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1. seminar
on
effect of various nutritional deficiencies on
human
growth and development

2. Content
roduction
mponent of nutrient
ssification
bohydrates
teins
amins (a) fat soluble vitamins
(b) water soluble vitamins
nerals

3. INTRODUCTION
l status of a society varies according to the socioeconomic conditions. In the weste
ritional imbalance is more often a problem accounting for increased frequency of
hile in developing countries of Africa , Asia and south America , chronic malnutriti
s problem in children.
ate diet should provide
, in the form of carbohydrate , fat, protein;
al and non essential amino acid and fatty acids to be used as a building blocks for
hesis of structural and functional proteins
ns and minerals which functions as coenzymes or hormones in vital metabolic pathw

4. Certain “CRITICAL PERIOD” exist during development of organ
characterized by HYPERPLASTIC AND HYPERTROPHIC
GROWTH
PHASES .Any dietary deficiency during these phases may cause
irreversible changes like growth retardation & orofacial alteration in
humans like:
1. Cleft lip and Palate
2. Reduced dental arch dimensions with inadequate spaces
3. Insufficient dental eruption
4. Short root and inter osseous rotation of per. Teeth
5. Shorter mandible in ant. And post. Direction
6. Reduction in ascending ramus
7. Dentoalveolar inclinations in the incisor region
8. Reduction in mesio – distal dimension of 3rd molar
ROLE OF VITAMINS IN GROWTH
AND
DEVELOPMENT

5. Component of nutrients
tial nutrients nonessential nutrient
teins 1. dietary fibres
s
bohydrates
amins
nerals
ter

6. CLASSIFICATIO
N
The nutritional deficiencies may be categories in two type
imary deficiency (b) secondary deficiency
o lake of essential nutrients 1. interference with ingestio
in diet. 2. interference with abs
3. interference with ut
4. increased excretion
5. increased nutritional

7. Primary deficiency secondary
deficiency
nutritional deficiency
depletion of nutrient
reserves
biochemical changes
functional changes
morphologic lesions and growth
retardation

8. Protein energy malnutrition
quate consumption of protein and energy as a result of primary dietary deficiencies
ioned deficiency may cause loss of body mass and adipose tissue ,resulting in protein
alnutrition. the primary deficiency is more frequent due to socioeconomic factors
the quantity and quality of dietary intake , particularly prevalent in the developing
of Africa Asia and south America .
iorkor : Which is related to protein deficiencies though calorie intake may be
sufficient.
mus : It is a starvation in infants occurring due to over all lack of calorie.

9. Contrasting features
Kwashiorkor
Marasmus: Protein deficiency with sufficient Starvation in infants w
calorie intake all lack of calories.
Occur in children between 6 month and In infants under 1 yea
3 years of age
Growth failure Growth failure
Wasting of muscle but preserved Wasting of all tissue
adipose tissue muscle and adipose
Oedema , localized or generalized Oedema absent
Enlarged fatty liver No hepatic enlarge
Serum protein low Serum protein low
Anemia present Anemia present
alternate band of light and dark Monkey like face, prot
bands. Abdomen ,thin lim

10. Disorder of vitamins
are organics substances which can not be synthesized with in the body and are esse
ance of normal structure and function of cell .Thus , these substance must be provide
uman diet .
eveloping countries, multiple deficiencies of vitamin and other nutrients are comm
alized malnutrition of dietary origin. In the developed country , individual vitam
ies are noted more often.

11. Fat soluble and water soluble vitamins
ble vitamins are vitamin A,D,E.K. They are absorbed from intestine in the prese
t and intact pancreatic function. Their deficiencies occur more readily due to
l factor ( secondary deficiency) . A state of hypervitaminosis may occur due to
vitamin A and D.
oluble vitamins are C and B complex group . These vitamins are absorb from sma
stine .being water soluble these vitamins are lost due to cooking or processing of f

12. Vitamin A
roup of related natural and synthetic chemicals that exert a hormone
ty or function.
nt dietary sources of vitamin A are
animal sources : liver , fish, eggs, milks, butter.
plant sources : yellow and leafy green vegetables eg
squash, spinach .
han 90% vitamin a is stored in liver. these reserve are adequate for 6
deprivation.
DFINED FUNCTIONS :
intaining normal vision in reduced light
fferentiation of specialized epithelial cells, mainly mucus secreting
nhancing immunity to infection.

13. Sign of deficiency
:
kening of corneal epithelium and eye become dry. Condition is called
pthalmia. Its leads to ulceraration of the cornea called keratomalacia ( softening o
ich may cause blindness.
ht blindness : ( nyctalopia) mostly seen in young adults. First sign of night vitamin
deficiencies
imal duct also shows hyperkeratosis . Corneal ulcer may occur which may get
fected and cause keratomalacia .
ots spots may appear which are focal triangular area of opacities due to
accumulation of keratinized epithelium..
us sign: skin develops papular lesions giving toad like appearance ( xeroderma )
sions : a. squamous metaplasia of respiratory epithelium.
b. Squamous metaplasia f pancreatic ductal epithelium .
c. Squamous metaplasia of urothilium.
d. Bone growth is retarded.

14. On jaws :
Excess of vitamin A during critical growth period markedly
inhibit the neural crest cell development and upset the
normal balance between bone formation and resorption –
CLEFT PALATE
Softening of cleft palate due to decrease in calcium
deposition
On Peridontium :
Leads to keratinizing metaplasia of epithelium .Increased
susceptibility
to infection .Disturbances in bone growth, shape and
texture.
On teeth :
Deficiency during matrix formation and matrix calcification
leads to ENAMEL HYPOPLASIA (atrophy of ameloblasts) &
hence increases caries susceptibility.

15. Hypervitamino
sis
arge dose of vitamin a can produce toxic manifestation in children. These may be a
nd chronic.
toxicity: single large dose of vitamin a. effects include neurological manifestation
ling brain tumour .eg headache, vomiting, stupor , papilloedema.
toxicity : a. neurological such as severe headache and distorted vision due to incr
intracranial pressure
b. Skeletal pains due to loss of cortical bone by increased osteoclasti
activity as well as due to exostosis .
c. Cutaneous involvement may be in the form of pruritus , fissuring,
sores, at the corner of the mouth and coarseness of hair.
d. Hepatomegaly with parenchymal damage and fibrosis .
e. hypercarotenaemia is yellowness of palm and skin due to excessive
of beta carotene containing food.

16. Vitamin
D
t soluble vitamin exit in 2 activated form
a. Vitamin D2 or calciferol
b. Vitamin D3 or cholecalciferol
2 main sources of vitamin D
(a) endogenous synthesis : 80 % body needs of vit
esis from 7 –dehydrocholestrol widely distributed in oily secretion of the skin.
(b) exogenous sources : such as sea fish , fish oil, egg

17. Main physiologic function
al absorption of calcium and phosphorus is stimulated by vitamin D.
: vitamin D is required for normal mineralization of epiphysis cartilage and
osteoid matrix . In hypocalcaemia vitamin D work synergistic with
parathyroid hormones and maintain the normal blood level of calcium and phosph
y : vitamin D stimulate reabsorption of calcium at distal renal tubular level.
regulation: it play an immune regulatory role due to presence of receptor for
lites

18. Lesions in vitamin D deficiencies
ed endogenous synthesis due to inadequate exposure to sunlight.
bsorption of lipids due to lack of bile salts such as intra hepetic biliary obstruction
gement of vitamin D metabolism as occur inkidney disorders.
deficiency of vitamin D from any of the above mechanism results in:
in growing children
malacia in adults
calcaemia tetany due to neuromuscular dysfunction.

19. Rickets
mary defect in rickets is : mineralization of bone ;
deranged endochondral and intramembranous bone g
ons occur from 6month to 2 years of age
changes
1. crainotabes : it is the earliest bony lesion occurring due to small roun
unossified area in the membranous bone of the skull ,disappearing wit
12 month of birth. The skull look like box or square .
2. Harrison sulcus : appear due to in drawing of soft ribs on inspiration.
3. rickety rosary :it is the deformity of chest due to cartilaginous over gr
at costocondral junction.
4. bow legs : occur in ambulatory children due to weak bone of lower leg
5. knock knees : it may occur due to enlarged ends of femur , tibia, and fi
6. lower epiphysis of radius may be enlarged.
7. lumbar lordosis is due to involvement of the spine and pelvis.

20. Retarded jaw, teeth and condoyle development
On jaws :
Maxillary dysplasia
Facial sutures difficult to close lead to open
bite
On teeth :
Hypoplastic changes during matrix
calcification
On Peridontium :
Osteoporosis of alveolar bone and cementaL
dysplasia
Vitamin D
deficiency

21. osteomalacia
Deficiencies in adult
ailure of mineralization of the osteoid matrix
may occur due to following (a) dietary deficiency
(b) poor endogenous synthesis of vit
eature : it is characterized by
(a) muscular weakness
(b) Vague bony pain
(c) fracture following trivial trauma
(d) green stick fracture
(e) psedofracture at weak places in bones

22. Hypervitaminosis D
mount of vit D causes increased intestinal absorption of calcium and phosphorus, lea
alcimia , hyper phosphatemia and increased bone resorption.
wing effects are seen :
increased urinary excretion of calcium and phosphate .
prediction of renal calculi.
osteoporosis
widespread metastatic calcification.

23. Vitamin E ( tocopherol)
y act as antioxidant activity . It prevent the oxidative degradation of cell membran
venges free radicals formed by redox reaction in the body .maintain the integrity of
mbrane.
n deficiency :
1) neurons with long axon develop degeneration in the posterior column of spi
2) peripheral nerve may also develop myelin degeneration in the axon ..
3) skeletal muscle may develop denervation.
4) retinal pigmentary degeneration .
5) reduced life span of RBC .
6) sterility in male and female.

24. Vitamin K
n two form :
vit k 1 or phylloquinine obtain from exogenous sources such as
green leafy vegetables .
vit k 2 or menadion : produced endogenously by normal intestinal f
nction of vit k is in hepatic microsomal carboxilation reaction for vitamin k depend
n vit k : (1) hemorrhagic diseases
(2) hypoprothrombina
f deficiencies
(a) hemorrhagic disease of new born
(b) biliary obstruction
(c) malabsorption syndrome .
(d) anticoagulant therapy.
(e) antibiotic therapy.

25. Vitamin C
c function of ascorbic acid.
(a) hydroxilation of proline to form hydroxiproline
(b) necessary for ground substance of other mesenc
such as osteoid , chondroid sulphate ,dentiin and cement substance of endothilium.
(c) hydroxilation of dopamine to norepinephrine.
(d) maintanance of folic acid level .
vitamin C deficiency :
(a) haemorrhagic diathesis .
(b) skeletal lesions : deranged formation of osteoid matrix
not deranged mineralisation.
(c) delayed wound healing .
(d) anaemia .
(e) lesions in teeth and gums .
( f) skin rashes .

26. Essential for dentin matrix formation
which take prior to enamel matrix formation.
Thereby deficiency of vit c
may lead to enamel hypoplasia
deficiency aggravates gingival response to plaque &
worsen edema,enlargement and bleeding .
On Peridontium :
Influence the metabolism of
collagen fibers thereby affect
Regeneration and Repair
It interfere with bone formation & remodelling
Its Study by McCanlies et al
On Teeth :

27. Vitamin B complex
al member of vitamin B complex .
1 . Thiamin ( vit b1)
2. riboflavin ( vit b2 )
3. niacin ( nicotinic acid )
4. pyridoxine ( vit b 6)
5. foliate ( folic acid )
6. cynocobolamin ( vit b 12)
7. biotin
8. pantothenic acid .
9 . choline

28. Thiamine ( vitamin B1)
logic function is in carbohydrate metabolism , act as coenzyme for carboxylic so a
ate pyruvic acid , synthesizes ATP and synthesis of fat from carbohydrate .
hiamine deficiency .
1.dry beri beri ( peripheral neuritis) : weakness , paraesthesia
sensory loss , polyneuritis , myelin degeneration and fragment of axons
2. wet beri beri ( cardiac manifestation ) : gen oedema , serous
heart is enlarge and
3. cerebral beri beri ( wernicke – korsakoffs syndrome)
a. Wernickes encephalopathy - degeneration of ganglia ce
demyelination and haemorrhage in the region of ventr
aqueduct.
b. korsakoffs psychosis : from brain haemorrhage .

29. Riboflavin ( vitamin B 2)
logy : it is called yallow respiratory enzyme or
hrome oxidase which is important in cellular respiration .
in riboflavin deficiency :
lesions : vascularisation of cornea , conjunctivitis ,
titial keratitis , and corneal ulcer
osis and angular stomatitis .
ongue : glositis red cyanosed and shiny tongue due to
y of mucosa of tongue .
hanges : scaly dermatitis

30. Niacin (nicotinic acid)
gy :
1. NAD ( nicotinamide adenine dinucleotide) required for dehydrogenation
in the metabolism of fat , carbohydrate , and protein.
2. NADP ( nicotinamide adenine dinucleotide phosphates ) . It is essential
dehydrogenation in the hexose monophosphate shunt of glucose metab
n niacin : Pellagra ( rough skin)
mainly seen in maize diet person .
dermatitis ; diarrhoea ; dementia

31. Pyridoxine ( vitamin B6)
ne occur in 3 closely related structure : 1. pyridoxine 2. pyridoxal 3. pyridoxamine
gic function are related to 1. fat metabolism
2 . Protein metabolism .
3. amino acid metabolism.
1. convulsion in infant .
2. dermatitis .
3. cheilosis .
4. glossitis ( bald tongue)
5. sideroblastic anemia .

32. Folate ( folic acid) / Cynocobolamin ( vit B 12)
ed for Rbc formation so deficiency lead to megaloblastic anemia .
lination of nerve take place leading to hemiplasia or paraplegia

33. Trace elements
Iron : microcytic hypo chromic anaemia
Copper : muscle weakness ,neurologic defect .
Iodine : goiter and hyperthyroidism .
Zinc : growth retardation , infertility .
Selenium : myopathy ,cardiomyopathy .

34. Guidelines for evaluation and assessment of
Nutritional status
R.D.A
Physical appearance
Clinical evaluation
Biochemical analysis
Anthropometrical data

35. Referenc
es
Concise medical physiology by Chaudhary
Text book of pathology by Harsh Mohan.
oral pathology by Shafer .
co journals.

36. Thank you
By :
Dr. Alok ojha
under guidance of : DR.