5.NUTRITION in humans and metabolism.doc

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1. NUTRITIONNUTRITION

2. INTRODUCTIONINTRODUCTION
The majority of opinions and research findings on the effects
of nutrition on oral and periodontal tissues point to the following
1. THERE ARE NUTRITIONAL DEFICIENCIES THAT
PRODUCE CHANGES IN ORAL CAVITY .
These changes include alterations of the lips, oral mucosa
and bone as well as of the periodontal tissues. These changes are
considered to be periodontal or oral manifestations of nutritional
disease.
2. THERE ARE NO NUTRITIONAL DEFICIENCIES THAT
BY THEMSELVES CAN CAUSE GINGIVITIS OR
PERIODONTAL POCKETS.
There are however nutritional deficiencies that can affect
the condition of the periodontium and there by aggravates the
injurious effects of local irritants and excessive occlusal forces.
Theoretically it can be assumed that there may be a “border

3. zone” in which local irritants of insufficient in severity could
cause gingival and periodontal disorders if their effect upon the
periodontium were aggravated by nutritional deficiencies. On the
basis of this speculation, some clinicians enthusiastically adhere
to the theory that would assign a key role in periodontal disease
to nutritional deficiencies and imbalances.
PHYSICAL CHARACTER OF THE DIETPHYSICAL CHARACTER OF THE DIET
Soft diets, although nutritionally adequate, may lead to
plaque and calculus formation. Hard fibrous food provides
surface cleansing action and stimulation, which results in less
plaque and gingivitis, even if the diet, is nutritionally
inadequate. Human diets also have a high sucrose content, which
favors the production of thick plaque.
THE EFFECT OF NUTRITION UPON ORAL MICROORGANISMS.THE EFFECT OF NUTRITION UPON ORAL MICROORGANISMS.
Although dietary intake is generally thought of in terms of
sustaining the individual it also source of bacterial nutrients.
Composition of the diet may influence the relative distribution of
types of microorganism their metabolic activity, their pathogenic
potential which in turn affects the occurrence and severity of oral
disease.
Morhant & Fitzgerald Year 1976 have presented an
excellent analysis of this subject. First effect upon the oral
organisms, so that their products become increasingly injurious
to the oral tissues. Sources of nutrients for the microorganisms

4. can be exogenous and endogenous. Exogenous factors are sugar
contents of the diet it has been demonstrated that the amount and
type of carbohydrates and the frequency of intake can influence
bacterial growth. The mechanisms of attachment and subsequent
colonization on the tooth surface by certain microorganisms may
also made possible by component of the diet.
VITAMINSVITAMINS
Vitamins can be defined as naturally occurring organic
substances which are required in minute amount to maintain
normal health of the organism and which have to be supplied in
food as they cannot be synthesized by the organism. They supply
very little energy by themselves, but they play an important role
in several energy transformation reactions in the body. They
differ from hormones in not being produced within the
organisms.
Vitamins are broadly classified into two groups.
Fat soluble vitamins  Vit A, D, E, K
Water soluble vitamins  Vit B, C
VITAMIN – AVITAMIN – A
McCollum is credited with the discovery of this vitamin. He
gave the name “Fat soluble A” to the substance.
SOURCESSOURCES
Vitamin A occurs only in animal tissues but it’s precursors,
carotenoid pigments occur extensively in the vegetable kingdom.
Cod liver oil and other fish liver oils, animal liver, milk and milk

5. products and eggs all contain Vitamin A. The carotenoid
pigments are present in carrots, sweet potatoes, green vegetables
like spinach and amaranth.
REQUIREMENTSREQUIREMENTS
The WHO group in 1967 recommended a daily intake of
750 microgram (2500 IU) of vitamin A or 3000 micrograms
(5000 IU) of beta carotene for an adult. The nutrition expert
group India (1968) also recommended the same intake. Pregnant
and Lactating women have to be provided 50% more.
VITAMIN – A DEFICIENCYVITAMIN – A DEFICIENCY
EYEEYE
Deficiency causes a condition known as night blindness
(Nyctalopia) that is inability to adapt when suddenly proceeding
from bright light to dim light.
LIVERLIVER
There is impairment of oxidative phosphorylation in the
liver mitochondria.
EPITHELIUMEPITHELIUM
Skin becomes dry, scaly and rough changes described as
keratinization. Similar changes occur in lacrimal glands leading
to dryness of conjunctiva and cornea (XEROPTHALMIA].

6. White opaque spots (Bitot’s spots) appear in the
conjunctiva on either side of the cornea in each eye. Corneal
epithelium also becomes keratinized and opaque may become
softened and ulcerated which is known as Keratomalacia.
Keratinization occurring in the mucous membrane of the
respiratory tract leads to increased susceptibility to infection and
lowered resistance to disease. Vit - A is also called as
anti - infective vitamin on account of its ability to prevent
infection.
Keratinization of urinary tract may lead to formation of calculi.
BONES AND TEETHBONES AND TEETH
Lowered osteoblastic activity, bones become cancellous,
defective resorption of the bone, diminished intracranial
capacity, compression of the brain and also cranial and spinal
nerves and central nerves system defect are most common. Teeth
also become unhealthy due to thinning of enamel and chalky
deposits on the surface.
VITAMIN-A DEFICIENCY AND PERIODONTAL DISEASEVITAMIN-A DEFICIENCY AND PERIODONTAL DISEASE
Gingival hyperplasia with inflammatory infiltration and
degeneration, pocket formation and formation of subgingival
calculus is reported. Local irritation is necessary before
abnormal epithelial tendencies associated with vitamin
deficiencies are manifested in the gingival sulcus. In animals

7. when local factors are present, the pockets are deeper than in
nondeficient animals.
There is little information regarding the effects of Vit – A
deficiency upon the oral structures in humans. Low daily intake
of Vit - A has been associated with periodontal disease. Marshall
Day reported a possible correlation between the incidence of
periodontal disease and dermatological lesions characteristic of
vit –A deficiency and Russell reported that populations with a
high incidence of periodontal disease tend to be deficient in vit-A
HYPERVITAMINOSIS - AHYPERVITAMINOSIS - A
Gingival erosions and ulcerations, loss of keratinization and
desquamation of lips were reported in one human case. Melanin
like pigmentation of skin, scaling dermatosis, disturbed
menstruation, itching, and exophthalmos have been identified
with hypervitaminosis in humans.
TREATMENT FOR VIT – A DEFICIENCYTREATMENT FOR VIT – A DEFICIENCY
Single large dose of 60mg retinol as given orally. If there is
vomiting or diarrhea 55mg retinol IM injection is recommended.
VITAMIN – DVITAMIN – D
The credit for demonstrating the antirachitic activity of cod
liver oils other than vitamin – A goes to MCCOLLUM.
Subsequently the vitamin was isolated in crystalline form by
ANGUS, WINDUS and others.

8. FORMSFORMS
Two main forms of the vitamin were discovered I.
Calciferol or vitamin D2, obtained by irradiating (with U.V –
light) the plant sterol ergosterol.
II. Vit – D3 formed by irradiating animal ergosterol and Vit
– D1 that is not sufficiently active.
SOURCESSOURCES
Egg yolk, milk, butter and fish liver oils contain varying
amounts of the preformed vitamin, the highest amounts being
present in fish liver oils.
FUNCTIONSFUNCTIONS
Vit – D promotes absorption of calcium & phosphorus.
Vit – D promotes growth in general.
It facilitates the normal functioning of parathormone.
It promotes mineralization of bone.
It is some times used in the treatment of tetany.
It some how acidifies the PH of distal ileum, colon and
caecum.
It increases citrate content of bone, blood and other tissues.
It exerts an antirachitic effect.
DAILY REQUIERMENTSDAILY REQUIERMENTS
The national research council (USA 1964) recommended
intake of 400 IU/day for infants and growing children. In tropical
countries with plenty of sunlight, smaller amounts may be

9. sufficient. The nutritional expert group India recommended a
daily supply of 200 IU.
PREVALENCE AND CONSEQUENCES OF A DEFICIENCYPREVALENCE AND CONSEQUENCES OF A DEFICIENCY
Rickets in growing children and osteomalacia in adults are
produced by a deficiency of Vit – D. These conditions may
appear whenever there is some derangement in Vit – D
absorption or metabolism or alternatively, in calcium or
phosphorus homeostasis
RICKETSRICKETS
The name Rickets came from the word “Wrikken” meaning
to bend or twist.
The conformation of the gross skeletal changes depends on
the severity of the rachitic process, its duration and in particular
the age of the patient and the stresses to which individual bones
are subjected. During the nonambulatory stage of infancy the
head and chest sustain the greatest stresses. The occipital bones
may become flattened, and the parietal bones can be buckled
inward by pressure, elastic recoil snaps the bones back in to their
original positions which is known as CRANIOTABES. An excess
of osteoid produces FRONTAL BOSSING and a squared
appearance of the head. Deformation of the chest results from
over growth of cartilage and osteoid tissue at the costochondral
junction, producing the RACHITIC ROSARY. The weekend
metaphyseal areas of the ribs are subject to the pull of the

10. respiratory muscles and thus bend inward, creating anterior
protrusion of the sternum which is known as PIGEON – BREAST
DEFORMITY.
The inward pull at the margin of the diaphragm creates
HARRISON’S GROOVE, girdling the thoracic cavity at the
lower margin of the ribcage also takes place in this condition.
The pelvis may become deformed. When the ambulating child
develops rickets, deformities are likely to affect the spine, pelvis
and long boned (Tibia) causing most notably
LUMBARLORDOSIS and bowing of the legs.
OSTEOMALACIA in the adult is much subtler and is
characterized by loss of skeletal mass or too little bone, referred
to as OSTEOPENIA. It must there fore be differentiated from
other osteopenias such as osteoporosis, osteitisfibrosa, and
certain stages of Paget’s diseases of the bone. In these conditions
there is no defect in mineralization. LOOSER’S ZONES or MILK
MANS fractures are sometimes present. This may be appreciated
only radiographically. Skeletal deformities don’t appear in
osteomalacia clinically. Radiograph or other techniques can
visualize only apparent loss of bone density and cortical
thickness. Not surprisingly, with marked osteomalacia the too
little bone is subject to fractures, most often the vertebrae, hips,
wrist, ribs and kyphoscoliotic deformity of the vertebral column.

11. HYPERVITAMINOSIS - DHYPERVITAMINOSIS - D
Nausea, vomiting, diarrhea, epigastricfullness, polyuria,
polydipsia, albuminuria, impaired renal function, hypercalcemia,
and hyperphosphatemia characteristics of hypervitaminosis – D.
In humans it may prove to be fatal.
The periodontal findings in experimental Hypervitaminosis
– D include osteosclerosis characterized by marked defects in the
endosteal and periosteal bone formation. Osteoporosis and
resorption of alveolar bone, dystrophic calcification in the
periodontal ligaments and gingiva, severe calculus formation,
deposition of a cementum like substance on the root surfaces
[hypercementosis and the ankylosis of many teeth] and extensive
periodontal disease.
ENAMAL HYPOPLASIAENAMAL HYPOPLASIA
A small number of patients with evidence of rickets develop
enamel hypoplasia. Whether these teeth are more susceptible
tooth dental caries is uncertain. The enamel does not appear to be
weakened, but the rougher surface may facilitate adherence of
dental plaque and food residue. In severe cases of Vit-D
deficiency, a calcitraumatic line may develop. [SWEENEY AND
SHAW 1988].
VITAMIN - EVITAMIN - E
In 1922 BISHOP and EVANS termed the food factor as
FACTOR’X’ which was subsequently renamed as Vit – E.

12. SOURCESSOURCES
Vegetable oils particularly wheat germ oil, corn oil,
cottonseed oil and sunflower oil are good sources.
It is also present in fair amounts in egg yolk and green leafy
vegetables like spinach and lettuce.

13. REQUIREMENTSREQUIREMENTS
Average human diets contain about 30 IU [20mg] of D –
alfatocopherol and since no deficiency is ever reported, this is
considered as adequate amount. Hypervitaminosis symptoms are
not reported.
PHYSIOLOGIC ROLESPHYSIOLOGIC ROLES
Vit – E is the most important fat-soluble ANTIOXIDANT.
Vit – E protects the integrity of normal cell membranes and
effectively prevents hemolysis of red blood cells, and also
protects Vit – A and unsaturated fatty acids from oxidation. Vit –
E supplementation has been shown to improve immune response
in healthy elderly patients; this effect may be mediated by
increase in prostaglandin that enhances growth of white blood
cells. These functions will promote resistance of the
periodontium to inflammation. Serum tocopherol [Vit – E] levels
may be associated with cancer risk.
HYPER AND HYPO STATESHYPER AND HYPO STATES
Oral Vit – E supplementation results in few side effects
even at doses as high as 3200mg/day [BENDICH and MACHLIN
1988].
Favorable response to Vit – E therapy has been reported in
patients with severe periodontal disease with a minimum of local
factors.

14. VITAMIN - KVITAMIN - K
DAM (1935) named the factor present in natural diets and
which protected against the hemorrhagic disease as Vit – K
(koagulation Vitamin). DAM and KARRER in 1939 isolated the
vitamin as crystalline form.
K1 (phylloquinone) which occurs in green plants, and K2
(menaquinone) which is formed by Escherichia coli bacteria in
the large intestine and is found in animal tissues and the fat
soluble synthetic compound menadione (K3).
PHYSIOLOGICAL ROLEPHYSIOLOGICAL ROLE
Vit – K functions principally as a catalyst for synthesis of
blood clotting factors primarily in maintaining prothrombin
levels.
REQUIREMENTSREQUIREMENTS
The RDA for adult men is 80mcg and for women 65mcg
with the exception of females between 25 – 30 years of age.
(BOOTH et al 1996)
SOURCESSOURCES
Green leafy vegetables are high in Vit -K, but meat and
dairy products provide significant amounts. Bacterial flora in the
jejunum and ileum synthesize Vit – K.

15. HYPER AND HYPO STATESHYPER AND HYPO STATES
Primarily Vit – K deficiency is uncommon, but disease or
drug therapy may cause deficiencies. Any condition of the biliary
tract affecting the bile prevents Vit – K absorption. Vit – K
deficiency is common in celiac disease and Sprue (which affect
absorption in the small intestine), and other diarrheal diseases
(Ulcerative colitis) as a result of malabsorption.
In Vi – K deficiency blood-clotting time is delayed
increasing the risk of bleeding. Newborn infants may develop
hemorrhagic disease secondary to Vit – K deficiency because the
gut is sterile during the first few days after birth. Newborn
infants are usually given a single dose of Vit - K intramuscularly
immediately after birth to prevent hemorrhage.
TREATMENTTREATMENT
100mg IM for 3 – 5 days.
VITAMIN – CVITAMIN – C
Scurvy was known for centuries. Lind gave accurate
description of the disease as early as 1757. Gyorgi in 1928
isolated a substance from adrenal gland called hexuronic acid,
which was later identified as Vit – C by Waugh and king (1932).
SOURCESSOURCES
Fresh green vegetables and salad vegetables like cabbage,
lettuce, spinach, amaranth and cucumber contain the vitamin.

16. The citrus fruits lemons and oranges and also berries and
melons are particularly rich in the vitamin. Tomatoes and
potatoes also contain good amounts. Gooseberry is one of the
richest sources of this vitamin.
REQUINRMENTSREQUINRMENTS
30mg for infants and 70mg for adults are recommended by
NRC (National Research Council). More is required during
pregnancy and lactation. The nutritional expert group (ICMR)
has recommended 50mg/day as adequate for Indians.
DEFICIENCYDEFICIENCY
Severe deficiency in humans results in scurvy
GENERAL SYMPTOMSGENERAL SYMPTOMS
Scurvy is uncommon in countries that have adequate food
supplies.
It is seen in infants in their first year of life because
formulas are not fortified with vitamins and in very old
especially those living alone and on restricting diets. Alcoholism
also predisposes for scurvy.
CLINICAL MANIFESTATIONSCLINICAL MANIFESTATIONS
Hemorrhagic lesions into the muscles of the extremities, the
joints, sometimes nail beds, petechial hemorrhage often seen
around hair follicles.

17. Increased susceptibility to infections, impaired wound
healing, bleeding and swollen gingiva loosened teeth, defective
formation and maintenance of collagen, retardation or cessation
of osteoid formation, impaired osteoblastic activity and increased
capillary permeability are most common. Susceptibility to
traumatic hemorrhages, hyporeactivity of the contractile
elements of the peripheral blood vessels is also seen.
POSSIBLE ETIOLOGICAL RELATIONSHIPS BETWEENPOSSIBLE ETIOLOGICAL RELATIONSHIPS BETWEEN
ASCORBIC ACID AND PERIODONTAL DISEASEASCORBIC ACID AND PERIODONTAL DISEASE
Low levels of ascorbic acid influences the metabolism of
collagen with in periodontium, there by affecting the ability
of the tissues to regenerate and repair it self.
Ascorbic acid deficiency interferes with bone formation,
leading to loss of periodontal bone (failure of osteoblast to
form osteoid).
Ascorbic acid deficiency increases the permeability of the
oral mucosa to tritiated endotoxin and tritiated inulin and of
normal human crevicular epithelium to tritiated dextran.
Increase in levels of ascorbic acid enhances both the
chemotactic and migratory action of leukocytes with out
influencing their phagocytotic activity.
An optimal level of ascorbic acid is apparently required to
maintain the integrity of the periodontal vasculature, as
well as the vascular response to bacterial irritation and
around healing

18. Depletion of Vit – C may interfere with the ecological
equilibrium of bacteria in plaque and thus increase its
pathogenicity.
GINGIVITISGINGIVITIS
Vit – C deficiency is an etiologic factor in gingivitis, which
is common at all ages.
Enlarged, hemorrhagic, bluish red gingiva is described.
Gingivitis in Vit – C deficiency patient is caused by
bacterial plaque.
Vit – C deficiency may aggravate the gingival response to
plaque and worsen the edema, enlargement and bleeding.
Correcting the deficiency may decrease the severity of the
disorder. Gingivitis will remain as long as bacterial plaque
factors are present.
PERIODONTITISPERIODONTITIS
Edema, hemorrhage in the periodontal ligament
Osteoporosis of alveolar bone,
Tooth mobility and degeneration,
Hemorrhage edema and degeneration of collagen fibers,
Retards gingival healing,
Periodontal fibers present below the junctional epithelium
and above the alveolar crest are least affected. (Explains
the infrequent apical down growth of the epithelium).

19. Vit – C deficiency does not cause periodontal pockets.
Local bacterial factors are required for pocket formation to
occur.
Vit – C deficiency accentuates destruction of the
periodontal ligament and alveolar bone. This is due to
inability to marshal a defensive delimiting connective
tissue barrier reaction to the inflammation and partly from
destructive tendencies of fibroblast formation and
differentiation to osteoblasts, as well as impaired formation
of collagen and mucopolysaccharide ground substance.
(A case reported by Charbeneau and Hurt showed worsening
of a preexisting moderate periodontitis with development of
scurvy)
Vit – C deficiency has its greatest impact on periodontal
disease when preexisting disease and other co destructive
factors are present.
TREATMENTTREATMENT
100mg Vit – C TID
B - COMPLEX GROUP OF VITAMINSB - COMPLEX GROUP OF VITAMINS
It is the anti beriberi factor present in rice polishing, yeast
and liver. It was originally called the water soluble Vit – B
to distinguish it from fat-soluble - A known of the time of
1920s.

20. In course of time several water-soluble factors acting as
vitamins were found to be the same sources like rice
polishing, yeast and liver and these were named B1, B2 etc.
Subsequently their normal structure was identified and they
were assigned more rational names based on their
chemistry.
Some of them are synthesized in the tissues of the higher
animals, and so do not strictly satisfy the definition of
vitamin.
SOURCESSOURCES
Generally they are rich in germinating seeds, rice polishing,
wheat germ, pulses, beans and lentils, yeast, liver and meat.
THIAMINETHIAMINE
Synonyms: - Vit – B1: anti beriberi substance; antineuritic
vitamin; aneurine
REQUIREMENTSREQUIREMENTS
They depend mainly upon, caloric intake and particularly
carbohydrate intake of the individual. For a adult taking 3000
calories/day. 1.5mg of thiamin is required.

21. DEFICIENCYDEFICIENCY
Called Beri – Beri
Characterized by
Paralysis
Cardiovascular symptoms
Edema
Loss of appetite.
ORAL DISTURBANCESORAL DISTURBANCES
Hypersensitivity to oral mucosa, minute vesicles
(simulating herpes) on the buccal mucosa, under the tongue
or in the palate and erosion of the oral mucosa.
TREATMENTTREATMENT
50mg thiamin for the first 3 days and 10mg 3 times a day
should be continued there after by mouth until convalescence is
established.
RIBOFLAVINRIBOFLAVIN – Vit – B2, Lactoflavin
The Vitamin was isolated by several people by different
names and named according to source as Lactoflavin (from milk),
ovoflavin (from egg yolk) and hepatoflavin (from liver). Warburg
pigments (Warburg’s yellow enzyme) from bottom yeast.
Subsequently the pure vitamin was isolated and synthesized.

22. SOURCESSOURCES
Milk, liver, kidney, heart, egg yolk and germinating seed.
Riboflavin is destroyed on exposure to light and is reduced to
colorless products.
REQUIERMENTSREQUIERMENTS
1.5 to 2.0 mg/day NEG, India, has recommended an intake
of 0.55mg/1000 calories, some as that recommended by WHO
group.
DEFICIENCYDEFICIENCY
Glossitis
Angular chelitis.
Seborrheic dermatitis.
Superficial vascularized keratosis.
Glossitis which is characterized by magenta discoloration &
atrophy of papillae. In mild to moderate cases the dorsum
exhibits a patchy atrophy of the lingual papillae and engorged
fungi form papillae, which project as pebble like elevations. In
severe deficiency entire dorsum is flat.
Angular chelitis begins as an inflammation of the
commissures of the lips, followed by erosion, ulceration and
fissuring.
(Riboflavin only is not cause for angular chelitis, loss of vertical
dimension together with drooling of saliva into the angles of the

23. lips may also play a important role. Candidiasis may develop in
the commissures of the debilitated persons.
Vascularization of conjunctiva and cornea are also observed in
its deficiency.
TREATMENTTREATMENT
5 mg 3 times a day.
NIACINNIACIN
Synonyms: P-P factor, pellagra preventing factor of Gold Berger,
Nicotinic acid.
Gold burger (1912) identified pellagra as a disease caused by
deficiency of dietary factor.
Elevehjem in 1937 isolated nicotinic acid and its amide from
liver extract and showed its efficiency in curing these conditions.
REQUIREMENTSREQUIREMENTS
National Research Council, U.S.A recommended
6.6mg/1000 calories (FAO/WHO group). Nutrition Expert Group
for Indian conditions also confirmed this. For a 3000 calories
diet, this works out 20mg/day.
DEFICIENCYDEFICIENCY
 General symptoms like
Dermatitis, Diarrhea, Pellagra, Dementia

24. ORAL SYMPTOMSORAL SYMPTOMS
Glossitis
Gingivitis
Generalized stomatitis.
Glossitis, stomatitis may be the earliest clinical signs. Gingiva
may be involved with or with out tongue changes.
The most common finding is necrotizing ulcerative gingivitis,
usually in areas of local irritation.
TREATMENT
100mg every 6 hours, smaller dose are likely to be
effective. Well absorbed parentally.
FOLIC ACIDFOLIC ACID
SynonymsSynonyms
Liver – L – Case factor; Vit – M; streptococcus Lactis
R(SLR) factor) vitamin - Bc , pteroylglutamic acid, norite eluate
factor, vitamin-B10; VitaminB11 – folacin)
Investigations at university of Wisconsin revealed in 1941
the common nature of a factor that is required for growth of
certain microorganisms and for the chick. This factor was
prepared in a concentrated form from spinach and from liver and
yeast by different group of workers. It was obtained in a pure
crystalline form and was also synthesized by the investigators in
the Lederle laboratories in 1946. Dr. Yellopragada Subba Rao, an
Americanized scientist from Andhra, had the distinction of being
associated closely with this work.

25. SOURCESSOURCES
Green leafy vegetables are good sources besides usual
sources of B – Complex.
REQUIREMENTSREQUIREMENTS
300 to 500 micrograms are adequate to maintain normal
health. The nutrition expert group (ICMR) recommends
100micrograms/day for an adult.
DEFICIENCYDEFICIENCY
Results in macrocytic anemia with megaloblastic
erythropoiesis.
 Oral changes like generalized stomatitis, Ulcerated
glossitis and Chelitis.
(Ulcerative stomatitis is an early indication of the toxic effect of
folic acid antagonists used in the treatment of leukemia)
 Gastrointestinal lesions like diarrhea, intestinal
malabsorption and sprue are seen. Significant reduction of
gingival inflammation has been reported after systemic or local
use of folic acid with no change in plaque reduction.
Changes associated with pregnancy and oral contraceptives
may be partly related to suboptimal levels of folic acid in the
gingiva. Reduction in gingival inflammation was seen in
pregnant women by using topical foliate mouth rinses.

26. PYRIDOXINEPYRIDOXINE
(Synonyms : Vitamin - B6; Rat antidermatitis factor, rat
acrodynia factors; adermin; Vit – H)
Gyorgy demonstrated Vit – B6
REQUIREMENTSREQUIREMENTS : - 2mg a day for adults
DEFICIENCYDEFICIENCY
Anemia, cardiovascular disturbances, convulsions,
retardation of growth and patchy atrophy of dorsum of the tongue
was seen in animals.
ORAL CHANGES IN HUMANSORAL CHANGES IN HUMANS
Angular chelitis glossitis with swelling atrophy of the
papillae, magenta discoloration and discomfort.
GENERAL SYMPTOMSGENERAL SYMPTOMS
Epileptic convulsions in human infants are common.
Treatment with INH in T.B patients induces a B6 deficiency state
manifested by neuropathy and excretion and abnormal tryptophan
in urine.
This Vitamin used in treatment of nausea, and vomiting of
pregnancy, radiation sickness and muscular dystrophy.
TREATMENTTREATMENT
30 mg as supplementation dose per day, 100mg per day is
required in penicillamine therapy.

27. PROTEIN DEFICIENCYPROTEIN DEFICIENCY
Protein depletion results in hypoproteinemia with many
pathologic changes, including muscular atrophy, weakness,
weight loss, anemia, leukopenia, edema, impaired lactation,
decreased resistance to infection, ability to form certain
hormones and enzyme systems.
Protein deficiency accentuates the destruction and negative
effects of local irritants and occlusal trauma upon the periodontal
tissues, but the initiation of the gingival inflammation and its
severity depends upon the local irritants. Tryptophan deficiency
in rats results in osteoporosis of alveolar bone.
PROLONGED PROTEIN DEFECIENCYPROLONGED PROTEIN DEFECIENCY
Calorie malnutrition produces a spectrum of syndromes
from kwashiorkor at one end caused by a critical lack of protein
despite a sufficient caloric intake, to marasmus at the other end,
caused by an overall lack of calories or more bluntly starvation.
KWASHIORKORKWASHIORKOR
Characterized by apathy, peripheral edema, subcutaneous
fat deposition, moon face, enlarged fatty liver, and low serum
albumin. Flaky paint areas of depigmentation and
hyperpigmentation. Hair often develops a fine texture is loosely
rooted and has a pale reddish hue. Moderate to severe anemia.
Fatty liver and hepatic damage are most common.

28. MARASUMSMARASUMS
Can be characterized by wasting, stunted growth, total loss
of subcutaneous fat with atrophy of muscle, producing
broomstick arms and legs from which skin hangs pathetically
loose. The faces are pinched and wizened imparting a
prematurely aged appearance. Children are alerting hungry and
will eat ravenously if given food.
TREATMENTTREATMENT
Daily requirement of 1gm per Kg is increased to 2 – 3 gm
per Kg per day.
STARVATIONSTARVATION
Starvation is the ultimate challenge without any food
intake, there is total lack of nutrients, no physical stimulation
and fuel for energy.
In a study of controlled semistarvation in young adults
there were no changes in the oral cavity or skeletal system
despite a 24% loss of body weight. Reduction in plaque index
scores and a considerable increase in gingival index scores were
seen as the fasting period lengthened.

29. MINERAL DEFICIENCIES AND TOXICITIESMINERAL DEFICIENCIES AND TOXICITIES
FLOURIDEFLOURIDE
Fluoride reduces the severity of cortisone induced alveolar
bone resorption. Prevents adverse effects of Hypervitaminosis -
D and inhibits bone resorption in tissue culture. Fluoride in
drinking water used to prevent tooth decay.
Higher levels may also produce dental fluorosis,
spondylosis deforms which is characterized by progressive
osteosclerosis, ossification of tendon and ligament insertions and
spinal rigidity.
MAGNESIUMMAGNESIUM
Altered alveolar bone architecture.
Increased bone resorption
Fibrosis of the marrow.
Calculus formation.
Loosening of teeth.
IN TOXICATIONSIN TOXICATIONS
MOLYBDENUMMOLYBDENUM
Mandibular exostoses
Cemental spurs
Hyper cementosis
Disorganization of odentobalstic layer.

30. BERYLLIUM AND STRONIUMBERYLLIUM AND STRONIUM
Hyper production of bone and cementum and dentin matrix
that doesn’t calcified leading to rickets like lesion.
PHYSICAL EFFECTS OF FOOD ON PERIODONTALPHYSICAL EFFECTS OF FOOD ON PERIODONTAL
HEALTHHEALTH
There are atleast 50 nutrients that are provided by food,
most of which are required for a healthy periodontium. An
imbalance of one or more nutrients can be a factor in the
disruption of tissue integrity and immune response. For instance
normal growth and development of periodontal and oral mucosal
tissues depends on sufficient intake of Vit – A (salivary glands,
epithelial tissue) Vit – C (Collagen, Connective tissue), and Vit –
B Complex (epithelial, connective tissue). Calcification of the
alveolus and cementum require amino acids, calcium, and
phosphorus, Vit - D and magnesium. Maintenance of oral tissues,
as well as the integrity of hosts immune and repair response,
requires sufficient amounts of Vit – A, C, D, Protein,
Carbohydrates, Calcium, Iron, Zinc and Folic acid. Poor nutrition
can affect the entire body and thus an adverse effect on the
periodontium.
FOOD CONSISTENCYFOOD CONSISTENCY
Chewing firm, coarse and fibrous foods such as raw fruits
and vegetables will stimulate salivary flow. The increase in
saliva will enhance oral clearance of food, there by reduction in
food retention. Nizel and papas (1989) reported that mastication

31. of firm, fibrous foods can also stimulate and strengthen the
periodontal ligament and perhaps may also increase the density
of alveolar bone adjacent to the roots.
INVOLVEMENT OF NUTRITION IN PERIODONTALINVOLVEMENT OF NUTRITION IN PERIODONTAL
DISEASEDISEASE
Growth and development.
Amount and type of supragingival plaque.
Inflammation and immune response.
Integrity of periodontium.
Amount and type of saliva.
Host resistance
Repair and healing process.
ACUTE NECROTIZING ULCERATIVE GINGIVITISACUTE NECROTIZING ULCERATIVE GINGIVITIS
ANUG is generally an acute disease prevalent in young
adults. ANUG is characterized by red and shiny marginal labial
and lingual gingiva, which bleeds when probed, crated
interdental papillae, grayish sloughing of marginal gingiva, foul
breath and metallic taste.
Nutrient deficiencies such as proteins or Vit – C and / or B
complex deficiency are contributing factors to ANUG. This
commonly occurs in a young adults who has poor eating habits
such as high fat and low nutrient intake, and who relies primarily
on convenience or fast food meals.

32. NUTRITIONAL MANAGEMENT FOR ANUGNUTRITIONAL MANAGEMENT FOR ANUG
Full liquid diets for one to two days along with calculus
removal. As tolerated mechanical soft diets avoidance of spicy
and acidic foods such as citrus fruits and tomatoes which will
irritates oral mucosa. Additional protein intake adequate fluid
intake is essential.
FOODS TO AVOID IN PATIENTS WITH ORALFOODS TO AVOID IN PATIENTS WITH ORAL
ULCERATIONSULCERATIONS
Caffeine containing beverages (coffee, tea, coca cola),
alcohol, pepper mint, chocolate, black and red pepper, chilly
pepper, chilly powder, acidic food, citrus fruits.
BLAND DIETBLAND DIET
PURPOSEPURPOSE
To provide a temporary well balanced diet for those with
ulcerations.
DIET IN PERIODONTAL SURGERY DIET IN PERIODONTAL SURGERY
PREOPERATIVEPREOPERATIVE
Periodontal surgery and healthy patients with an adequate
in take don’t require special dietary modification. Surgery on a
chronic alcoholic would most likely require preoperative
replenishment of several nutrient deficiencies. Recommendation
of a liquid nutritional supplements or multivitamins may be
warranted. Surgery may be postponed for one to two weeks to
allow nutritional status to improve.

33. POST OPERATIVE CAREPOST OPERATIVE CARE
The requirements for calories, protein, vitamins, minerals
and water may be double the speed recovery time (Nizel and
papas 1989), liquid diet may be required for the first one to two
days. This can be progressed in to a mechanical soft diet after
one to two days for 3 to 5 days. A liquid supplements and is a
multivitamin may be recommended to ensure adequate nutrition
and to shorten duration of recovery.
JOURNALS REVIEWJOURNALS REVIEW
The affect of calcium and periodontal disease are likely
related to alveolar bone. Change which eventually results in
greater clinical attachment loss.
J.Periodontal 2000, 71, 1057 – 1066 (by Mieko Nishida et al)
Vit – C known as one of the powerful scavenger of super oxide
anions, smokers, may need more antioxidants to prevent the
harmful influences of tobacco products on periodontal tissue.
Low levels of dietary Vit – C were associated with more severe
periodontal disease in tobacco users but not in non-tobacco
users.
J.Periodontal 2000, 71,1215 – 1223 (by Mieko Nishida et al)
In vitro treatment with ascorbate containing Vit-C metabolites
enhanced the formation of mineralized nodules and collagenous
proteins.
J.Periodontal 1999,70,992 – 999 (by Dorothy J Rowe et al)

34. Osteoporosis is multifactorial and genetic factor plays an
important role. The polymorphism in Vit – D Receptor gene is
linked to decrease bone mass in postmenopausal women.
Genes and Osteoporosis 1997; 8; 232 – 286 [STRUAN et al]
Even in the continuing presence of plaque, gingival health can be
significantly enhanced by improved nutrient intake suggests
important implications for the maintenance care of marginally
deficient individual.
J.Periodontal; 1985;56;558 – 561 [By Barry Webb Jones, et al)

35. CONCLUSIONCONCLUSION
The involvement of nutrition in periodontal disease is not
as clear as it is for dental caries however the primary initiating
agent is bacterial plaque accumulation around the teeth and
gingiva. Nutritional deficiencies do not initiate periodontal
disease nor does megadoses of supplement prevent or cure
periodontal disease.
Nutrition may alter development, resistance and repair of
periodontium. Which ultimately affects the severity and extent of
the disease. Food choices influence the properties of plaque and
saliva. A change in salivary flow can influence the growth of
plaque.
A lack of nutrients does not cause the gingival
inflammation, but may be a predisposing factor, which may
disrupts the process of tissue repair. Adequate nutrients can
hasten the healing and repair process

36. CONTENTS
INTRODUCTION
VITAMINS
Sources
Physiological role
Role in periodontal diseases
Daily requirements
Deficiencies
Treatment
PROTEINS
MINERALS
NUTRITION IN PERIODONTAL DISEASES
NUTRITION IN DEVELOPMENT OF PERIODONTAL TISSUES
ANUG
ORAL ULCERATIONS
NUTRITION IN PRE AND POSTOPERATIVE CARE
CONCLUSION