effect of various nutritional deficiencies on human growth and development
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Content
roduction mponent of nutrient ssification bohydrates
teins amins (a) fat soluble vitamins (b) water soluble vitamins nerals www.indiandentalacademy.com
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
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ROLE OF VITAMINS IN GROWTH AND DEVELOPMENT 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. 2. 3. 4. 5. 6. 7. 8.
Cleft lip and Palate Reduced dental arch dimensions with inadequate spaces Insufficient dental eruption Short root and inter osseous rotation of per. Teeth Shorter mandible in ant. And post. Direction Reduction in ascending ramus Dentoalveolar inclinations in the incisor region www.indiandentalacademy.com Reduction in mesio – distal dimension of 3rd molar
tial nutrients teins s bohydrates amins nerals ter
Component of nutrients
nonessential nutrient 1. dietary fibres
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CLASSIFICATIO N The nutritional deficiencies may be categories in two type
imary deficiency
(b) secondary
o lake of essential nutrients in diet.
1. interference with ingestio 2. interference with abs 3. interference with ut 4. increased excretion 5. increased nutritional
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deficiency
Primary deficiency deficiency
secondary
nutritional deficiency depletion of nutrient reserves biochemical changes functional changes morphologic lesions and growth retardation
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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 :
mus :
Which is related to protein deficiencies though calorie intake may be sufficient. It is a starvation in infants occurring due to over all lack of calorie.
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Contrasting features Kwashiorkor : Protein deficiency with sufficient Marasmus calorie intake
Starvation in infants w all lack of calories.
Occur in children between 6 month and 3 years of age Growth failure Wasting of muscle but preserved adipose tissue Oedema , localized or generalized Enlarged fatty liver Serum protein low Anemia present alternate band of light and dark bands.
In infants under 1 yea
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Growth failure Wasting of all tissue muscle and adipose Oedema absent No hepatic enlarge Serum protein low Anemia present Monkey like face, prot Abdomen ,thin lim
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.
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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
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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. www.indiandentalacademy.com
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. www.indiandentalacademy.com
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 On teeth : susceptibility
Deficiency matrix formation and matrix to infectionduring .Disturbances in bone growth, shapecalcification and leads to ENAMEL HYPOPLASIA (atrophy of ameloblasts) & texture. hence increases caries susceptibility.
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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. www.indiandentalacademy.com
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 窶電ehydrocholestrol widely distributed in oily secretion of the skin.
(b) exogenous sources : such as sea fish , fish oil, egg
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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
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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.
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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. www.indiandentalacademy.com
Vitamin D deficiency 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
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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
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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.
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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.
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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) (b) (c) (d) (e)
hemorrhagic disease of new born biliary obstruction malabsorption syndrome . anticoagulant therapy. antibiotic therapy. www.indiandentalacademy.com
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 . www.indiandentalacademy.com
On Teeth : 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 www.indiandentalacademy.com
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
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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 .
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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
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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
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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 .
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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
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Trace elements
Iron : microcytic hypo chromic anaemia Copper : muscle weakness ,neurologic defect . Iodine : goiter and hyperthyroidism . Zinc : growth retardation , infertility . Selenium : myopathy ,cardiomyopathy .
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Guidelines for evaluation and assessment of Nutritional status R.D.A Physical appearance Clinical evaluation Biochemical analysis Anthropometrical data
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Referenc es
Concise medical physiology by Chaudhary Text book of pathology by Harsh Mohan. oral pathology by Shafer . co journals.
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