VITAMINS IN PERIODONTICS

BRIEF DESCRIPTION OF ALL THE VITAMINS AND THEIR ROLE IN PERIODONTAL HEALTH

1. Presented by,
ZUNAIDHA

2. Contents
•Introduction
•Classification
•Fat soluble –vitamin A , D , E, K
•Water soluble Vitamins -Vitamin C
Thiamine (B1)
Riboflavin (B2)
Niacin ( B3)
Pyridoxine (B6)
Biotin (B7
Folic acid
Vitamin B12

3. VITAMINSmay be regarded as organic compounds required in the diet in
small amounts to perform specific biological functions for normal
maintenance of optimum growth and health of organism.

4. FAT SOLUBLE WATER SOLUBLE
Vitamin A
Vitamin D
Vitamin E
Vitamin K
Non B-ComplexB-Complex
Vitamin C
Energy-releasing Hematopoietic
Thiamine (B1)
Pantothenic acid
Biotin (B7)
Pyridoxine (B6)
Niacin ( B3)
Riboflavin (B2)
Folic acid
Vitamin B12

5. HISTORY
HOPKINS –“Accessory factors” to the unknown and essential nutrients
present in natural food.
FUNK (1913) –isolated an active amine from rice polishings, later in yeast
which could cure Beri-Beriin pigeons.
Coined the term “Vitamine”.
McCollum and Davis (1915) –usage of A, B, C introduced.
1920-1930 –many investigators carried out extensive research and
discovered B-complex vitamins.

6. Synthesis of Vitamins by Intestinal Bacteria
Bacteria of the gut can produce some of vitamins, required by man and
animals.
Vitamin K and Biotin may be sufficient to meet the body requirements
due to normal bacterial synthesis
Synthesis and absorption of B-complex vitamins are relatively less.
Antibiotics often kills the vitamin synthesizing bacteria present in the gut.
Hence additional consumption of vitamins is recommended.

7. •A,D,E,K
•Availability in diet,absorptionand
transport are associated with fat.
•Soluble in fats, oils, fat solvents.
•Can be stored in liverand
adipose tissue.
•Not readily excreted in urine.
•Excess consumption results in
toxic affects. ( A, D)
•B1, B2, B3, B6, B7, B9, B12,
folic acid , vitamin C.
•Soluble in water.
•Readily excreted in urine and not
toxic to the body
•Not stored in body in large
quantities (B12).
•Metabolic stores are depleted
within weeks, hence requires
continuous supply through diet.
FAT SOLUBLE
WATER SOLUBLE

8. VITAMINA
Hippocratescured night blindness (500 B.C ) by prescribing Ox liver in
honey, which in is now known to contain high quantity of vitamin A.
McCollum and Davis (1917) –fat soluble factor of butter was needed for the
proper growth of rats, fed a synthetic diet.
Stunbock(1919) -Vitamin A activity of carotenoids.
Karrer(1931) –structure.
Kuhn and Morris ( 1937) –synthesized in laboratory.
Fat soluble vitamin-present only
in foods of animal origin.
ProvitaminsCarotenes are found in
plants

9. RETINOL
RETINAL
RETINOIC
ACID
β-CAROTENE
RETINOL( VitA Alcohol)
β-ionone ring
Not destroyed by heat
Double bond-Susceptible to
oxidation.
Animals –retinylesters with long
chain fatty acids.
RETINAL( VitA Aldehyde)
Oxidation of retinol
Interconvertible
RETINOICACID( VitA Acid)
Oxidation of retinal.
Cannot be converted to retinal or
retinol.
β-carotene (ProvitaminA )
Plant foods
Cleaved in intestine to form two
moles of retinal.
FORMS OF VITAMIN A

10. RDA
Males = 5000 IU
Females = 800 IU
1 IU= 0.3μg of Retinol
Adult = 750 μg/day
DIETARY SOURCES :
Serum retinol = 30-65mg/dl
Cod liver oil, carrots, capsicum, liver,
sweet potato, broccoli, leafy vegetables
Milk, cheese , butter
Dark green and yellow veg
-B –carotene.
Pregnant and Lactating women have to be provided 50% more.
Dietary deprivation -daily
supplement of 800 to 1,500 μgRE
(2,666 to 5,000 IU)

11. Lymph
Intestinal brush border hydrolases
β-carotene 15-15’-
dioxygenase
2 moles of retinal
ZINC
Absortion, Transport and Mobilization
RAR-Retinoid Acid Receptor
RXR-RexinoidReceptors

12. VISION -Normal functioning of Retina
CELL GROWTH & DIFFERENTIATION –Regulate protein synthesis.
HEALTHY EPITHELIAL TISSUE-
Prevents keratin synthesis,
Formation of muccopolysaccharides, thus maintains moist cell surface.
Synthesis oftransferrin –RETINOL AND RETINOIC ACID
Maintains IMMUNE SYSTEM
Carotenoids –Antioxidant , thus reduces the risk of cancer.
Haematopoiesis
FUNCTIONS OF VITAMIN A

13. Vitamin A Deficiency
Vitamin A deficiency blindness is most common in children
Initial
Irreversible damage to the visual cells
Xerophthalmia
Bitotspots
Corneal ulceration
Keratomalacia
Growth Retardation:
Impairment in skeletal formation
REPRODUCTION :
Sterility in males : degeneration
of germinal epithelium .
Fetaldeath
SKIN & EPITHELIAL CELLS :
Rough and dry skin.
Keratinization of GIT, Urinary
tract,Respiratorytract.
Increased bacterial infection
Urinary stones
Alterations in mucosal surfaces

14. HypervitaminosisA
SYMPTOMS
Dermatitis (drying and redness of skin )
Enlargement of liver
Skeletal decalcification
Tenderness of long bones
Loss of weight
Irritability
Loss of hair
Joint pains
Pregnancy : Congenital malformation in
fetus.
Raised intracranial pressure.
Total serum vitamin level is elevated.
Retinol + lipoproteins =harmful to the body.
Retinol binding protein exceeds
Higher retinol = increases the synthesis of lysosomalhydrolases = destructive action of
hydrolases, particularly on the cell membranes.
Impairs epithelial tissue integrity.
TOXICITY -> 3000 μg/day

15. EFFECT OF VITAMIN A ON PERIODONTIUM
Major function of vitamin A –Maintain health of the epithelial cells
of skin and mucous membrane.
Plays an important role in protecting against microbial invasion by
maintaining epithelial integrity
Several epidemiological studies have failed to demonstrate any relationship
between this vitamin and periodontal disease in humans .
Absence of Vitamin A :
degenerative changes in epithelial tissues = keratinizing metaplasia.
•Experimental animals –hyperkeratosis and hyperplasia of gingiva
increased tendency of pocket formation
•Rats –proliferation of JE, Retardation of gingival wound healing.
pocket formation (local factors )

16. Linden et al. evaluated the correlation between periodontal health and
serum levels of multiple antioxidants.
Henoticedthatlevelsofαandβcarotene,βcryptoxanthin,andzeaxanthin
weresignificantlylowerinmoderateandsevereperiodontitispatientshowever
nosuchassociationwasfoundinthelevelsoflutein,lycopene,αtocopherolor
retinolwithperiodontitis.
Walstonet al found that patients with low levels of α-and β-carotene and
total carotenoids were more likely to have high interleukin-6.

18. Vitamin D, the sunshine vitamin, has long been recognized as essential for
bone and mineral metabolism.
Fat soluble vitamin
Resembles sterols and functions as hormones.
History :
Mellanby(1919) discovered that administration of
cod liver oil could prevent the development of rickets
in experimental dogs.
Augus(1931) isolated Vitamin D and named it as
calciferol.
Ergocalciferol(vitamin D2) :Plants.
Cholecalciferol (vitamin D3) :Animals.
Forms of Vitamin D

19. 1.Consumption of natural foods
2.Exposure of skin to sunlight for synthesis of vitamin D
3.By irradiation of foods (yeast ) which contains precursors
of vitD and fortification of foods
(milk, butter etc.)
RDA
400IU/ 10μg
In countries with good sunlight
(like India), the RDA is 200 IU or 5 μg.
Serum Vit. D = 24-65 pg/ml
main source of vitamin D isde novosynthesis
in the skin. (95% )
AMERICAN MEDICAL ASSOCIATION
•400 IU in children –to prevent rickets
NATIONAL OSTEOPOROSIS FOUNDATION
•800-1000 IU –Prevents fracture
•> 50 YRS OLD

20. BIOSYNTHESIS OF VITAMIN D
25-hydroxylase
1-Hydroxylase
Calcitriol

21. Vitamin D3 is synthesized in the skin by UV rays of sun.
The biologically active form of vitamin D, calcitriolis produced in the kidney.
Calcitriolhas target organs –intestine , bone and kidney.
Action is similar to steroid hormones.
binds to a receptor in the cytosol
( calcitriolreceptor complex )
this complex acts on DNA to stimulate the synthesis of
calcium binding protein
Calcitriolsynthesis is self-regulated by a feedback mechanism.
It acts in association with other hormones , parathyroid hormone and
calcitonin to regulate calcium and phosphate level in plasma.
HALF LIFE = 10 hrs
Features of Vitamin D comparable with Hormones

22. Biochemical function of Vitamin D
Biologically active form –Calcitriol(1, 25 DHCC)
It regulates the plasma levels of calcium and phosphate
I.Increases the absorption of Calcium and phosphate.
Binds to a receptor in the cytosol
( calcitriolreceptor complex )
this complex acts on DNA to stimulate the synthesis of
calcium binding protein
Cauptake
II. Reservoir of calcium and phosphate
In osteoblasts , calcitriolstimulates calcium uptake.
Calcitriol+ PTH increases the mobilization of calcium and
phosphate from the bone.
III. Reabsorption of Calcium and Phosphate.
Decresesthe excretion

23. VITAMIN D DEFICIENCY
Insufficient exposure to sunlight
Consumption of diet lacking Vitamin D.
Strict vegetarians
Chronic alcoholics
Liver and kidney diseases.
Fat malabsorption syndromes.
Prevalantin northern latitudes.
RICKETS (Children)
OSTEOMALACIA (Adult)
RENAL RICKETS
RICKETS
Bone deformities due to incomplete
mineralization
Soft and pliable bones
Delay in teeth formation
Decreased plasma level of calcitriol
Alkaline phosphatase activity is
elevated.
RENAL RICKETS
Chronic renal failure
Decreased synthesis of calcitriolin
kidney

24. Dental Manifestation :
Mellanby:
Developmental abnormalities of dentin
and enamel (enamel hypoplasia).
Delayed eruption
Malalignedteeth
Human rachitic teeth:
abnormally wide predentinzone and
interglobulardentin
HypervitaminosisD
Vitamin D is mostly stored in liver and slowly
metabolized.
Most toxic in overdoses (10-100 times RDA).
Bone resorptionand hypercalcemia
Renal calculi
Loss of appetite, nausea, increased thirst and
loss of weight.

25. VITAMIN D ON BONE METABOLISM
vitamin D appears to stimulate bone resorption, which is necessary for bone
remodelling and formation of new bone, but after longer periods of exposure
and it may facilitate osteoblast proliferation and differentiation.
remodeling

26. VITAMIN D AND PERIODONTAL HEALTH
•Mainatainscalcium –phosphorus balance
•Experimental dogs –osteoporosis of alveolar bone
•Osteiodformation is normal –uncalcifiedand fails to resorb.
•Reduction in width of PDL space –normal rate of cementumformation,
coupled with effective calcification and distortion of growth pattern of
alveolar bone.
OSTEOMALACIC ANIMALS :
Rapid,severegeneralized osteoclasticresorptionof alveolar bone
Proliferation of fibroblasts
Radiographically–partial /complete disappearance of Lamina Dura
Reduced density of supporting bone.
Loss of traberculae

27. More recent studies showed significant associations between periodontal health and
intake of vitamin D and calcium,andthat dietary supplementation with calcium and
vitamin D may improve periodontal health, increase bone mineral density in the
mandible and inhibit alveolar bone resorption.
In a recently published longitudinal study, Garciaet al. reported that calcium and
vitamin D supplementation may reduce the severity of periodontal disease if used at
doses higher than 800-1,000 IU daily .
They also noted that vitamin D, in addition to its role in bone and calcium
homeostasis, acts as an anti-inflammatory agent because it inhibits immune cell
cytokine expression and causes monocyte/macrophages to secrete molecules that
have a strong antibiotic effect.
Indeed, vitamin D deficiency may be linked to increased risk of infectious diseases.
This suggests that vitamin D may be of benefit in the treatment of periodontitis, not
only because of its direct effects on bone metabolism, but also because it may have
antibiotic effects on periodontopathogensand inhibit inflammatory mediators that
contribute to the periodontal destruction.

28. sunlight (about 3,000 IU vitamin D3/5-10 min of mid-day,
midyear exposure of arms and legs for a light-skinned .

30. Naturally occurring anti-oxidant.
Anti-sterility vitamin –essential for normal reproduction.
Evans and Bishop (1922) –fat soluble factor , present in vegetables
was responsible for the normal reproduction in rats.
1936 –isolated the compounds of Vitamin E activity and named
TOCOPHEROLS.
Most active –αtocopherols.
Chemistry –derivatives of 6-hydroxychromane (tocolring) with
isoprenoidside chain.
Antioxidant property –chromanering

32. •ANTIOXIDANT PROPERTY –
Prevents non enzymatic oxidations of various cell components by molecular
O2 and free radicals ( superoxide and hydrogen peroxide )
•Essential for membrane structure and integrity of the cell.
•It prevents hemolysisof RBC by oxidizing agents.
•It is required for proper storage of creatinein skeletal muscle.
•Essential for optimum absorption of amino acid from the intestine.
•Helps in proper synthesis of nucleic acid.
•It works in association of vitamin A, and C , to delay the onset of cataract
•Recent studies have shown that high intake of vitamin E (200-300mg/dl)
protects against the development of heart diseases.
BIOCHEMICAL FUNCTION OF VITAMIN E

33. MALE = 10mg/dl
FEMALE = 8mg/dlSerum level = 5-20 mg/ml

34. DEFICIENCY OF VITAMIN E
Sterility
Muscular dystrophy and paralysis
Megaloblasticanemia
CNS-minor neurological symptoms.
Increased fragility of erythrocytes.
Abnormal cellular membrane
Defect in fat absorption and transport
TOXICITY: least toxic
No toxic effect has been reported even after ingestion of 300mg/day for 23
years.

35. VITAMIN E AND PERIODONTAL HEALTH
Antioxidant–limits free-radical reactions and protects cells from lipid
peroxidation and improves stability and integrity of biologic membranes.
As consequence, vitamin E stops the production of ROS.
Systemic and local Superoxide dismutase levels are lowered in chronic
periodontitis patients when adjunctive vitamin E along with SRP was given ,
indicating improved periodontal healing as well as antioxidant defense.
Systemic vitamin E appears to accelerate gingival wound healing in rats.
-Jungnamego kim
The effect of vitamin E on healing ulcers was first reported by Lee in 1953,
who demonstrated improvement in frequency and healing time when
compared to placebo.

36. Serum levels of α-tocopherolhave been inversely associated with mean
PPD and periodontitis (defined according to CDC/AAP criteria) in a
subset of participants in the 1999–2001 NHANES
Vitamin E can help to control periodontal disease through its ability to prevent
inflammation.
Goodson and Bowles(1973) used vitamin E to treat 14 patients with
periodontal disease and found a reduction in inflammation after 21 days, as
determined by crevicular fluid flow.
Cernaet al showed that long term (12 weeks) administration of 300 mg of
Vitamin E significantly reduced inflammation of the periodontal tissues

37. Only fat soluble vitamin with specific co-enzyme function.
Its is required for the production of blood clotting factors, essential for
coagulation.
In 1934, Dam Schonleyderdiscovered that a hemorrhagicdisease of chicks,
characterized by severe bleeding, could be cured by alfaalfaand fish meal.
On isolation of the active principle they named it Koagulationvitamin or
Vitamin K.
K1
Phylloquinone
(plants)
K2
Menaquinone
(Intbacteria/animals)
K3
Menadione
(synthetic form)
Naphthoquinonederivates
Activity is lost –oxidizing agents, irradiation, strong acids and alkalies

38. Plants sources: mostly phylloquinone, accounts 90% of intakes.
green leafy vegetables; spring (collard) greens, spinach, Brussels sprouts.
-soybean, cottonseed, and olive oil are relatively rich in vitamin K
Animal sources:
milk and milk products, meat, liver, fermented foods.
Exposure to light and heat can result in significant destructionof vitamin K
RDA = 70-140μg/day

40. Biochemical functions of Vitamin K
The function of vitamin K are concerned with blood clotting process.
It brings about post-translational modification of certain blood clotting
factors . ( II, VII , IX , X )
vitamin K also required for the carboxylation of glutamic acid residues of
osteocalcinand periostin.
VITAMIN K
GLUTAMATE (GLU )
γ–Carboxyglutamate(GLA)
WARFARIN

41. DEFECIENCYOF VITAMIN K
Rare in humans except for newborns–
•Insufficient gut bacteria
•Poor placental transport of vitamin K
•Low Prothrombin synthesis capacity of neonatal liver
•Human milk is very low in Vitamin K ( 2.5μg / L )
•Malabsorption( ulcerative colitis ) / Diarrhea
•Bleeding episodes may occur in patients with low vitamin K status on long term
Antibiotic treatment ( loss of colonic bacteria )
•Anticoagulant therapy .
Vitamin K injections ( 0.5-1mg ) or 2mg orally

42. HYPERVITAMINOSIS OF VITAMIN K
Hemolyticanemia
Jaundice in infants
Antagonists to Vitamin K
Heparin and Coumarinderivatives
Warfarin
Salicylates

43. Vitamin K and Periodontal tissues:
The most common oral manifestation is gingival bleeding and post surgical
hemorrhage.
If antibiotics are to be made part of periodontal therapy for a long period
of time, coagulopathies might be observed.
Vitamin K is an important pharmacological agent used to reverse the
anticoagulant effects of warfarin and routinely administered for patients
undergoing hemodialysis.
Hence, if periodontal therapy is to be performed in patients with kidney failure,
vitamin K can be used to treat any bleeding incidents.
However, a patient with digestive disorder or who has been using antibiotics for
a long period of time must be investigated for vitamin K deficiency.
Although vitamin K deficiency may lead to gingival bleeding, a recent study by
Aral et al. has found that vitamin K supplementation was not able to reduce pro-
inflammatory factors in the periodontium.

45. James Lind –surgeon of English Navvy (1753) discovered
that citrus foods helped to prevent scurvy.
Ascorbic acid was identified in 1932 as the antiscorbotic
vitamin.
Chemistry–hexose derivative
Citrus fruits,gooseberry,
guava ,green vegetables,
tomatoes,potatoes.
RDA=60-70 mg/day
Man and other primates cannot synthesize Vitamin C due to deficiency
of enzyme L-gluconolactone oxidase

46. BIOCHEMICAL FUNCTION OF VITAMIN C
•Collagen synthesis : necessary for normal c.t and wound healing process.
•Bone formation ( organic matrix, collagen ,inorganic calcium , phosphate )
•Iron and haemoglobin metabolism: enhances iron absorption ,
formation of ferritin
mobilization of ferritin.
•Metabolism of tryptophan , tyrosine , cholesterol and folic acid.
•Synthesis of corticosteroid hormone ( high vitC is present in adrenal gland )
•Cellular respiration :
Electron transport chain exhibits optimum activity in the presence of Vitamin C
•Immunological functions: enhances the synthesis of antibodies,
increases the phagocytic action of leucocytes.
•Prevents cataract formation.
•Chronic diseases –free radicals are constantly produced.(ANTIOXIDANT)

47. Deficiency of Vitamin C :
Impairment in the synthesis of collagen
Antioxidant property of ascorbic acid
Impairment / cessation of osteoid formation and osteoblasticfunction
SCURVY
Spongy and sore gums
Loose teeth
Swollen joints
Anemia
Fragile blood vessels
Decreased immunocompetance
Delayed wound healing
Osteoporosis
Haemorrhage
Increased suceptiblityto infection
Mental Disorders
Unusual eating habits,
Alcoholism
Intestinal Malabsorption
Dialysis

48. VITAMIN C AND PERIODONTAL HEALTH
Low levels of ascorbic acid influence the metabolism of collagen within the
PDL, affecting the ability to repair and regeneration.
Interferes with bone formation leading to loss of alveolar bone.
Osteoporosis of alveolar bone of scorbutic monkeys results from increased
osteoclasticresorption( not associate with Pocket formation).
Optimum level would maintain the epithelial barrier function to bacterial
products.
Optimum level is required to maintain the integrity of periodontal
microvasculature, vascular response to bacterial plaque and wound healing.

49. GINGIVITIS :
Acute vitamin C deficiency does not cause or increase the incidence of
gingivitis, but increases its severity.
It may aggravate the gingival response to bacterial plaque -edema,
enlargement and bleeding.
PERIODONTITIS:
Impairs gingival healing
Osteoporosis of alveolar bone.
Edemaand haemorrhage of PDL
Tooth mobility.

50. May interfere with the ecologic equilibrium of bacteria in plaque and thus
increase the pathogenicity. ( no evidence )
Leggottet al.studied the effect of a nutrient rich diet but lacking vitamin C, on
periodontal health. The results suggested that ascorbic acid may influence
early stages of gingivitis, particularly increased crevicular bleeding.
Based on NHANES III , Nishida et al.revealed that they have a weak, but
statistically significant dose response relationship between the dietary vitamin C
to periodontal disease in current and former smokers.
Chappleet al. found a strong and consistent inverse association between serum
vitamin C levels and the prevalence of periodontitis.
A case report by Charbeneauand Hurt : worsening of pre existing moderate
periodontitis with development of scurvy

51. THIAMINE ( B1)
Anti-beriberivitamin / antineuriticvitamin.
Jansen and Donath(1926) –isolated from rice polishings.
It is a white crystalline water soluble solid destroyed by heat in alkalized
neutral condition
Special coenzyme –thiamine pyrophosphate (TPP)
physiologically active form.
RDA
ADULTS –1-1.5mg/day
CHILDREN –0.7-1.2
mg/day
Cereals,pulses,oilseed,
nuts ,yeast.
Outer layer of cereals-
bran
Dietary sources :

52. Biochemical functions of B1
Thiamine pyrophosphate is intimately connected with the energy releasing
reactions in carbohydrate metabolism.
Important role in transmission of nerve impulses.
Accumulation of
pyruvate
Crosses the BBB-
POLYNEURITIS
Lack of energy –
adversely effects the
cellular functions.
Decreased activity of
transketolasein erythrocytes

53. DEFECIENCY OF B1
BERI BERI
Populations consuming extremely polished rice as staple food.
WET BERI BERI
Edemaof legs,face,trunk
Breathlessness , palpitations
Swollen calf muscles
BP : Systolic –increased
diastolic –decreased
Fast and bouncing pulse
Heart becomes weak –death
DRY BERI BERI
Neurological manifestations
Peripheral neuritis
Edemais not common
Weak muscles and difficulty in
walking
Mixed BERI BERI
INFANTILE BERI BERI
Born to thiamine deficient mother
Sleeplessness
Restlessness
Vomiting
Convulsions
Cardiac dialatation
death
Wernicke-Korsakoffsyndrome
TOXICITY : Repeated I.V injection may result in anaphylactic shock
Oralmanifestation:
Hypersensitivity of oral mucosa, minute
vesicles on buccalmucosa , the tongue or
palate, and erosion of oral mucosa

54. Thiamine deficiency occurs in individuals with diabetes, which leads to
hyperglycaemic-induced damage…
•Thiamine administration can prevent the formation of harmful by-products of
glucose metabolism, reduce oxidative stress and improve endothelial function.
•The potential benefit of long-term replacement in those with diabetes is not yet
known but may reduce cardiovascular risk and angiopathiccomplications.
(Alamet al, 2012), used 300 mg of thiamineach day for 3 months in type 2 DM.
In this study, low thiaminlevels did not appear to be related to dietary intake,
rather to enhanced excretion through the renal system.
Alamrecommended that people with type 2 diabetes take 300 mg of thiamindaily
to prevent depletion of thiaminlevels in the body.

55. RIBOFLAVIN ( B2)
Riboflavin is the first B complex vitamin that was isolated in pure state (KUHN 1933)
GOLDBERGER (1926) –PELLAGRA could be cured by dietary factor Vitamin B2
Stable to heat but sensitive to light.
COENZYMES –Flavinmononucleotide (FMN)
Flavinadenine dinucleotide (FAD)
RDA
1.2-1.7mg/day
DIETARY SOURCES :
Milk and milk products,
meat,egg,
liver,kidney,Cereals ,fruits,
vegetables , fish

56. BIOCHEMICAL FUNCTIONS
The flavincoenzymes participate in many Redox reactions responsible for
energy production.
The functional unit –isoalloxazinering which serves as an acceptor of two
hydrogen atoms.
FMNH2 / FADH2
The coenzymes are associated with certain enzymes involved in carbohydrate,
lipid, protein and purine metabolism.

57. DEFECIENCY OF RIBOFLAVIN
Associatedwithinadequateconsumptionofmilkandanimalproducts.
Mostcommoninchronicdiarrhea,liverdisease,chronicalcoholism
angular stomatitis
perleche
Seborrhea dermatitis

58. NIACIN (B3)
Nicotinic acid –chemical compound formed due to oxidation of nicotine.
Pellagra preventive factor (P.P) of Goldberg.
Co-enzyme = NAD+ and NADP+ (Synthesized by tryptophan)
Administration of dried meat and liver cured pellagra (Goldberg, 1928 )

59. DIETARY SOURCES :
Liver , yeast , whole grains , cereals , pulses , peanuts
Milk ,fish , egg .
EAA : tryptophan serves as precursor for synthesis of
Nicotinamidecoenzymes.
RDA
Adult : 15-20 mg
Children : 10-15 mg

60. FUNCTIONS :
•Essential for cell functioning.
•Constituent of NAD and NADPH needed for the energy release
from carbohydrates, proteins , and fats .
•Steroid and RBC formation.

61. 1)Deficientintake(stapledietofcornandmaize)
2)Defectivedigestionasindiarrhea
3)Increaseddemandduringpregnancy,thyrotoxicosis,fever
PELLAGRA –skin , GI tract , CNS
DERMATITIS
Neck , dorsal part of feet ,ankle , face
(butterfly-like pattern)
DIARRHEA
Loose stools with blood and mucous
Prolonged –weight loss
DEMENTIA
Degeneration of nervous tissue
Anxiety, irritability , poor memory
Insominia
Death-rarely
DEFECIENCY OF B3
LEUCINE–inhibits the synthesis of NAD+
and NADP+
Drug therapies(e.g. isoniazid)
can lead to niacin deficiency

62. Glossitis
Tongue is “beefy red”,
glossodyniaand glossopyrosis.
Profuse salivation.
The most common finding is NUG usually in areas of local irritation.
Necrosis of gingiva and leukopenia-terminalfeatures

63. THERAPEUTIC USES OF NIACIN
2-4g/ day (200 times more the RDA )
•Inhibits lipolysis in adipose tissue and decreases the circulatory free fatty acids.
•Decreases the triacylglycerol synthesis in liver.
•Decreases serum levels of LDL , VLDL , Cholesterol (Hyperlipoproteinemia)
•The vasodilator effect = angina pectoris and cerebral thrombosis.
•Sublingual niacin has helped in the relief of pain and shock.
Glycogen and fat reserve of skeletal and cardiac muscles are depleted.
Tendency for the increased levels of glucose and uric acid.
Serum levels of certain enzymes may be elevated (LIVER )
High doses may produce resistance to insulin.

64. EFFECT ON PERIODONTIUM
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.

65. PYRIDOXINE (B6)
Active form –Pyridoxalphosphate (PLP )
B6 compounds are Pyrimidine derivatives
Synthesized by Kuhn and co-workers (1939)
RDA
ADULT=2-2.2mg/day
Pregnancy/lactation
=2.5mg
DIETARY SOURCES :
•Egg yolk, fish , milk ,meat
•Wheat , corn , cabbage , roots.

66. BIOCHEMICAL FUNCTIONS OF B6
Closely associated with metabolism of amino acids .
Synthesis of serotonin , histamine , niacin co-enzyme from amino acid is
dependant on PLP.
PLP participates in reactions like
Transamination
Decarboxylation
Transulfuration
Condensation

67. DEFECIENCY OF B6
NEUROLOGICAL SYMPTOMS
Depression
Irritability
Nervousness
Mental confusion
Convulsions
Peripheral neuropathy
Demyelination of neurons
Decreased Haemoglobin level
Hypochromic microcytic anemia
women under OCP
Infants
Alcoholics

68. Anti-egg white injury factor or vitamin H
Sulphur containing vitamin.
Glycoprotien-Avidinand biotin
RDA
Adults-100-300 μg/day
BIOTIN
Sources: liver, kidney, eggyolk, milk,
tomatoes, grains, vegetables

69. Biochemical function of BIOTIN
Essential in many metabolic pathways including citric acid
cycle and Glycolysis.
Involved in the synthesis of fatty acid and amino acid
Biotin is a coenzyme for carboxylase enzymes
• Acetyl coenzyme A carboxylase
• Pyruvate carboxylase
• MethylcrotonylCoA carboxylase
• PropionylCoA carboxylase

70. •Rare
Biotin Deficiency
1.Dermatitis-red rash around the eyes, nose,
mouth, and genital area.
2.Alopecia-Hair loss
3.Lethargy
4.Acidosis
5.Neurological abnormalities-depression
6.Hallucinations
Sulfonamides –destroys intestinal flora
High consumption of raw eggs –avidinwhich blocks the absorption of Biotin .
20 raw eggs / day
Major gut resection

71. F
O
L
I
C
A
C
I
D
Wills (1934) reported that macrocytic anemiain humans could be cured
by a vitamin present in autolysedyeast extract
Angier (1946) –established the structure and synthesized it chemically.
Synthesis –Amino Acids
Purines
Pyrimidine -Thymine
Three components :
Pteridinering
p-amino benzoic acid ( PABA)
Glutamic acid
Active form = tetrahydrofolate(THF / FH4)

72. Green leafy vegetables , whole grains,
cereals , liver ,kidney , yeast , milk
RDA
ADULT = 100μg/day
Pregnancy =300μg/day
Lactation = 150μg / day
Folic acid is important during periods of rapid cell division and growth.
Both children and adults require folic acid to produce healthy red blood cells and
prevent anemia.

74. Most common vitamin deficiency in pregnant women .
Lactating women , OCP , alcoholics are more susceptible
Methotrexate –inhibits DHFR.
Decreased production or purines –impairs DNA synthesis.
DEFECIENCY SYMPTOMS
Inadequate dietary intake
Defective absorption
Impaired metabolism
Increased demand
Maturation of RBC slows down
Cell division in bone marrow is affected
Macrocytic anemiawith megaloblasticchanges in bone marrow
Neural tube defects –cleptlip and palate.

75. Abnormalities in rapidly proliferating epithelial cells.
The maturation of junctionalepithelium, which has a rapid turnover rate, is
a prime importance in the prevention and control of periodontal disease.
Folic acid deficiency is associated with severe gingival inflammation
(Vogel).
Folic acid deficiency in gingivitis patients as compared to patients
supplemented with folic acid have shown to increase bleeding on probing,
increase gingival exudate, and both clinical and histological evidence of
severe gingival inflammation.
Absence of keratinization of gingival surface.
Decreased resistance to infection is also noted among folic acid-deficient
individuals

76. Folic acid supplementation and its influence in gingival and periodontal health
and disease
systemically and topically
Mouthwash, tablets, capsules, and injections
Dietary supplementation of 2 mg systemic folic acid showed an increase
In the resistance of gingivato local irritants and thus led to a reduction in
inflammationover a 30-day period (Vogel, 1976).
use of 5 ml folate mouthwash rinse twice-daily for 4 weeks for 1 min on
established gingivitis in non-pregnant women showed improved gingival health
(Angela R C Pack, 1984)

77. Systemic folic acid (5 mg/day) in combination with oral hygiene measures
in prevention of phenytoin-induced gingival overgrowth showed that after
one year, gingival overgrowth was delayed in children (Prasad V N, 2004).
In folic acid deficiency-prone situation, the management and maintenance
of periodontal health and disease will be positively influenced by folic acid
supplementation.
Oral folic acid supplementation, 0.5 mg/day, is associated with prevention
of gingival overgrowth in children taking phenytoin monotherapy

78. COBALAMINE B12
•Anti-pernicious anemiavitamin.
•Synthesised only by microoragaisms.
•It is the only vitamin containing the element cobalt.
•It is red crystalline substance, red colourbeing due to cobalt.
•It is destroyed by prolonged exposure to sunlight

79. Liver , kidney .milk , curd ,
eggs, fish , pork , chicken
Syntheseizedonly by micro organism .
Hence never found in plants .
RDA
ADULT = 3μg/day
Children = 0.5-1.5 μg/day

80. Absortptionand transport
FUNTION :
Formation of mature RBC
Synthesis of DNA and RNA

81. DEFECIENCY OF VITAMIN B12
PERNICIOUSANEMIA–Lowhaemoglobinlevels
Decreasedno.oferythrocytes
Neurologicalmanifestations
DEMYELINATION OF NERVOUS SYSTEM –
paresthesiaof fingers and toes
confusion , loss of memory,psychosis
CAUSES :
AI destruction of parietal cells
Hereditary malabsorption
Partial or total gastrectomy
Insufficient production of IF
Dietary insufficiency

82. THERAPEUTIC DOSES
100-1000μg i.m
Megaloblasticanemia–combined supplements of folic acid and B12
ORAL MANIFESTATIONS
Glossitis, angular cheilitis,
Recurrent oral ulcer,
Oral candidiasis,
Diffuse erythematous mucositis
pale oral mucosa,
Haemorrhagic gingiva,
Oral paresthesia,
Sore and burning mouth
Detachment of PDL fibers,
Loss of taste, xerostomia

83. Although vitamins are required in minute quantities , they are indispensable
for maintaining the integrity and proper functioning of various body systems.
It is important for us to have basic knowledge about different vitamins that
are required for body to educate and motivate the patient thereby preventing
any mineral deficiency.
CONCLUSION

84. REFERENCES
•Textbook of biochemistry : U sathyanarayana
•Textbook of Diet and Nutrition in Oral Health : Carole A Palmer.
•Nutritional Care ,third edition , Cynthia A. Stegeman,JudiRatliff Davis
•Nutraceuticals in periodontal health: a systematic review on the role of
vitamins in periodontal health maintenance,
•The role of nutrition in periodontal health:anupdate :shariqnajeeb,
muhammadsohailzafar,zohaibkhurshid, sanazohaibkhalidalmas
•Vitamin A and immune function:Richard D. Semba

85. •Role of dietary antioxidants in periodontitis: a preventive approach: journal
of dental and medical sciences
•Effect of High Dose Thiamine Therapy on Risk Factors in Type 2 Diabetics
SaadiaShahzadAlam, SamreenRiazand WaheedAkhtar M.
•Vitamin E Supplementation, Superoxide Dismutase Status, and Outcome of
Scaling and Root Planing in Patients With Chronic Periodontitis: A
Randomized Clinical Trial :NehaSinghet al.
•Hormonal actions of vitamin D and its role beyond just Being a vitamin: A
review article KhurshidAhmad Khan1,2*, Professor JavedAkram1 and
MariumFazal1
•Folic acid: A positive influence on periodontal tissues during health and
disease

86. Thankyou …