from the Scadinavian word koagulation.

7. • Vitamin discovery, both accidental and deliberate, was spread out over 40 years. By
1940, all 13 currently recognized vitamins had been discovered and given a sequential
letter of the alphabet.

8. DEFINITION:
• However, vitamin D, which can be made in the skin after exposure to sunlight,
and niacin which can be formed from the essential amino acid tryptophan, do
not strictly confirm to this definition.
• Vitamins like vitamin k and biotin are secreted by the bacteria of the gut.

9. CLASSIFICATION
Vitamins can be divided into 2 main groups
VITAMINS
FAT SOLUBLE WATER SOLUBLE
Stored in the liver Not stored extensively
Not absorbed or stored easily Required regularly in the diet
Sometimes toxic in excess Generally non-toxic in excess
All B vitamins are coenzymes

11. DIGESTION AND ABSORPTION
• Vitamins are released from food during the digestive process.
• Water-soluble vitamins (vitamin B-complex and C) that are utilized by the body for
metabolic processes are absorbed through the small intestine.
• Any excess that is not used right away is excreted by the kidneys in the urine.
• Fat-soluble vitamins (vitamins A, D, E, and K) are absorbed with dietary fats through the
small intestine.
• After absorption, they are sent to the liver and fat deposits and circulate through the
blood with the help of chylomicrons and lipoproteins.

12. TOXICITY / IMBALANCE
• Eating too many fortified foods or taking a mega dose of vitamin supplements—more
than the recommended daily intake can produce toxic effects.
• Fat-soluble vitamins are more toxic than water-soluble vitamins because they can be
stored and accumulated in adipose tissues.
• Vitamin D is the most toxic of all vitamins because of its ultimate effect on the human
body.
• Vitamin D enhances the absorption of calcium, and so an excess of vitamin D causes an
excess of calcium circulating in the blood, which is detrimental to the heart.

13. • Two water-soluble vitamins can be somewhat toxic: vitamin B-6 and niacin.
• Both can have detrimental effects if the amount ingested is more than the kidney can
handle and excrete.

14. VITAMIN A
Recommended dietary allowance:
Adult 600 μg of retinol
Lactation 950 μg of retinol
Children 400-600 μg of retinol
Infants 350 μg of retinol
• In a patient with cirrhosis of the liver, the stores of this vitamin are markedly reduced.

16. Functions of vitamin A:
There are 3 active forms of vitamin A
 Retinoic acid
 Retinaldehyde
 -carotene
 Retinal has a role in Vision
 Retinoic acid has a role in regulation of gene expression and tissue differentiation
 -carotene is an antioxidant and has possible roles in atherosclerosis and cancer
prevention.

17. Clinical manifestation of deficiency of vitamin A :
• Night Blindness
• Xerophthalmia
• Keratomalacia
• Irreversible Blindness.
• Vitamin A also has an important role in differentiation of immune system cells, and
mild deficiency leads to increased susceptibility to infectious disease.

18. EFFECTS OF VITAMIN A DEFICIENCY ON ORAL STRUCTURES:
• Animal studies have shown vitamin A to be indispensable to the proper growth and
development of periodontium, teeth, salivary gland, and oral epithelium.
• In humans, the teeth are less sensitive to vitamin A deficiency, although some studies
suggest that it can exacerbate existing periodontitis.
• Little information is available regarding the effects of vitamin A deficiency on the oral
structures in humans. Several epidemiologic studies have failed to demonstrate any
relation between this vitamin and periodontal disease in humans.

19. • In experimental animals, vitamin A deficiency results in hyperkeratosis and
hyperplasia of the gingiva with a tendency for increased periodontal pocket
formation.
• As vitamin A deficiency is associated with epithelial metaplasia and hyper-
keratinization, it has been postulated that oral leukoplakia (thickened white patches
on mucous membranes) might response to large doses of vitamin A.

20. Diagnosis and treatment:
It is usually on the basis of clinical features.
The following can also be measured:
 Plasma concentration of vitamin A (normal 20 μg/dl ) and retinol binding
protein.
THERAPY:
• Treatment with vitamin A (as retinol palmitate) orally or IM prevents blindness.
• If the deficiency is severe and has already caused keratomalacia, eyesight
cannot be restored.

21. HYPERVITAMINOSIS-A
• Excessive consumption of vitamin A leads to toxicity.
• The symptoms of hypervitaminosis-A include dermatitis (drying and redness of skin),
enlargement of liver, skeletal decalcification, tenderness of long bones, loss of weight,
irritability, loss of hair, joint pains.
• It is now believed that the vitamin A toxicosis symptoms appear only after retinol binding
capacity of retinol binding protein exceeds.

22. Beneficial effects of β.carotene:
• Increased consumption of β-carotene is associated with decreased incidence of heart
attacks, skin and lung cancers.
• This is attributed to the antioxidant role of β-carotene which is independent of its role as
a precursor of vitamin A.
• Ingestion of high doses of β-carotene for long periods are not toxic like vitamin A.

23. VITAMIN D
Recommended dietary allowance:
• There are three types of vitamin D, but only two; vitamin D2 and vitamin D3 are
of nutritional importance.
Adults 2.5μg (100 I.U.)
Infants and children 5μg (200 I.U.)
Pregnancy and lactation 10μg (400 I.U.)

24. • Vitamin D2 (ergocalciferol) is derived from the provitamin ergosterol, which is
present in plants, especially in fungi and yeasts.
• Vitamin D3 (Cholecalciferol) , the naturally occurring form of the vitamin in animal
tissues, is produced in the skin.
• Its precursor (intermediate compound) 7-dehydrocholesterol is converted into D3
when exposed to sunlight.

26. Functions:
Vitamin D functions both as a vitamin and as a hormone.
1. The principal action of vitamin D is to promote intestinal calcium and phosphate
absorption.
2. Vitamin D is necessary for the formation of normal bone and teeth, and the
calcification or repair of diseased bone.
3. There is speculation that vitamin D stimulates a calcium-dependent ATPase and / or
alkaline phosphatase in mucosal cells and also promotes synthesis of a calcium-binding
protein.

27. BONE DISEASES ASSOCIATED WITH VITAMIN D DEFICIENCIES:
Vitamin D deficiency has its most pronounced effects on bones and teeth.
RICKETS
• Lack of orderly change from cartilaginous material to calcified bone & mineralization of the
osteoid matrix does not occur.
• An overgrowth of cartilage at the rib-cartilage junctions causes beading of the ribs known as
rickets rosary.
• Protrusion of the sternum and depression of the sides of the rib cage produce the condition
known as pigeon breast.

28. OSTEOMALACIA
• Osteomalacia is the adult counterpart of rickets.
• In osteomalacia, the bones become soft as a result of a failure of mineralization as
they undergo remodeling.
• Wide zones of demineralized osteoid tissue are found at the junctions of mineralized
bone and the layers of osteoblasts.
• Clinically, the patient experiences pain in the ribs, spine, pelvis and legs.
• Bone tenderness to pressure is common.
• There is a tendency of the leg bones to bend, which leads to a waddling gait.

29. Dental implications
• Eruption of permanent teeth may be delayed
• Enamel defects ranging from pitting to complete absence of enamel
• Markedly decreased calcification of cementum and dentin.
• Vitamin D and calcium deficiency have been found to result in generalized jaw bone
resorption and loss of PDL (Dorsky 2001).
• Enamel hypoplasia.
• The enamel calcifies poorly and may in some areas fail to form. In the dentin, spaces that
represent un calcified dentin matrix occur.

30. Vitamin D deficiency or imbalance on the periodontal tissues of young dogs:
• Osteoporosis of alveolar bone
• Osteoid that forms at a normal rate but remains uncalcified.
• Failure of osteoid to resorb, which leads to its excessive accumulation.
• Reduction in the width of the pdl space.
• A normal rate of cementum formation, but defective calcification and some
cementum resorption.
• Distortion of the growth pattern of alveolar bone.

31. THERAPY:
• Rickets: Vitamin D 1000 to 5000 IU / day is prescribed, depending on the severity of the
disease. Exposure to sunlight is helpful.
• Vitamin D supplements should be gradually reduced to prophylactic doses of 400 IU daily
after serum alkaline phosphatase decreases to normal levels.
• Osteomalacia: The biochemical test that may point toward a diagnosis of vitamin D
deficiency is an elevated serum alkaline phosphatase.

32. • The treatment for osteomalacia is 5000 to 20,000 IU of vitamin D accompanied by 5 g of
calcium gluconate or calcium lactate three times a day.

33. VITAMIN E
Recommended dietary allowance:
The current estimate of vitamin E requirement is about 0.8 mg/g of essential fatty acids.
Function:
• Vitamin E exists in more than one form. The most active form is -tocopherol. The exact
mechanism by which vitamin E functions in body is unknown.
• Vitamin E serves as a biological antioxidant to limit free-radical chain reactions and to
protect body cells from lipid peroxidation and ultimate destruction.
• Inhibits prostaglandin synthesis.

34. • Vitamin E affects arachidonic acid release from phospholipid; consequently, platelet
thromboxane A2 biosynthesis is lowered.
• Corrigan found that Vitamin E which normally has no effect on the coagulation
mechanism has been shown to enhance the coagulation defect in vitamin K deficient rats,
dogs, chick and humans.
• He suggested that vitamin E acts at the vitamin K carboxylase step of carboxylation of the
precursor prothrombin.
• Vitamin E has been assigned hypothetical functions in conditions such as cancer, muscular
dystrophy, or sterility. However proof of its contribution or curative properties in mankind
is lacking.

35. Clinical findings of vitamin E deficiency:
Vitamin E deficiency is rare in human beings.
Causes:
• Congenital atresia (closure) of the bile ducts
• Malabsorption syndromes
• Steatorrhea
• Xanthomatosis
• Biliary cirrhosis

36. • Vitamin E deficiency may cause impaired neuromuscular function.
• 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.
Treatment of deficiency:
• In the treatment of vitamin E deficiency (less than 0.5 to 2.02 mg/ 100 ml of plasma), 30 to
100 mg daily may be prescribed.

37. VITAMIN K
Recommended dietary allowances:
The vitamin K requirement of man is met by a combination of dietary intake and microbial
synthesis in the gut. The daily requirement for man appears to be about 0.03 mg/kg for the
adult.
Function:
1. The primary function of vitamin K is to catalyze the synthesis of a blood clotting factor,
prothrombin, by the liver.Vitamin K is also essential for the production of other clotting factors
– factors VII (proconvertin), IX (Christmas factor), and X (Stuart factor).
2. Promotion of the fibrin clot formation.

38. 3. It has been postulated that vitamin K acts as a cofactor in oxidative phosphorylation in
the mitochondria.

39. Deficiency:
Vitamin K deficiency is rather rare in humans because of the intestinal synthesis of the
vitamin by microorganisms and because it is quite widely distributed in foods.
Causes:
• Bilary disease
• Fat malabsorption
• Prolonged use of antibacterial drugs
• Surgical operation such as a cholecystectomy
• Certain drugs can affect its metabolism

40. • Vitamin K compounds have been found to be required for the growth of Bacteroides
melaninogenicus, an organism closely associated with periodontal disease.
• It is speculated that a suitable antimetabolite of vitamin K might interfere with the
growth of this organism and, consequently, prevent the occurrence of periodontal disease.
Therapy:
Newborn infants tend to be deficient in vitamin K due to minimal stores of prothrombin at
birth and lack of an established intestinal flora. Soon after birth, all infants or those at
increased risk should receive a single intramuscular dose of a vitamin K preparation (0.1-0.2
mg of menadione sodium bisulphite or 0.5 mg of vitamin K) by way of prophylaxis.

41. • The treatment of hypoprothrombinemia (prothrombin deficiency) because of vitamin K
deficiency resulting from any of the conditions consists of the administration of 2 to 5 mg
daily of a synthetic, water – soluble vitamin K tablet.

42. THAIMINE (VITAMIN B1)
It is also, known as ‘Anti beri-beri’ or ‘Antineuritic’ vitamin.
Recommended Dietary Allowance:
Men 1.2 – 1.6 mg/day
Woman
0.9 -1.2 mg/day
Pregnancy
+0.2 mg/day
Lactation +0.3 mg/day

43. Function:
1. Thiamin pyrophosphate (TPP) has a role in carbohydrates metabolism:
a)It acts as a coenzyme in the production of ribose, the sugar needed by all cells for the
formation of ribonucleic acid (RNA), which helps produce protein and deoxyribonucleic
acid (DNA), the basic substance of genes.
b) It is involved in reactions of oxidative decarboxylation of alpha-keto acids to aldehydes.
This reaction is particularly important in conversion of pyruvate to acetate just prior to
Kreb’s cycle, and in the conversion of alpha ketoglutarate to succinyl coenzyme A within
the Kreb’s cycle.

44. c) Thiamine is also a cofactor for transketolase. This enzyme is involved in the conversion
of sugars containing 3,4,5,6 or 7 carbons.
2. Thiamin is also been shown to play a role in pathways involved with proteins and fat
metabolism.
3. Thiamin has a specific role in neurophysiology that is independent of its coenzyme
function.

45. Deficiency:
• Severe thiamin deficiency is called beriberi. It affects principally the cardiovascular,
muscular, and nervous systems. Beriberi may manifest in one of the three forms:
• In the dry beriberi, there is loss of appetite, tingling and numbness in hands and legs and
also dropping of the feet.
• In wet beriberi, there is dropsy, palpitation and breathlessness and weakness of heart
muscle leading to heart failure and edema of the legs.
• Infantile beriberi, caused by inadequate thiamine in breast milk, is characterized by
dyspnea, cyanosis and cardiac failure.

46. In the alcoholic, a severe thiamin deficiency may lead to Wernicke’s syndrome, which is
characterized by confusion, paralysis of eye muscles, and loss of memory. Peculiar gait and
foot and wrist drop are seen in advanced cases.
The possible oral manifestations of a deficiency of this vitamin are hyper sensitivity of the
oral mucosa, glossitis and loss or diminution of taste, minute vesicles (simulating herpes) on
the buccal mucosa, under the tongue or on the palate; and erosion of oral mucosa.

47. Therapy:
• A good diet and administration of 5 to 10 mg of thiamin hydrochloride three times a day
will help the usual cases of nutritional polyneuropathy (a disease involving several nerves).
• Alcoholics or others who may develop beriberi should also have some multivitamin B
complex tablet supplement in a therapeutic dose (which is two or three times the supportive
dose).

48. RIBOFLAVIN (VITAMIN B2)
Recommended dietary allowances:
Men 1.4 – 1.9 mg/day
Woman 1.1 -1.5 mg/day
Pregnancy +0.2 mg/day
Lactation +0.4 mg/day

49. Function:
• Riboflavin is an electron-transfer vitamin participating in the exchange of oxygen and
hydrogen between plasma and tissue cells.
• Riboflavin is a cofactor for hydrogen transfer compounds, Flavin adenine dinucleotide
(FAD) and riboflavin-5-phosphate.
1. FAD is involved in initial oxidation steps for both glucose and fatty acids as well as in the
oxidative deamination of amino acids.
2. FAD also activates pyridoxine and converts folic acid to its active (cofactor) form.

50. 3. Riboflavin is necessary for the
i) Synthesis of corticosteroids,
ii) RBC metabolism,
iii) Gluconeogenesis and
iv) Thyroid activity.
4. Most cellular pathways depend on this vitamin at one step or another, and growth
cannot occur without it.

51. Deficiency:
The causes for riboflavin deficiency are
 Inadequate dietary intake, most often seen in alcoholics and the economically deprived.
 Severe gastrointestinal disease that causes vomiting and hypermotility of the
gastrointestinal tract.
 Polyuria resulting from uncontrolled diabetes.

52. • Clinically, riboflavin deficiency may be found in conjunction with a lack of other B
vitamins such as pyridoxine, niacin, and folic acid.
• The reason for the multiplicity of vitamin deficits is that dietary deficiencies tend to be
multiple because the food sources are similar.
• The symptoms of riboflavin deficiency (ariboflavinosis) include glossitis, angular
cheilitis, seborrheic dermatitis, and a superficial vascularizing keratitis.

53. Therapy:
• In the treatment of riboflavin deficiency, a good diet of liver, meat, eggs, and enriched
cereals plus, a special emphasis on a quart of milk daily is a first consideration.
• Also, a therapeutic multivitamin capsule containing at least 5 mg of riboflavin should be
taken two or three times a day.

54. NIACIN (Vitamin B3)
Niacin should be used as the generic description for derivatives exhibiting qualitatively the
biological activity of nicotinamide.
Recommended dietary allowance:
Men 16 – 21 mg/day
Woman 12 – 16 mg/day
Pregnancy + 2 mg/day
Lactation + 3 mg/day

55. Function:
• Niacin functions as part of two major coenzymes in energy metabolism, nicotinamide
adenine dinucleotide (NAD) and NAD phosphate (NADP).
• These coenzymes are hydrogen carriers, they are essential in many energy transfer
pathways e:g Kreb’s cycle, intracellular respiration, and fatty acid synthesis.
• Both of these coenzymes work with TPP and FAD in the net yield of energy from
carbohydrates, fats and proteins.
• Therefore, niacin is vital in the normal function of the central nervous system, in
maintaining the integrity of the skin and mucous membranes, and especially in supplying
the needed coenzyme for the energy cycles.

56. • Niacin inhibits lipolysis in the adipose tissue and decreases the circulatory free fatty
acids.
• Triacylglycerol synthesis in the liver decreased.
• The serum levels of low density lipoproteins (LDL), very low density
lipoproteins(VLDL), triacylglycerol and cholesterol are lowered.
• Hence niacin is used in the treatment of hyperlipoproteinemia type II b (elevation of
LDL and VLDL).

57. Deficiency:
• Pellagra is a niacin deficiency disease caused by primary inadequate dietary intake or by a
secondary conditioning (systemic) factor such as alcoholism, gastrointestinal disease,
hyperthyroidism, or infection that inhibits absorption and use of nutrients.
• Pellagra is characterized by dermatitis, diarrhea, dementia, glossitis, gingivitis, and
generalized stomatitis.
• Early symptoms of pellagra are similar to those produced in other B complex deficiency
states: weakness, persistent fatigability, irritability, headache, and depression.

58. • Soreness and inflammation of the tongue (glossitis) and mouth (stomatitis) aggravated by
highly seasoned food.
• Oral manifestations of vitamin B-complex and niacin deficiency in experimental animals
include black tongue and gingival inflammation with destruction of the gingiva, periodontal
ligament, and alveolar bone.
• Necrosis of the gingiva and other oral tissues, as well as leukopenia, is terminal features of
niacin deficiency in experimental animals.
• The tongue is sore, swollen, scarlet in color, and smooth.

59. Therapy:
• In treatment of mild niacin deficiency, administration of 50 mg of nicotinamide orally
three times a day is recommended.
• For the treatment of pellagra, 300 to 500mg of nicotinamide daily in divided doses, as
well as supplements of other nutrients that are frequently deficient, is prescribed.
Although mega-doses of niacin are useful for the treatment of hyperlipidaemia there are
certain harmful side effects also.
• Glycogen and fat reserves of skeletal and cardiac muscle are depleted.

60. • 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.

61. PANTOTHENIC ACID
Recommended dietary allowance:
Function:
• Pantothenic acid is a critical component of coenzyme A (CoA). In this manner, it is
involved in acyl-transfer reactions of fat, carbohydrates and protein metabolism.
• This vitamin is also active in the synthesis of cholesterol, steroid hormones, porphyrins (a
component of Hb) and phospholipids.
Adult 4 – 7 mg / day,
Children 3 – 4 mg / day.

62. • Another function of CoA is the transfer of succinyl and malonyl groups, it also carries the
acyl units for fatty acid synthesis and amino acid activation. It initiates the Krebs cycle
and releases ATP.
Deficiency:
• In humans, a deficiency is rare and can be induced experimentally.
• The symptoms are fatigue, sleep disturbances, headaches, malaise, nausea, and
abdominal stress.
• Burning, prickling sensation (paresthesia) of the hands and feet, cramping of the leg
muscles, and impaired coordination are additional findings.

63. Therapy:
• No definite therapeutic regimen for dealing with pantothenic acid deficiency has been
presented.
• Multivitamin B complex preparations usually contain pantothenic acid and are given as
supplements twice or thrice a day.

64. BIOTIN
• Biotin (formerly known as anti-egg white injury factor or vitamin H)
• It is a sulphur Containing B –complex vitamin.
• It directly participates as a coenzyme in the carboxylation reactions.
Recommended dietary allowance: 100 – 200 μg /day
Function:
1. The most important role of biotin is in carboxylation reactions, particularly in fatty acid
synthesis. Biotin functions in the enzyme pyruvate carboxylase, during the conversion of
pyruvate to oxaloacetate in Krebs cycle.

65. 2. Biotin is involved in deamination reaction with aspartic acid, serined threonine.
3. Biotin functions as a coenzyme involving the addition of carbon dioxide in the
formation of purines, which are important constituents of DNA and RNA.
Deficiency:
• Biotin deficiency is uncommon, since it is well distributed in foods and also
supplied by the intestinal bacteria. The deficiency may however, be associated with
the following two causes.

66. • Human biotin deficiency has been encountered in infants treated with sulfa drugs and in
adults whose diet consisted mainly of raw egg whites.
• Biotin deficiency has been reported in patients maintained for long periods of time on
intravenous feeding.
• Deficiency causes inflammation of the skin and the tongue (dermatitis and glossitis), loss
of hair (alopecia) and skin disease (dermatosis), loss of appetite and sleep, nausea,
muscular pains, increased skin sensitivity (hyperesthesia), and burning and prickling
sensations (paresthesia).
• Consumption of an occasional raw egg, will not precipitate deficiency symptoms. It is only
when large amounts (20 or more eggs per day) are consumed that a problem occurs.

67. PYRIDOXINE (VITAMIN B6 )
Vitamin B6 is not a single vitamin but rather a group of metabolically and functionally
interrelated pyridines namely, pyridoxine, pyridoxamine (the amine of pyridoxine), and
pyridoxal. Each of these substances is widely distributed in foods and is present in both
free and bound forms.
Recommended dietary allowance:
Adult 2 mg /day
Lactation 2.5 mg/day
Children 1.6 – 2 mg/day

68. Function:
The principal vitamin activity resides in the enzymatically active coenzyme form, pyridoxal-5
phosphate.
1. Role in protein metabolism:
a) Transamination, deamination, desulfuration and decarboxylation reaction
b) Needed for porphyrin formation
c) Conversion of tryptophan to niacin.

69. 2. Role in carbohydrate metabolism – Pyridoxine acts with enzyme phophorylase in the
breakdown of glucose to glucose-1-phosphate.
3. Role in fat metabolism:
i) Conversion of linoleic acid to arachidonic acid
ii) Formation of sphinogolipids in myelin sheath.
4. It is also involved in CNS:
It helps in metabolism of substances like serotonin, dopamine and others.

70. Clinical diagnosis of deficiency:
• A frank deficiency of Vitamin B6 in humans is rare because of its widespread distribution in
natural foodstuffs.
• An experimental deficiency produced cheilosis, glossitis and stomatitis, and an itching and
burning dermatitis with redness in the nasolabial folds.
• Subjective symptoms accompanying these signs were loss of appetite, nausea, drowsiness,
and peripheral neuropathy.

71. Therapy:
• When primary deficiency of this vitamin is suspected in an adult, a daily dosage of 10 mg
is given.
• In iron-resistant hypochromic anemia, doses up to 100 mg / day have been given.
• Certain drugs, such as isoniazid, produce a need for a supplement of vitamin B6.

72. FOLACIN
The term folacin is the generic descriptor for folic acid, pteroylmonoglutamin acid and
related compounds exhibiting the biological activity of folic acid.
Recommended dietary allowance:
• Consumption of alcohol will increase the body’s folic acid requirements.
Adult 100 mg/day
Pregnancy 400 mg/day
Lactation 150 mg/day

73. Function:
1. Tetrahydrofolate (THF), an active form of this enzyme, is a cofactor for enzymes involved
in the synthesis of purines and pyrimidine's, which form DNA and RNA.
2. THF is of particular importance in the formation of both RBC and WBC.
3. Folic acid coenzymes are also responsible for the formation of body protein from glycine
and serine.
4. THF acts as a cofactor in methylation of homocysteine to methionine. This reaction is
linked to vitamin B12 metabolism.

74. FOLIC ACID DEFICIENCY:
• Folic acid deficiency is probably the most common vitamin deficiency in humans
because body’s stores of folate are relatively low which can last for upto 4 months only.
• Folic acid deficiency may cause megaloblastic anemia.
• Clinically, the patient has tissue anemia characterized by weakness, fainting attacks,
severe paleness of skin, and congestive heart failure.
• There are no central nervous system abnormalities, which is a key factor in distinguishing
between folic acid deficiency and vitamin B12 deficiency.

75. • It should be stressed that a folacin supplement will cure the anemia caused by vitamin
B12 deficiency but will not alleviate the neurological symptoms that accompany this
anemia.
• In folate deficiency, there are impaired production of DNA and unsynchronism
between protein synthesis and cell division which prevent cell maturation from
reaching completion. A consequence is that the epithelial barrier function is affected.
• Folate deficiency has also been related to decrease in host immune-competence.

76. ORAL CHANGES:
• Folic acid-deficient animals demonstrate necrosis of the gingiva, periodontal ligament, and
alveolar bone without inflammation.
• The absence of inflammation is the result of deficiency-induced granulocytopenia.
• In humans with folic acid deficiency states, generalized stomatitis occurs, which may be
accompanied by ulcerated glossitis and cheilitis.
• Angular cheilosis and gingivitis are also present.
• Folic acid deficient animals have shown to be vulnerable to ulcerations and infections of
lips, tongue, gingiva, periodontium and oropharynx.

77. • They show decrease in cell-mediated immune responses and in impairment in the
permeability barriers of oral mucosa.
• Vogel et al (1980) found that folic acid supplementation may increase resistance to
the development of periodontal inflammation in humans.
• Vogel hypothesized that phenytoin-induced aberration of folate metabolism could
render the gingiva more susceptible to irritation from local etiologic factors, thereby
enhancing susceptibility to gingival overgrowth.

78. VITAMIN B12 (COBALAMIN)
Recommended dietary allowance:
Adults 1 μg/day
Pregnancy 1 μg/day
Lactation 1.5 μg/day
Children 0.2 – 1 μg/day

79. Functions:
1. Vitamin B12 works in conjunction with THF in the synthesis of nucleoproteins for
DNA and RNA synthesis and for the formation of Hb.
2. Vitamin B12 functions in the synthesis of myelin sheath and the transfer of folate into
cells.
3. The replication of gastrointestinal cells, bone cells and nerve cells depend on vitamin
B12 involvement in DNA synthesis.
4. Vitamin B12 also functions in protein, fat and carbohydrate metabolism.

81. Vitamin B12 Deficiency:
A deficiency of Vitamin B12 is usually not due to a dietary inadequacy.
Causes:
 Absence of the intrinsic factor
 Severely shrunken gastric mucosa
 Tapeworms
 Resection of the stomach or the ileum
 Vegetarians

82. • The most important disease associated with vitamin B12 deficiency is pernicious anemia
• Characterized by low hemoglobin levels, decreased number of erythrocytes and
Neurological manifestation
• B12 deficiency is also associated with neuronal degeneration and demyelination of
nervous system
• The symptoms include paraesthesia (numbness and tingling) of fingers and toes.
• In advanced stages,confusion, loss o f memory and even psychosis may be observed
• The neurological symptoms of pernicious anemia are believed to be due to the
accumulation of methylmalonyl CoA that interferes in myelin sheath formation

83. Therapy:
A deficiency caused by inadequate ingestion of the vitamin (i.e., strict vegetarian
patients) can be effectively treated by oral ingestion of 0.001 to 0.003 mg (1 to 3 g) of
the vitamin daily.

84. VITAMIN C (ASCORBIC ACID)
• Vitamin C is a water soluble versatile vitamin.
• It plays an important role in human health and disease.
• Vitamin C has become the most controversial vitamin in recent years. This is
because of the claims and counter-claims on the use of vitamin C in mega doses to
cure everything from common cold to cancer.
Recommended dietary allowance:
Adult 40 mg/day
Lactation 80 mg/day
Infants 25 mg/day
Children 40 mg/day

85. Functions:
1. Vitamin C has a key role in the formation of collagen & intercellular material, bone &
teeth, & in the course of wound healing.
2. Ascorbic acid functions as a cofactor for hydroxylation reactions such as formation of
hydroxyproline and hydroxylysin which is necessary in the synthesis of collagen.
3. Vitamin C is involved in phagocytosis and acts as a detoxifying agent.
4. Vitamin C is involved in reduction of minerals, eg., ferric iron to ferrous iron and hence
vitamin C enhances iron absorption and plays a number of roles that relate to hematology.

86. 5. The participation of vitamin C in the synthesis of hormones by the adrenal glands
may account for its high concentration in adrenal tissues.
6. Although it had been thought that vitamin C supplementation might exert an
antistress action, this has not shown to take place in humans. Ascorbic acid is used as a
food additive antioxidant to prevent enzymatic browning of fruits and potatoes.

87. DEFICIENCY OF VITAMIN C:
Severe vitamin C deficiency results in scurvy.
Clinical Features:
• Hemorrhagic diathesis
• Retardation of wound healing
• Bleeding, swollen, spongy gingiva
• loosened teeth
• Hemorrhagic lesions into the muscles of the extremities, the joints, and sometimes the
nail beds
• Petechial hemorrhages, often around hair follicles
• Increased susceptibility to infections

88. • Defective formation and maintenance of collagen
• Retardation or cessation of osteoid formation
• Impaired osteoblastic function
• Increased capillary permeability
• Susceptibility to traumatic hemorrhages
• Hyporeactivity of the contractile elements of the peripheral blood vessels,
• sluggishness of blood flow

89. Gingival and periodontal tissues:
• Redness
• Swelling
• Tendency towards bleeding upon minimal stimulation
• An alteration towards spongy consistency
• Gingivitis is not caused by lack of vitamin C
• Alfono et al 1994 demonstrated an impairment of barrier function of oral epithelium
basement membrane to bacterial endotoxin in scorbutic guinea pigs.
• A deficiency in vitamin C would impair bone formation and could even cause bones to
fracture.

90. • Barnes stated that defects in collagen synthesis, its tertiary structure and turnover may
explain the observed weakness of periodontal collagen fibers in ascorbic acid deficiency.
• Vitamin C deficiency has been found to increase the risk of periodontal disease among
the smokers and diabetics.
• In vitamin C deficiency, gingiva have decreased ability to resist inflammation and
bleeding, and hence gingivitis occurs even with the presence of small amount of irritants.
• Fontana found that in periodontal disease, the local irritation is the causative agent, and
vitamin C deficiency may be an aggravating factor not the cause.

91. POSSIBLE ETIOLOGIC RELATIONSHIPS BETWEEN ASCORBIC ACID AND
PERIODONTAL DISEASE
Woolfe et al., 1980 have suggested that ascorbic acid may play a role in periodontal disease by
one or more of the following mechanisms:
1. Low levels of ascorbic acid influence the metabolism of collagen within the periodontium,
thereby affecting the ability of the tissue to regenerate and repair itself.
2. Ascorbic acid deficiency interferes with bone formation, leading to loss of periodontal bone.
3. Ascorbic acid deficiency increases the permeability of the oral mucosa and of normal
human crevicular epithelium.

92. 4. Increasing levels of ascorbic acid enhance both the chemotactic and migratory action of
leukocytes without influencing their phagocytic activity.
5. An optimal level of ascorbic acid is apparently required to maintain the integrity of the
periodontal microvasculature, as well as the vascular response to bacterial irritation and wound
healing.
6. Depletion of vitamin C may interfere with the ecologic equilibrium of bacteria in plaque and
thus increase its pathogenicity.

93. Acute vitamin C deficiency accentuates the destructive effect of gingival inflammation on
the underlying periodontal ligament and alveolar bone.
Vitamin C deficiency has its greatest impact on periodontal disease when preexisting
disease and other codestructive factors are present.
Wolbach and Howe (1925) have shown
• Ameloblasts and odontoblasts exhibit loss of polarity and atrophy in scorbutic guinea
pigs.
• The dentinal tubules that are laid down lack their parallel arrangement resulting in an
irregular dentin or no dentin at all.
• The pulp is engorged and dilated from the increased blood.

94. Therapy:
• In treating infantile scurvy, 50 to 100 mg of ascorbic acid may be added to the milk four
times daily.
• In treatment of adult scurvy, 250mg should be administered four times daily for a week,
after which the dose may be decreased to 50 to 100mg four times daily until normal
vitamin C plasma levels of 0.6 to 1.5 mg/100 ml are attained.

95. ROLE OF VITAMINS ON IMMUNE SYSTEM
• Vitamins are essential constituents of our diet that have long been known to
influence the immune system.
• Vitamins A and D have received particular attention in recent years as these
vitamins have been shown to have an unexpected and crucial effect on the immune
response.
• vitamins has role in modulating a broad range of immune processes, such as
lymphocyte activation and proliferation, T-helper-cell differentiation, tissue-specific
lymphocyte homing, the production of specific antibody isotypes and regulation of
the immune response.

96. • The influence of VD3 metabolites in the immune system, particularly of 1,25(OH)2VD3,
has been known for more than 20 years.
• In vitro, 1,25(OH)2VD3 exerts a marked inhibitory effect on adaptive immune cells .
• It inhibits T-cell proliferation, the expression of interleukin- 2 (IL-2)and interferon-γ (IFNγ)
and protein in T cells.
• 1,25(OH)2VD3 enhances nonspecific T-cell suppressor activity.

98. Immunomodulatory role of vitamin A
• Effects on adaptive immune-cell subsets.
• Vitamin A metabolites can also affect some aspects of the adaptive immune response.
• Retinoic acid enhances cytotoxicity and T-cell proliferation, the latter probably mediated,
at least in part, by enhancing Il-2 secretion and signalling in T cells.
• Consistent with an in vivo role for vitamin A in T-cell function, vitamin A deficient mice
have shown defects in TH-cell activity.

99. Forkhead Box Protein 3 (FOXP3) , Receptor-related Orphan Receptor-γt (Rorγt), Antibody-secreting Cells (Ascs), Mucosal-associated
Lymphoid Tissues (MALT), BAFF (B-cell-activating Factor), APRIL (A Proliferation-inducing Ligand), Thymic Stromal Lymphopoietin
(TSLP), Inducible nitric oxide synthase (iNOS),Gut-associated Lymphoid Tissue-GALT.

100. CONCLUSION:
• Although vitamins are required in minute quantities, they are indispensable for maintaining
the integrity and proper functioning of various body systems.
• A sound knowledge regarding dosage of different vitamins and the clinical presentation of
their deficiencies help in properly identifying and curing different disease conditions.

101. 1. Palmer CA. Diet and Nutrition in Oral Health 1st ed, Pearson education 2003.
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3. Kaye E K. Nutrition, dietary guidelines and optimal periodontal health. Periodontol 2000.
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fads. Periodontol 2000 2009;50(2):78–89
5. Kuzmanova D, Jansen IDC, Schoenmaker T, Nazmi K, Teeuw WJ, Bizzarro S,Loos BG,
Velden van der U. Vitamin C in plasma and leucocytes in relation to periodontitis. J Clin
Periodontol 2012; 39: 905–912.
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