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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 differentiationinc 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 matrixenamel
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
hydrolasesdestructive 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 individualsdecrease 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)
THANK YOU!!!!
Vitamin B
VITAMIN B
 Eijkman (1897) polyneuritis in fowlscured 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 lipserosion, ulceration and fissuring.
 Candidiasis may develop in the commissures of
debilitated personsperleche
 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 B3intake.
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 B6deficiency
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.
Deficiency Symptoms:
 Large amounts of uncooked eggs .
High intake of avidin, +biotinunavailable.
 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
Biochemical Functions:
1) 3 vitaminB12-dependent enzymes:
 methionine synthetase,
 methylmalonyl CoA mutase
 leucine aminomutase.
2) metabolism of cyanidecyanocobalamin.
Estimation of Methylmalonic acid and serum B12
levelsassess 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
acid
Folic
acid
Biochemical Functions:
 Tetrahydrofolate (THF), the coenzyme of folic acid is
actively involved in this one-carbon metabolism.
 Synthesis of purines, pyramidines, glycine, serine and
choline
Deficiency Symptoms:
 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 oxidizeddehydroascorbic 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) DopamineNorepinephrine
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)
 Gingivitisbacterial 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) . petechiaechymoses
 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.
Studies
Animal 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 B16mouse
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.
REFERENCES
 Essentials of Biochemistry- Satyanarayanan. 2nd
edition
 Biochemistry and Oral Biology – A.S Cole, J.E. Eastole. 2nd
edition
 Drugs, Diseases and Periodontium – Robin Seymour
 Clinical Periodontology, Carranza. 10th
edition
 Shafer’s Textbook of Oral pathology. 5th
edition
 Schafer et al. In vivo evaluation of an oral health toothpaste with 0.1%
Vitamin E acetate and 0.5% sunflower (with vitamin F). International
Dental Journal (2007); 87: 119-123.
 Essentials of medical pharmacology, KD Tripathi. 5th
edition
 Drug update, July-Oct 2008 Vol 5, Issue IV
 A. C. de Menzes et al. Clinical manifestations of Hypervitaminosis A in
human gingiva. J Periodontol 1984:55; 474-476.
 Iain L.C. Chapple and John B. Matthews. The role of reactive oxygen
and antioxidant species in periodontal tissue destruction. Perio 2000 Vol
43; 2007, 160-232.
 Robert E. Schifferle. Periodontal disease and nutrition: separating the
evidence from current fads. Periodontology 2000, Vol. 50, 2009, 78–
89.
 Iain L.C. Chapple. Potential mechanisms underpinning the
nutritional modulation of periodontal inflammation. JADA 2009, Vol
140; 178-184.
 Robert K. Murray, Daryl K. Granner, Peter A. Mayes, Victor W.
Rodwell. Harper’s Illustrated Biochemistry. 26th
edition.
 Yasuko Shimada et al. Effects of ascorbic acid on gingival melanin
pigmentation in vitro and in vivo. J Periodontol 2009; 80: 317-323.
 Vogel R. I. et al. The effects of megadoses of ascorbic acid on PMN
chemotaxis and experimental gingivitis. J Periodontal 1986, 57; 472-
479.
 Poppell T.D. et al. Effect of folic acid on recurrence of phenytoin
induced gingival overgrowth following gingivectomy. J Clin
Periodontol 1979; 18,134-139.
 Pack A.R. Folate mouthwash: effect on established gingivitis in
periodontal patients. J Clin Periodontol 1984; 6, 619-628.
 Dreizen S et al. Studies on the biology of the periodontium of
marmosets. XIII. Histpathology of niacin deficiency stomatitis in the
marmoset. J Periodontol 1977; 8, 452-455.
 vitamins

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vitamins

  • 1.
  • 2. CONTENTS  Introduction  Terminologies  Classification  Vitamin A  Vitamin D  Vitamin E  Vitamin K  Vitamin B  Vitamin C  Conclusion  References
  • 3. 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.
  • 5. • Vitamins = 'vital' and 'amine'. Cashmir Funk 1911- ‘Vitamine’  Other names: accessory food factors, food hormones  Vitamers
  • 7.
  • 9. VITAMIN A  2 groups: McCollum,Davis;Osborne and Mendel.(1913)  Fat soluble vitamin- present only in foods of animal origin.  Pigmented carotenoids - plants
  • 10. 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
  • 11. Biochemical functions:  Normal function of the retina  Growth and differentiation of epithelial tissues  Bone growth  Gene transcription  Immune function  Embryonic development and reproduction
  • 12.  Haematopoiesis  Skin and cellular health:Isotretinoin  Antioxidant activity
  • 13. RDA: 5000 IU (1000 retinol equivalents*) 4000 IU (800 retinol equivalents*) * 1 IU = 0.3 µg of retinol Serum retinol = 30-65mg/dl
  • 15. 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
  • 16.  In developing tooth, odontogenic epithelium fail to undergo differentiationinc 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 matrixenamel hypoplasia  Atypical dentin cellular and vascular inclusions  Alveolar bone  retarded rate of formation.  Eruption rate retarded Dental Manifestations
  • 17. 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 hydrolasesdestructive action of hydrolases, particularly on the cell membranes
  • 18. 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)
  • 19.  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
  • 20.  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)
  • 21. 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).
  • 22.  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
  • 23.  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
  • 25.  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
  • 29. 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.
  • 30. 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
  • 31.  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
  • 32. Dental Manifestations Mellanby:  Developmental abnormalities of dentin and enamel  Delayed erption  Malaligned teeth  Human rachitic teeth: abnormally wide predentin zone and interglobular dentin
  • 33. 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.
  • 34. 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
  • 35.  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.
  • 36.  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.
  • 37.  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
  • 39. VITAMIN E  Herbert Evans and Katherine Bishop in green leafy vegetables (1922)  “Antisterility vitamin.”  Fat soluble  Naturally occurring antioxidant.  Tocopherols
  • 40. Biochemical functions:  Antioxidant property  Membrane antioxidant- membrane integrity.  prevents the oxidation of Vitamin A and carotenes.  Prevents peroxidation of PUFA. Aging.
  • 41.  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.
  • 42.  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.
  • 43.  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
  • 45. 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.
  • 46. 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
  • 47.  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
  • 49. 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 individualsdecrease in the concentration of prothrombin in the blood.
  • 51. 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
  • 52.  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
  • 54. 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
  • 55. Antagonists to Vitamin K  Heparin and Coumarin derivatives  Warfarin  Salicylates
  • 56. 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)
  • 58.
  • 60. VITAMIN B  Eijkman (1897) polyneuritis in fowlscured by feeding extracts of polished rice  Jansen And Donalto (1926 )
  • 61.
  • 62. THIAMINE Admiral Takaki (1880) Jansen and Donath(1926)  Anti beri beri or anti neurotic vitamin.  Chemistry:
  • 64. 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
  • 65. 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
  • 66. 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
  • 67. 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
  • 68. 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
  • 69. RIBOFLAVIN  Warburg and Christian (1932) identified a yellow enzyme which contained riboflavin.
  • 70. 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
  • 72. 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.
  • 73.  Angular cheilitis begins as an inflammation of the commissure of the lipserosion, ulceration and fissuring.  Candidiasis may develop in the commissures of debilitated personsperleche  Riboflavin deficient monkeys include severe lesions of the gingiva, periodontal tissues and oral mucosa, including noma.
  • 74. NIACIN  Also known as “Pellagra preventive factor of Goldberg.” Coenzymes synthesized by tryptophan Redox reaction
  • 76. 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)
  • 77.  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
  • 78.  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 B3intake.
  • 79. 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
  • 80. PANTOTHENIC ACID Derived from a Greek word Pantos - everywhere. RDA Adults: 5-10 mg/day Synthesis of CoA in fatty acid synthesis.
  • 81. 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
  • 82. PYRIDOXINE The active form of Vit B6 is the coenzyme- pyridoxal phosphate.
  • 84.   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
  • 85. Deficiency:  Rare. Foods,intestinal flora  Depression, nervousness, convulsions, peripheral neuropathy. Demyelination of neurons  associated with a poor prognosis in women with breast cancer.
  • 86.  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
  • 87.  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 B6deficiency
  • 88. 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.
  • 89. Deficiency Symptoms:  Large amounts of uncooked eggs . High intake of avidin, +biotinunavailable.  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
  • 90. 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
  • 92. Biochemical Functions: 1) 3 vitaminB12-dependent enzymes:  methionine synthetase,  methylmalonyl CoA mutase  leucine aminomutase. 2) metabolism of cyanidecyanocobalamin. Estimation of Methylmalonic acid and serum B12 levelsassess Vit.B12 deficiency
  • 93. 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
  • 94. 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
  • 95. 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
  • 97. Biochemical Functions:  Tetrahydrofolate (THF), the coenzyme of folic acid is actively involved in this one-carbon metabolism.  Synthesis of purines, pyramidines, glycine, serine and choline
  • 98. Deficiency Symptoms:  macrocytic anemia with megaloblastic erythropoiesis,  Glossitis – swelling of lateral borders and tip of the tongue.  depression, cognitive impairment and dementia
  • 99. 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
  • 101. 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
  • 102.  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
  • 103.  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
  • 104.  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.
  • 106. 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.
  • 107.  Chemistry:  Ascorbic acid is a six carbon ketolactone  Structurally related to glucose and other hexoses.  Reversibly oxidizeddehydroascorbic 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
  • 109. 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
  • 110. 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) DopamineNorepinephrine
  • 111. 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
  • 112. Gingiva:  Classic sign: Gingivitis with enlarged, hemorrhagic, bluish red gingiva  But gingivitis is not caused by vitamin C deficiency. (Woolfe et al 1980)  Gingivitisbacterial plaque.  Aggravate the gingival response to plaque and worsen the edema, enlargement, and bleeding.
  • 113.  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)
  • 114.  Long standing case: Purple swellings and gingival bleeding (capillaries fragile and susceptible to rupture) (Thomas 1997) . petechiaechymoses  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
  • 115.  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)
  • 116.  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).
  • 117.  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
  • 118. 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)
  • 119. 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.
  • 120. Studies Animal 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
  • 121.  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)
  • 122. 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.
  • 123.  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)
  • 124.  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
  • 125.  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
  • 126.  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
  • 127.  Yasuko Shimada et al ascorbic acid significantly inhibited tyrosinase activity and melanin formation in B16mouse melanoma cells.  concluded that ascorbic acid has potential for the treatment of gingival melanin pigmentation J Periodontol 2009; 80: 317-323
  • 128. 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,
  • 129. 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.
  • 130. REFERENCES  Essentials of Biochemistry- Satyanarayanan. 2nd edition  Biochemistry and Oral Biology – A.S Cole, J.E. Eastole. 2nd edition  Drugs, Diseases and Periodontium – Robin Seymour  Clinical Periodontology, Carranza. 10th edition  Shafer’s Textbook of Oral pathology. 5th edition  Schafer et al. In vivo evaluation of an oral health toothpaste with 0.1% Vitamin E acetate and 0.5% sunflower (with vitamin F). International Dental Journal (2007); 87: 119-123.  Essentials of medical pharmacology, KD Tripathi. 5th edition  Drug update, July-Oct 2008 Vol 5, Issue IV
  • 131.  A. C. de Menzes et al. Clinical manifestations of Hypervitaminosis A in human gingiva. J Periodontol 1984:55; 474-476.  Iain L.C. Chapple and John B. Matthews. The role of reactive oxygen and antioxidant species in periodontal tissue destruction. Perio 2000 Vol 43; 2007, 160-232.  Robert E. Schifferle. Periodontal disease and nutrition: separating the evidence from current fads. Periodontology 2000, Vol. 50, 2009, 78– 89.  Iain L.C. Chapple. Potential mechanisms underpinning the nutritional modulation of periodontal inflammation. JADA 2009, Vol 140; 178-184.  Robert K. Murray, Daryl K. Granner, Peter A. Mayes, Victor W. Rodwell. Harper’s Illustrated Biochemistry. 26th edition.
  • 132.  Yasuko Shimada et al. Effects of ascorbic acid on gingival melanin pigmentation in vitro and in vivo. J Periodontol 2009; 80: 317-323.  Vogel R. I. et al. The effects of megadoses of ascorbic acid on PMN chemotaxis and experimental gingivitis. J Periodontal 1986, 57; 472- 479.  Poppell T.D. et al. Effect of folic acid on recurrence of phenytoin induced gingival overgrowth following gingivectomy. J Clin Periodontol 1979; 18,134-139.  Pack A.R. Folate mouthwash: effect on established gingivitis in periodontal patients. J Clin Periodontol 1984; 6, 619-628.  Dreizen S et al. Studies on the biology of the periodontium of marmosets. XIII. Histpathology of niacin deficiency stomatitis in the marmoset. J Periodontol 1977; 8, 452-455.

Editor's Notes

  1. Vitamins not synthesized in the body however,vit K and biotin may be sythesized by the intestinal bacteria .Antibiotics may suppress these bacteria and hence vit supplements is advised. Micronutrients are substances required in very small amounts (mg or μg) and that mainly function as co-factors of enzymes ( &amp;lt; 0.005% body weight).eg vitamins and minerals.their deficiency and overdose can produce similar problems
  2. Casimir Funk, was a Polish biochemist. A son of Polish Jews[1] , he was generally credited with the first formulation of the concept of vitamins in 1912[2] , which he called vital amines or vitamines Vitamers:chemically similar structure and qualitatively similar vit.activity.
  3. 15 vitamins.all water soluble act as coenzymes….only vit k in fat soluble acts as coenzyme….energy releasing and hematopoeitic.they r soluble in fats and fat solvents-alcohol and acetone.stored in liver and adipose tissue
  4. The long chain hydrocarbon structure of vitamin A means that the vitamin is essentially non-polar. Hence it is fat soluble rather than water soluble.
  5. Conversion of b carotene inefficient-hence it produces only 1/6th vit A activity compared to retinol. Retinoids toxic in high doses. B cartotene not so. At the low partial oxygen pressures found in most tissues β- carotene acts as an antioxidant but this initial activity is followed by pro-oxidant behavior at higher oxygen tensions, associated with substantial detrimental effects upon the surrounding tissues35. Over 500 carotenoids found in nature Less than 10% with provitamin A activity -carotene highest activity Must be acted upon in the gut or by the liver to form retinol
  6. Retinol is oxidized to retinal, which combines with the protein opsin to form rhodopsin. Rhodopsin is the active agent which converts light signals to electrical impulses that the optic nerve transmits to the brain Vision Gene transcription Immune function Embryonic development and reproduction Bone metabolism Haematopoiesis Skin and cellular health:Isotretinoin Antioxidant activity
  7. Night blindness-earliest symptom of vit A def.individuals hav difficulty to see in dium light. Xerophthalmia-severe def of vit A. dryness of conjuctiva and cornea, keratinization of epithelial cells. white,triangular spots-bitot spots seen Vit A def blindness common in children of developing countries Epi cells fail to differentiate. Basal layer lose their specificity and tend to form str.sqamous epithelium with keratin production.occus in mucous membrane of trachea,conjunctiva,ureter,salivary gland
  8. Headache:due to raised intracranial pressure which resembles the symptoms of brain tumour. Pregnancy:is associated with the risk of congenital malformations in the developing fetus.
  9. Thus tissue can be easily invaded with bacteria and cause periodontal disease and microabscess formation
  10. (from diet and body-due to exposure to sunlight) Both chole and ergo are provitamins.ergo has an additional methyl group and a double bond It resembles sterol and functions like a hormone??????more on that….. Preg and lactation also 5 mcg
  11. During the course of cholesterol biosynthesis, 7-dehydrocholesterol is formed as an intermediate. On exposure to sunlight, 7-dehydrocholesterol is converted to cholecalciferol in the skin4. 1, 25-DHCC contains 3 hydroxy groups hence referred to as calcitriol4. Calcitriol (1, 25-DHCC) is the biologically active form of vitamin D. It regulates the plasma levels of calcium and phosphate. Calcitriol acts at three different levels (intestine, kidney and bone) to maintain plasma calcium (normal 9 – 11mg/dl).
  12. to keep normal calcium and phosphorus levels in the body which helps to maintain and build strong bones, teeth and nails By controlling the supply of calcium between the bones and the blood, it supports bone mineralization and bone remodelling by osteoblasts and osteoclasts. supports cell functions and other neuromuscular functions in the body dealing with skin problems such as psoriasis Being a powerful antioxidant and anti-carcinogen, it helps combating depression, prostate cancer, breast cancer, high blood pressure, cardiovascular diseases, phagocytosis activity and boosts anti-tumor activity. Vitamin D also helps treating conditions like diabetes and obesity, and prevents the onset of multiple sclerosis. Hence, we can say vitamin D helps maintaining a healthy immune system and is important for body&amp;apos;s overall growth and development
  13. There is an overproduction of alkaline phosphatase related to more cellular activity of the bone. It is believed to be due to a vain attempt to result in bone formation. Affects epiphyseal plate,shaft and metaphysis.
  14. Affects only long bone and diaphysis of long bones Seen in post menopausal women with low ca intake. It is endemic in certain countries like japan,china and india Malabsorption is also another eitiology
  15. Sites in subjects of the highest 25-hydroxyvitamin-D quintile were 20% less likely to bleed on gingival probing than sites in subjects of the lowest 25-hydroxyvitamin-D quintile.
  16. found that female rats required a then unrecognized dietary principle to sustain a normal pregnancy
  17. Antioxidant property due to: Its limited mobility within cell membranes. prevents enzymatic oxidation of various cell components by molecular oxygen and free radicals such as superoxide and hydrogen peroxide. Its lack of water solubility (many ROS are generated in the aqueous phase) Aging due to progressive accumulation of cellular damage resulting from free radicals.As an antioxidant, vit e may prevent free radical damage
  18. by enhancing the activity of enzyme δ - amino levulinic acid (ALA) synthase and ALA dehydratase.
  19. It is believed that vitamin E prevents the oxidation of low density lipoprotein (LDL). The oxidized LDL has been implicated to promote heart diseases4.
  20. maintains germinal epithelium of gonads for proper reproductive function Vitamin E supplemented diet is advised for pregnant and lactating women.
  21. These are mostly associated with a defect in fat absorption and transport4.
  22. Tooth paste containing vit E
  23. Independently.almquist..described the same hemorrhagic disease in chickens and the method for its prevention the relationship between vitamin K, adequate hepatic function, and the physiological mechanisms operating in the normal clotting of blood was established12.
  24. only natural vitamin K available Considerable synthesis of menaquinones occurs in gram-positive bacteria, and bacteria in the intestinal tract are responsible for the large amount of vitamin K contained in human and animal faeces Phylloquinone and menaquinone are relatively nontoxic Jaundice; brain damage Menadione toxic to skin and respiratory tract in high doses.causes hemolytic anaemia and hypobilirubinemia in infants when given parentarally in large doses.
  25. Vitamin K acts as a coenzyme for the carboxylation of glutamic acid residues present in a)proteins b)osteocalcin (Calcium binding protein) Catalysed by a carboxylase (microsomal). The formation of γ carboxyglutamate (Gla) is inhibited by dicoumarol. Warfarin is a synthetic analogue that can inhibit vitamin K action. Gla residues (-ve ) + calcium ions (+ve)to form a complex The prothrombin-Ca complex binds to the phospholipids (platelets). Inc. conversion Prothrombin  thrombin. Structurally related to ubiquinones…..which is a component of mitochondrial ETC
  26. The formation of γ carboxyglutamate (Gla) is inhibited by dicoumarol. Warfarin is a synthetic analogue that can inhibit vitamin K action. inhibiting vitamin K quinone reductase and epoxide reductase
  27. Normal prothrombin level-11-15 sec Defic
  28.   Deficiencies of vitamin B-complex can cause the absence of disturbed protein, carbohydrate, and fat metabolism. Deficiencies can also decrease resistance to infection secondary to antibody formation, and some WBC functions may be impaired (Yates et al. 998)37.
  29. 1880, when Admiral Takaki greatly reduced the incidence of beriberi in the Japanese Navy by adding fish, meat to the sailors’ diet of polished rice. . The active factor subsequently was named vitamin B1; in1926 it was isolated in crystalline form by Jansen and Donath The conversion of thiamine to its coenzyme form is carried out by the enzyme thiamine diphosphokinase, with adenosine triphosphate (ATP) as the pyrophosphate (PP) donor11.
  30. Cereals, pulses, oil seeds, nuts and yeast are good sources. Thiamine is mostly concentrated in the outer layer (bran) of cereals. Also present in animal foods like pork, liver, heart, kidney, milk etc. since thiamine is a water soluble vitamin, it is extracted into the water during cooking process. Such water should not be discarded4.
  31. Specific diagnostic test is based upon measurement of transketolase activity in erythrocytes (Brin, 1968).
  32. Beri beri : commonly in people eating polished rice as their staple food. The hyperesthesia extends in the form of a band around the limb, the so-called
  33. The arteriolar dilatation, and possibly also the edema, probably results from high circulating concentrations of
  34. although memory for past events may be unimpaired.
  35. called flavin mononucleotide (FMN), and flavin adenine dinucleotide (FAD). Riboflavin is converted to FMN and FAD by two enzyme-catalyzed reactions:
  36. the physiologically active forms of riboflavin, serve a vital role in metabolism as
  37. Nicotinamide adenine dinucleotide , Nicotinamide adenine dinucleotide phosphate.
  38. The coenzymes, bound to appropriate dehydrogenases, function as oxidants by accepting electrons and hydrogen from substrates and thus becoming reduced. The reduced pyridine nucleotides, in turn are
  39. , affecting all parts of the skin that are exposed to sunlight. Similar skin lesions may also occur in areas not exposed to sunlight, but subject to pressure, such as the knees, elbows, wrists, and ankles.
  40. cotton top marmosets were made vitamin B3 deficient by long term dietary deprivation. The results showed that the animals developed anorexia, weight loss, weakness etc and the stomatitis
  41. A
  42. It is widely distributed in foods, intestinal bacterial synthesis
  43. terminating the action of the hormones.
  44. These symptoms are related to the decreased synthesis of biogenic amines (serotonin, GABA, norepinephrine and epinephrine). Demyelination of neurons is also observed in B6 deficiency38.
  45. This drug also reacts with PLP to form inactive thiazolidine derivative. The drug pencillamine is used in the treatment of patients with rheumatoid arthritis, Wilson’s disease and cystinuria. This drug also reacts with PLP to form inactive thiazolidine derivative.
  46. The dermatitis is similar to that seen in zinc and essential fatty acid deficiency, and is commonly associated with Candida albicans infection The dermatitis is because of impaired metabolism of polyunsaturated fatty acids as a result of low activity of acetyl CoA carboxylase38.
  47. synthesized by only microorganisms and not by animals and plants. It was the last vitamin to be discovered. Vitamin B12 is present in the diet in a bound form to proteins. It is liberated by the enzymes (acid hydrolase) in the stomach38.
  48. Curd is a better source than milk due to synthesis of B12 by lactobacillus. Animals obtain it either by eating foods, derived from other animals or from the intestinal bacterial synthesis
  49. This prevents the binding of cyanide to cytochrome oxidase and permits (relatively slow) metabolism to yield thiocyanate
  50. because of the neurological damage that accompanies the megaloblastic anemia of vitamin B12 deficiency, the condition is generally known as
  51. gingival changes associated with pregnancy and oral contraceptives may be partly related to suboptimal levels of folic acid in the gingiva.
  52. On days 0 and 30 of a double blind study, two groups of 15 subjects each were evaluated using plaque index (PI), gingival index (GI), gingival crevicular fluid (GCF) and fasting plasma folic acid levels. One group received 2 mg of vitamin Bc twice daily for 30 days, while the control group received a placebo.
  53. 30 pregnant females in their 32nd week of pregnancy were randomly divided into 3 groups. One group received placebo mouthwash and placebo tablets; another group received placebo mouthwash and one 5 mg vitamin Bc tablet daily; and a third group received placebo tablets and rinsed with vitamin Bc mouthwash twice daily for 1 min.
  54. Treatment group had significantly less recurrence of gingival overgrowth, the mean difference amounted to only 6-7% at 3 and 6 months.
  55. Long sea voyages of exploration in the sixteenth to eighteenth centuries, which were undertaken without a supply of fresh fruits and vegetables, resulted in large number of crews dying from scurvy.
  56. Oxidation rapid in the presence of copper.hence vit C becomes inactive when prepared in copper vessels. Usually, animals can synthesize Vit C from gluycose ia uronic acid pathway.however man,guinea pigs,bats,primates cannot.
  57. High content of vitamin C is found in adrenal gland and gonads. Milk is a poor source of ascorbic acid4. Additional intakes (20-40% increase) are recommended for women during pregnancy and lactation. Smoking, chronic alcoholism, use of oral contraceptives and administration of aspirin lower serum levels of ascorbic acid (normal 0.5-1.5 mg/dl) 4.
  58. At the tissue level, a major function of ascorbic acid is related to the synthesis of collagen, proteoglycans and other organic constituents of the intercellular matrix in diverse tissues such as tooth, bone and capillary endothelium. Collagen is a major component of the periodontium, being one of the major proteins present in the gingival connective tissues and bone. For collagen maturation to occur, adequate vitamin C must be available within the body to permit the hydroxylation of lysine and proline.+ Lysyl hydroxylase and prolyl hydroxylase Hydroxyproline and hydroxylysin help in cross linking of the collagen and inc. the strength of the fibre. Inc iron absorption by intestine keeping it in the ferrous state.due to the reducing property of vitamin C.
  59. Adrenal gland possesses high levels of vit C esp in periods of stress.helps in the hydroxylation reactions in the synthesis of corticost hormones Sparing effect;Prevents their oxidation due to its strong antioxidant property
  60. Acute vitamin C deficiency does not cause or increase the incidence of gingival inflammation, but it does increase its severity
  61. Ulceration and secondary infection.
  62. Scurvy is associated with a defect in collagen synthesis that is apparent in the failure of wounds to heal, in defects in tooth formation, and in the rupture of capillaries, which leads to numerous petechia and their coalescence to form ecchymoses12.
  63. Hydroxyproline and hydroxylysine are essential for the collagen cross-linking and the strength of the fiber. Although there is fibroblast proliferation in the wound area, the fibroblasts appear immature and fail to produce collagen..form a fluid like material around themselves….a weak attempt to form collagen
  64. Failure of osteoblasts to form osteoid takes place—later in the disease Osteoporosis of alveolar bone in scourbutic monkeys take place due to inc osteoclastic resorption Histologic picture-fracturing of the calcified matrix material…region of complete degeneration. The area beneath this is free of hematopoeitc cells and made of ct cells..
  65. Any bacterial attack..first line of defense of the dentogingival unit will be impaired.
  66. Check If this is known as the cork screw apperance., add a pic for the 2nd point if possible.
  67. Vit c def cannot be an initiating factor but may enhance plaque induced lesion