vitamins

CONTENTS Introduction Terminologies Classification Vitamin A Vitamin D Vitamin E Vitamin K Vitamin B Vitamin C Conclusion References

INTRODUCTION

Definition:

Vitamins may 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 the organism

-Harper’s Illustrated Biochemistry.26th edition.

Terminologies

• Vitamins = 'vital' and 'amine'.

Cashmir Funk 1911- ‘Vitamine’

Other names: accessory food factors, food hormones

Vitamers

Classification

Vitamin A

VITAMIN A

2 groups: McCollum,Davis;Osborne and Mendel.(1913)

Fat soluble vitamin- present only in foods

of animal origin.

Pigmented carotenoids - plants

Chemistry Retinol→ß-ionone ring and the side chain

contains two isoprenoid rings,four double bonds(oxidation) ß carotenes- cleaved in the intestine to produce 2 mol.of

retinal, hence called provitamins. Antioxidant property.

Carotenes

Biochemical functions:

Normal function of the retina

Growth and differentiation of epithelial tissues

Bone growth

Gene transcription

Immune function

Embryonic development and reproduction

Haematopoiesis

Skin and cellular health:Isotretinoin

Antioxidant activity

RDA:

5000 IU (1000 retinol equivalents*)

4000 IU (800 retinol equivalents*)

* 1 IU = 0.3 µg of retinol

Serum retinol = 30-65mg/dl

Vitamin AVitamin A

Deficiency:

Night blindness (nyctalopia) Xeropthalmia Bitot’s spots Corneal ulceration – Keratomalacia

Degenerative changes-keratinizing metaplasia-bacterial inf General defense mechanism of the body-impaired Growth retardation:impairment of skeletal formation Degeneration of germinal epithelium leads to sterility in

males and termination of pregnancy (fetal death) also seen

In developing tooth, odontogenic epithelium fail to undergo differentiationinc rate of cell proliferation epithelial invasion of pulpal tissue

Mothers (5 months before birth)distortion of shape of incisors and molars.

Poor calcification of enamel matrixenamel hypoplasia

Atypical dentin cellular and vascular inclusions

Alveolar bone retarded rate of formation.

Eruption rate retarded

Dental Manifestations

Hypervitaminosis Symptoms: include dermatitis, enlargement of liver, skeletal

decalcifications, tenderness of long bones, loss of weight, irritability, loss of hair, joint pains.

Constant headache

pregnant women

Total serum vitamin level is elevated.

retinol + lipoproteins =harmful to the body.

retinol binding protein exceeds=toxicosis.

Higher retinol =increases the synthesis of lysosomal hydrolasesdestructive action of hydrolases, particularly on the cell membranes

Vitamin A and periodontal diseases

Avitaminosis has been shown to produce localized gingival recession, epithelial hypertrophy, and hyperplasia in monkeys, guinea pigs and dogs.

(Mellanby and King 1934; King 1935, 1937, Topping and Fraser 1939; Mellanby 1941; Glickman and Stoller 1948; Miglani 1959)

The following periodontal changes have been reported in vitamin A deficient rats:– Hyperplasia and hyperkeratinization of the gingival

epithelium.– Proliferation of junctional epithelium.– Retardation of gingival wound healing.– Deep periodontal pockets

Transient inflammation ,gingivitis and pocket formation have been reported in dogs

( Mellanby and King,1934)

However later it was indicated that local irritation was necessary before an inflammatory response is observed.

( Boyle 1941; Glickman and Stoller 1948; Frandsen 1963)

Vitamin A is controversial in its antioxidant property

At the low partial oxygen pressures- antioxidant and vice-versa and can cause detrimental effects on the tissues

(Iain L.C. Chapple and John B. Matthews,2007)

Contradictory findings i.r.t bone:

Replacement of bony trabeculae with fibrous connective tissue ( Marshall 1927, King 1935)

Reduced bone formation ( Boyle 1941; Miglani 1959)

Increased thickness of bone and greater deposition on the labial cortical plates. (Irving 1949,1956; Schour et al 1941).

Frandsen (1963) put forth a theory that the

main effect of Vitamin A deficiency is to suppress resorption by inhibiting osteoclast function.

Osteoblast function may also be reduced (Frandsen and Becks 1962), although if the magnitude of suppression is greater in favour of the resorbing cells, then bone deposition will continue but at a slower rate. The time interval-significant factor

In a case report, a 20- year old woman presented with gingival erosions, ulcerations, bleeding, swelling and a loss of keratinization.

Headache, dry mouth and loss of hair were also noted. History of taking 200,000 IU of vitamin A daily for 6

months was given. When the vitamin supplementation was stopped, gingival

improvement was noted in 1 week. At 2 months, the appearance of the oral tissues was found to be normal.

A. C. de Menzes et al,1984

Vitamin D

Vitamin D can be considered as a conditional vitamin

Cholecalciferol (vitamin D3) :animals.

Ergocalciferol (vitamin D2) :plants.

RDA: 400 IU or 10µg of cholecalciferol.

In countries with good sunlight (like India), the RDA is 200 IU or 5 µg.

Serum Vit. D = 24-65 pg/ml

Vitamin DVitamin D

Biosynthesis

skin

1-hydroxylase

Biological functions

Deficiency

Less common (synthesized in the body).

Occurs in strict vegetarians, chronic alcoholics, individuals with liver and kidney diseases or fat malabsorption syndrome.

Leads to demineralization of bone. Rickets- children

osteomalacia - adults.

Rickets Derived from an old English word

wricken = twist. Antirachitic vitamin.

Rickets in children is characterized by : bone deformities due to incomplete

mineralization, resulting in soft and pliable bones

delay in teeth formation.

calcitriol

alkaline phosphatase

Osteomalacia: Osteomalacia is derived from Greek (osteon - bone;

malakia - softness). Demineralization of the bones occurs increased

susceptibility to fractures.

Taylor and Day :50 % incidence of severe periodontitis in a series of 22 indian women with osteomalacia

Renal Rickets (renal osteodystrophy): It is seen in patients with chronic renal failure.

decreased synthesis of calcitriol in kidney. It can be treated by administration of calcitriol

Dental Manifestations

Mellanby:

Developmental abnormalities of dentin and enamel Delayed erption Malaligned teeth

Human rachitic teeth:

abnormally wide predentin zone and interglobular dentin

Hypervitaminosis D

Vitamin D is mostly stored in liver and slowly metabolized.

Most toxic in overdoses (10-100 times RDA).

Bone resorption and hypercalcemia

Renal calculi

Loss of appetite, nausea, increased thirst and loss of weight.

Periodontal Implications

Oliver et al studied that deficiency of calcium + vitamin D there was a reduction of alveolar bone mass and greater areas of unmineralized osteoid.

In the periodontal ligament, the number and diameter of the dentoalveolar fibres were reduced alteration in the masticatory activity due to loss of the mineralized tissue

The periodontal effects of overdosing with vitamin D in dogs have also been described (Becks 1942).

Increased osteoblastic activity, included : pathological calcification of the periodontal membrane

and gingiva Osteosclerosis of the alveolar bone, Marked hypercementosis.

The effect of vitamin D deficiency or imbalance on the periodontal tissues of young dogs results in :

osteoporosis of alveolar bone; osteoid that forms at a normal rate but remains uncalcified; failure of osteoid to resorb, which leads to excessive accumulation

reduction in the width of the periodontal ligament space

a normal rate of cementum formation, but defective calcification and some cementum resorption

and distortion of the growth pattern of alveolar bone.

Data from the NHANES III :

Low serum levels of vitamin D have been linked with a loss of periodontal attachment. (immunomodulatory effect-50 years of age.)

The association between serum conc. of 25-hydroxyvitamin-D and gingival inflammation were evaluated .

It was concluded that the anti-inflammatory effects of vitamin D might reduce the susceptibility to gingivitis

Vitamin E

VITAMIN E

Herbert Evans and Katherine Bishop in green leafy vegetables (1922)

“Antisterility vitamin.”

Fat soluble

Naturally occurring antioxidant.

Tocopherols

Biochemical functions:

Antioxidant property

Membrane antioxidant- membrane integrity.

prevents the oxidation of Vitamin A and carotenes.

Prevents peroxidation of PUFA. Aging.

nitric oxide production by vascular endothelium.

synthesis of heme- ALA synthase and dehydratase

cellular respiration through ETC

Synthesis of nucleic acids.

Protects liver –(carbon tetrachloride)

Inhibition of protein kinase C -platelet aggregation.

Storage of creatine in skeletal muscles.

Absorption of amino acids from the intestine.

in association with vitamins A, C and β carotene, to delay the onset of cataract.

Recent studies have shown that high intake of vitamin E (about 200 – 300 mg/day) protects against the development of heart diseases.

Protects RBC from hemolysis by oxidizing

agents.

Associated with reproductive functions and prevents sterility (anti-sterility vitamin).

RDA

10 mg (15 IU*)

8 mg (12 IU*)

*1 mg of alpha tocopherol = 1.5 IU

Serum level = 5-20 mcg/ml

Vitamin E

Vitamin E

Deficiency:

Neurological problems due to poor nerve

conduction.

Erythrocyte membrane fragility results as the erythrocytes are oxidized.

Degenerative changes in muscles

Megaloblastic anaemia

Depresses immunological responses to antigens, lymphocytic proliferative responses, delayed dermal hypersensitivity and general resistance.

Vitamin E and periodontal tissues:

Ability to interfere with the production of prostaglandins.

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.

Cerna et al showed that long term (12 weeks) administration of 300 mg of Vitamin E significantly reduced inflammation of the periodontal tissues

In contrast, a cross-sectional study showed that no significant difference existed in the serum level of vitamin E in patients with periodontal disease when compared to healthy controls (Slade et al. 1976).

Schafer et al – toothpaste containing Vit E and F maintained the bio-availabilty of zinc and triclosan and provided with anti plaque and anti-gingivitis properties

Vitamin K

VITAMIN K

In 1934, Dam discovered that a nutritional disease of chicks, characterized by severe bleeding, could be cured by alfalafa and fish meal.

On isolation of the active principle they named it Koagulations vitamin or Vitamin K.

Almquist and Stokstad

Quick and co-workers (1935) :coagulation defect in jaundiced individualsdecrease in the concentration of prothrombin in the blood.

Chemistry

Physiology: Carboxylation of certain glutamate residues in proteins

to form γ-carboxyglutamate residues.(Gla)

The Gla-residues play key roles in the regulation of three physiological processes:

1. Blood Coagulation

2. Bone metabolism

3. Vascular biology.

ETC and oxidative phosphorylation

Blood clotting : It brings about the post-translational modification of certain blood clotting factors. (Factor II,VII, IX, and X )

RDA

• No RDA

120 µg

80 µg

Serum level= 1-2 mcg/kg

Vitamin K

Vitamin K

Deficiency

Uncommon

It may occur in newborn infants and in patients on antibiotics which suppress the gut flora.

Prolonged clotting time

Increased risk of fractures or reduced bone density-production of osteocalcin affected

Antagonists to Vitamin K

Heparin and Coumarin derivatives

Warfarin

Salicylates

Vit K and Periodontal tissues:

The most common oral manifestation is gingival bleeding and post extraction hemorrhage.

Prothrombin level < 35% - bleeding on brushing.

< 20% - spontaneous bleeding occurs Diagnosis made on : Elevated prothrombin time or reduced clotting factors Rx: parental dose of 10 mg

Some studies indicated an association between vitamin K and osteoporosis; however, the relationship between vitamin K and bone health remains unclear (Hendler 1983)

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Vitamin B

VITAMIN B Eijkman (1897) polyneuritis in fowlscured by feeding

extracts of polished rice

Jansen And Donalto (1926 )

THIAMINE

Admiral Takaki (1880)

Jansen and Donath(1926)

Anti beri beri or anti neurotic vitamin.

Chemistry:

Vitamin B1

Vitamin B1

1.4mg/day

1mg/day

Biological functions:

carbohydrate metabolism as a coenzyme in the decarboxylation of :

pyruvate

α-ketoglutarate

Utilization of pentose in the HMP shunt;enzyme transketolase.

Transmission of nerve impulse , acetylcholine synthesis

Dry Beriberi :symmetrical ascending peripheral neuritis.

Initially: weakness, stiffness, and cramps in the legs, can walk only short distance.

numbness of the dorsum of the feet and ankles, vibration sense dec.

Hyperesthetic (stocking and glove distribution)

Anesthesia.

Terminal stages:patient-bedridden

Wet Beriberi

Heart: dilatation of arterioles, rapid blood flow, inc pulse rate and pressure, inc JVP RHF & edema.

The signs of CHF may be seen without peripheral neuritis.

lactate and pyruvate

pyruvate dehydrogenase

Wernicke-Korsakoff Syndrome

Chronic alcoholics.

The body needs of thiamine increases + Insufficient intake or impaired intestinal absorption

Korsakoff’s psychosis:confusion, loss of recent memory

Wernicke’s encephalopathy: nystagmus and extraocular palsy

Oral Manifestations

Hypersensitivity of the oral mucosa

Minute vesicles (simulating herpes) on the buccal mucosa, under the tongue, or on the palate

Erosion of the oral mucosa

RIBOFLAVIN Warburg and Christian (1932) identified a yellow enzyme

which contained riboflavin.

Physiological Functions:

FMN and FAD- coenzymes for a wide variety of respiratory flavoproteins.

Redox reactions energy production.

Carbohydrate, lipid, protein and purine metabolism

Glutathione reductase in erythrocytes-assess deficiency

Vitamin B2

Vitamin B2

1.7mg/day

1.3mg/day

Deficiency: (ariboflavinosis) Cheilosis, glossitis and seborrhic

dermatitis, superficial vascularizing keratitis

Mild to moderate cases : dorsum → magenta, patchy atrophy of the filiform papillae and engorged fungiform papilla (pebble-like elevations)

Severe deficiency : dorsum is flat, with a dry and fissured surface.

Angular cheilitis begins as an inflammation of the commissure of the lipserosion, ulceration and fissuring.

Candidiasis may develop in the commissures of debilitated personsperleche

Riboflavin deficient monkeys include severe lesions of the gingiva, periodontal tissues and oral mucosa, including noma.

NIACIN Also known as “Pellagra preventive factor of Goldberg.”

Coenzymes synthesized by tryptophan

Redox reaction

Vitamin B3

Vitamin B3

18mg/day

12-16mg/day

Deficiency

Pellagra- 3 D’s

Photosensitive dermatitis, like severe sunburn (butterfly-like pattern)

Physiological conditions (e.g. Hartnup disease and malignant carcinoid syndrome)

Drug therapies (e.g. isoniazid) can lead to niacin deficiency (Carpenter 1983)

Glossitis and stomatitis .

Tongue is “beefy red”, glossodynia and glossopyrosis. (Bald tongue of Sandwith)

Profuse salivation.

The most common finding is NUG usually in areas of

local irritation.

Necrosis of gingiva and leukopenia-terminal features

Dreizen et al(1977) stomatitis was highlighted by a necrotizing gingivitis and periodontitis and an ulcerative and atrophic glossitis.

These results showed a possible predisposition of the periodontium to aggressive forms of periodontal disease due to a deficiency of vitamin B3 intake.

Taguchi, S. Nippon Shishubyo

The effects of a vitamin B3-supplemented toothpaste

(1% nicotinate ethyl ester paste )

gingival blood circulation of plaque induced gingivitis were evaluated in a nonhuman primate model.

gingival inflammation

PANTOTHENIC ACID

Derived from a Greek word Pantos - everywhere.

RDA

Adults: 5-10 mg/day

Synthesis of CoA in fatty acid synthesis.

Deficiency Symptoms:

Rare

Dr. Gopalan:burning feet syndrome (pain and numbness in the toes, sleeplessness, fatigue)

Anemia, fatty liver, decreased steroid synthesis

Oral changes seen in animals but not in humans

PYRIDOXINE

The active form of Vit B6 is the coenzyme- pyridoxal phosphate.

Vitamin B6

Vitamin B6

RDA:Adult- 2-2.2 mg/day

Biochemical Functions:

PLP- coenzyme amino acid metabolism (transamination and decarboxylation)

Cofactor of glycogen phosphorylase

steroid hormone action where it removes the hormone-receptor complex from DNA binding

Deficiency:

Rare. Foods,intestinal flora

Depression, nervousness, convulsions, peripheral neuropathy.

Demyelination of neurons

associated with a poor

prognosis in women with

breast cancer.

skin lesions (e.g., acrodynia in the rat) and fissures or ulceration at the corners of the mouth and over the tongue

Patchy atrophy of the tongue, angular cheilitis and glossitits. Magenta discoloration of the tongue.

hypochromic microcytic anemia (the first step of heme biosynthesis is PLP dependent)

changes in leukocyte count and activity

impairment of immune responses

endocrine abnormalities

defects in the metabolism of tryptophan, methionine, and other amino acids

Drug Induced B6 Deficiency:

Isoniazid and penicillamine should be accompanied by pyridoxine supplementation to avoid B6 deficiency

BIOTIN Anti-egg white injury factor or vitamin H

It plays a role in gluconeogenesis and fatty acid synthesis.

RDA:

Adults- 100-300 µg/day.

Sources: liver, kidney, egg, milk, tomatoes, grains etc.


Large amounts of uncooked eggs .

High intake of avidin, +biotinunavailable. Major resection of the gut. Alopecia and a scaly erythematous dermatitis, especially

around the body orifices.

Histology : absence of sebaceous glands and atrophy of the hair follicles.

Oral Manifestations: Glossitis and atrophy of the lingual papillae

CYANOCOBALAMIN

Anti-pernicious anaemia vitamin.

Unique vitamin.(microorganisms)

RDA Adults- 3 µg/day

Pernicious anemia is the megaloblastic anemia specifically due to vitamin B12 deficiency

Vitamin B12

Vitamin B12

Extrinsic factor of Castle


1) 3 vitaminB12-dependent enzymes:

methionine synthetase, methylmalonyl CoA mutase leucine aminomutase.

2) metabolism of cyanidecyanocobalamin.

Estimation of Methylmalonic acid and serum B12 levelsassess Vit.B12 deficiency

Deficiency Symptoms: spinal cord degeneration and

peripheral neuropathy. (Seen in 2/3rd of the cases)

gait ataxia and loss of position & vibratory sense. cutaneous sensation and tendon reflexes

synthesis of TNF-α

epidermal growth factor in the spinal cord

Oral Manifestations:

Glossitis:50-60% .(Moeller’s glossitis or Hunter’s glossitis)

stomatitis and mucosal ulcerations.

Epithelial cell abnormalities.

More susceptible to epithelial dysplasia or malignant transformation

Treatment: Vit B12 (100-1000µg)-IM

FOLIC ACID

Lucy Wills in 1931 identified folate as the

nutrient needed to prevent anemia during pregnancy.

Derived from Latin word Folium-leaf

RDA Adults- 400 µg/day

Folic acidFolic acid


Tetrahydrofolate (THF), the coenzyme of folic acid is actively involved in this one-carbon metabolism.

Synthesis of purines, pyramidines, glycine, serine and choline


macrocytic anemia with megaloblastic erythropoiesis,

Glossitis – swelling of lateral borders and tip of the tongue.

depression, cognitive impairment and dementia

Periodontal Implications:

Animals: necrosis of the gingiva, periodontal ligament, and alveolar bone without inflammation (granulocytopenia). (Shaw JH, 1962)

humans :generalized stomatitis,ulcerated glossitis and cheilitis.

Ulcerative stomatitis is an early indication of the toxic effect of folic acid antagonists (e.g., methotrexate)-Rx of leukemia

B-Complex Supplements

Studies

Vogel(1976) evaluated the effects of vitamin Bc supplementation in humans. (2 mg ,twice daily,30 days)

resistance of the gingiva to local irritants

gingival inflammation

Pack A.R. (1980) The effect of systemic and topical Vit. Bc on gingival inflammation during pregnancy

Improvement in GI despite no significant changes in PI. Vitamin Bc can improve the resistance of the periodontium to bacterial plaque

Pack (1984) effects of a vitamin Bc mouthwash (5 mg/5 ml, twice daily for 4 weeks) on established gingivitis .

Influence on gingival health through local rather than systemic influence

Drew(1987) effects of both systemic and topical administration of vitamin Bc

Topical vitamin Bc significantly inhibited gingival overgrowth to a greater extent than either the systemic vitamin Bc or placebo groups

A similar finding was also reported by Backman(1989) who suggested that folate levels should be checked and supplementation with vitamin Bc considered in patients on long term anticonvulsive diphenylhydantoin therapy

On the contrary, Brown et al.(1991) found a single daily oral 3 mg capsule of vitamin Bc did not show efficacy as the sole therapeutic agent in the reduction of PIGO

Poppel et al(1979) examined the effect of vitamin Bc on the recurrence of PIGO following gingivectomy and observed less recurrence in these patients.

Vitamin C

VITAMIN C

In 1747, the Scottish surgeon James Lind discovered that citrus foods helped to prevent scurvy.

First vitamin to be artificially synthesized in 1935.

Seen among: elderly living alone,alcoholics,dietary faddists,and infants only on sterilized milk and foods.

Chemistry:

Ascorbic acid is a six carbon ketolactone

Structurally related to glucose and other hexoses.

Reversibly oxidizeddehydroascorbic acid. (possesses full vitamin C activity). Copper.

Man cannot synthesize it due to the deficiency of a L-gulonolactone oxidase.

Threshold substance-degree of saturation

Vitamin C

Vitamin C

Males:90 mg/day

Females:75 mg/day

Physiological functions:

1) Collagen formation:

proline lysine

hydroxyproline hydroxylysine

2) Intercellular ground substance, dentin, bone and CT

3) Iron and Haemoglobin metabolism

4) Tryptophan,tyrosine, folic acid metabolism

5) Synthesis of corticosteroid hormones by hydroxylation

6) Sparing effect on Vit A,Vit E, Vit B complex

7) Immunological function: Igs and phagocytic action of leucocytes

8) Antioxidant property: prevents damage to cellular structures and implicated in dev. of cancer,heart diseases and ageing

9) Carnitine biosynthesis

10) DopamineNorepinephrine

Dentin: Hojer and Crampton

Atrophy and disorganization of the odontoblasts

Irregularly laid down dentin with irregular tubules

Dentin formation ceases & predentin becomes hypercalcified

Producing heavy basophilic line between the dentin and the pulp

Odontoblasts become indistinguishable from pulpal cells

Gingiva: Classic sign: Gingivitis with enlarged,

hemorrhagic, bluish red gingiva

But gingivitis is not caused by

vitamin C deficiency.

(Woolfe et al 1980)

Gingivitisbacterial plaque.

Aggravate the gingival response to plaque and worsen the edema, enlargement, and bleeding.

Goldman: Hypertrophy of the gingiva covering the entire crowns

Subperiosteal hemorrhage lifted the gingiva from underlying bone

Focal areas of necrosis of free margin of the gingiva

Interdental and marginal gingiva-bright red with swollen,smooth,shiny surface.

Fully developed scurvy: gingiva becomes boggy,ulcerates and bleeds easily on slight stimulation like chewing (Stolman 1961)

Long standing case: Purple swellings and gingival bleeding (capillaries fragile and susceptible to rupture) (Thomas 1997) . petechiaechymoses

Gingival epithelium undergoes thinning-spongiosis

When severe atrophy occurs, blood exudes through the breaks in the epithelial layer.

Tritated inulin and endotoxin-oral mucosa

Tritated dextran-human crevicular epithelium

Periodontal Ligament:

Formed collagen-unaffected by deficiency.

Thus alteration in the fibres of the periodontal ligament—due to inability of the host to synthesize and repair rather than inability to maintain mature fibres.(Waerhaug 1958)

Doesnot reduce the no: of fibroblasts present in the CT(Gersh and Catchpole 1949; Chen and Postlewait 1961)

The periodontal fibers that are least affected :just below the junctional epithelium and above the alveolar crest

infrequent apical down growth of the epithelium.

Chronic cases: Hemorrhages into and swelling of the periodontal ligament

High conc. of alkaline phosphatase in vicinity of collagen (Jenkins, 1978).

Alveolar bone Alveolar bone resorption with increased tooth mobility

(Shaw 1978) although true loss of attachment and pocket formation do

not occur as a result of ascorbic acid deficiency alone

((Boyle 1937; Waerhaug 1958)

Shows atrophic changes; marrow space replaced with fibroblasts

Histologic changes:

Trummerfeld zone

Gerustmark

Vitamin C and PMNs

Conc. of Vit C in PMNs = 16 mg/ dl

in plasma = 0.5-1 mg/ dl Plasma level sensitive to diet change,stress, nicotine intake,

use of oral contraceptives.within 3 weeks it is depleted.

Invitro (Nugester, Ames,1948)-Impaired phagocytic activity Invivo- bactericidal activity of leucocytes impaired when

daily intake of ascorbate increased to 2g (Shilotri,Bhat,1977)

But inc. chemotactic and migratory action of leukocytes. Mungster and Ames (1948)

Long bones and hair If haemorrhage in the subperiosteal region of the long

bones-severe pain and tenderness occurs

Petechiae, ecchymoses and spontaneous bruising of the extremities.

Vascular congestion of the hair follicles leads to enlargement, keratosis and localized reddening of the skin.

StudiesAnimal Studies:

The effects of vitamin C deficiency in periodontal tissues were first studied by Glickman (1948)

Guinea pigs were placed on a vitamin C free diet and sacrificed after 35 days.

Histological examination revealed :

Deeper periodontal pockets in animals fed on vitamin C free diet.

Gingival edema and hemorrhage were also seen in the test group

Boyle (1937,1938) believed that the deficiency produced atrophic changes in the gingiva and underlying bone in guinea pigs .

There is bleeding, osteoporosis and resorption of alveolar bone, rupture of periodontal ligament fibers, widening of periodontal ligament space and increased tooth mobility. (Topping and Fraser 1939;Turseky and Gilckman 1954;Dunphy et al 1956; Waerhaug 1958)

Human studies Studies have shown that low levels of plasma Vit C are

associated with some degree of gingivitis and periodontitis. (Blockley and Baenziger 1942 ;

Stuhl1943; Kyhos et al 1944).

Crandon et al. (1940).He consumed a vitamin C-deficient diet for six months and after the fifth month a slightly boggy gingival appearance was noticed.

Cohen (1955) showed that, in absence of local periodontal treatment, a 500 mg oral tablet of ascorbic acid improved the gingival condition in teenagers after 90 days.

Over a similar trial period, daily doses of ascorbic acid (1-3 g) have reduced irregularities in the lamina dura of young adults.

It is due to the consolidation of collagen at the alveolar bone/cementum interface. (Cowan,1976)

Nishida et al. in the NHANES III, evaluated the effect of dietary intake of vitamin C and the presence of periodontal disease.

There was a weak, but statistically significant, relationship with periodontal disease in current and former smokers, as measured by clinical attachment.

Those taking the lowest doses of vitamin C, and who also smoked, had the greatest negative clinical effect on their periodontal tissues

J Periodontol 2000; 71: 1215-1223

Vogel et al.(1986) evaluated the role of mega doses of vitamin C on PMN chemotaxis and on the progression of experimental gingivitis.

Four months of daily vitamin C (500 mg, three times daily) supplementation

resulted in a significant increase in plasma ascorbate levels, but did not increase host resistance to experimental gingivitis

In a later analysis, Chapple et al.(2007) reviewed the data of 11,480 adult participants (> 20 years of age) in the NHANES III.

They demonstrated that increased serum concentrations of vitamin C, billirubin and total antioxidant levels were associated with reduced relative risk of periodontitis in both smokers and nonsmokers

Yasuko Shimada et al ascorbic acid significantly inhibited tyrosinase activity and melanin formation in B16 mouse melanoma cells.

concluded that ascorbic acid has potential for the treatment of gingival melanin pigmentation

J Periodontol 2009; 80: 317-323

Rx

Drug name Dosage Vitamins present

Tab Limcee 500 mg Vit C

Inj Vitcofol 10 ml Folic acid, B12,B3

Tab Nurokind -OD 150µg Vit B12

Cap Becosules –Z Vit B-complex, Vit C and Zinc

Tab A to Z Vit C, Vit B-complex, Vit A, Vit D3, Vit E,

Inj, Tab Zincovit Vit C, Vit B-complex, Vit A, Vit D3, Vit E,

CONCLUSION

Nutritional deficiencies and imbalances have a significant impact on the periodontal tissues.

Hence, a sound understanding of the various vitamins and their effects on the periodontium is crucial for every clinician.

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