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GOOD MORNING
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Contents
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 History
 What is vitamin D
 Production and its metabolism
 Sources
 Functions
 RDA
 Biomarkers
 Laboratory methods for testing vitamin d
 Vitamin D deficiency General disorders
Dental considerations
 Take home points
 References
 History 6

 1600 1st description of rickets by Whistler & Glisson

 1918 Sir Edward Mellanby linked with fat-soluble nutrient

 1923 Goldblatt & Soames demonstrated exposure to

sunlight or UV light produced a substance with similar properties

 1936 Identification of Vitamin D by Windaus

What is Vitamin D..?? 7

 Fat Soluble Vitamin

 Known as calciferol

 Absorbed through sunlight exposure

 Converted to hormone form through liver and

kidney
Two Major Forms of Vitamin D 8

 Vitamin D2, ergocalciferol

 Vitamin D3, cholecalciferol

Other Forms of Vitamin D 9

 Vitamin D1: molecular compound of

ergocalciferol with lumisterol, 1:1

 Vitamin D4: 22-dihydroergocalciferol

 Vitamin D5: sitocalciferol (made from 7-

dehydrosisterol)
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Production and metabolism
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SOURCES
What are the sources? 15

 Fish (salmon,tuna,mackerel)
 Cod liver oil
 Milk, cheese. (vitamin D fortified)
 Margarine,
 Dry cereal (Vitamin D fortified)
 Liver, meat
 Egg
 Exposure to sunlight 16

 Important source of vitamin D

 Season, latitude, time of day

17
Functions 18
What does Vitamin D do? 19

 Maintain normal blood levels of Calcium and

Phosphorus
 Aids in absorption of calcium
 Promotes bone mineralization
 Prevents rickets in children and Osteomalacia in
adults
20
21
Amount of vitamin D in foods…
22
 Egg – 100 gms boiled egg – 871 IU
 Sea fish – 100 gms - 759 IU
 Mushrooms – 100gms - 446 IU
 Cereals (fortified) – 100gms – 333 IU
 Butter – 100 gms – 110 IU
 Processed cheese(fortified) – 100 gms – 300 IU
 Almond milk – 100 ml – 531 IU
 Soy milk – 100 ml – 431 IU
 Infant formula – 100 ml – 300-350 IU (depending on manufacturer)
Role in immunomodulation 23

 Binds to nuclear Vitamin D receptors (VDR)

 Immune enhancing and immunosuppressive
effects
 Increase activity of NKCs
 Increased production of cathelicidin
 Therepeutic Clinical Applications
Vitamin D in INDIA 24
 Vitamin D deficiency is epidemic in India despite of
plenty of sunshine.
 All Indian studies uniformly point to low 25(OH)
 All studies have uniformly documented low dietary
calcium intake compared to Recommended
Daily/Dietary Allowances (RDA) by Indian Council
of Medical Research (ICMR)
 The vitamin D status of children is very low in both
urban and rural population studied.
 Pregnant women and their new born had low vitamin
D status. The effect of short course of loading doses
of vitamin D doesn’t have a lasting effect and a
maintenance dose is needed
TABLE I Etiology of Vitamin D Deficiency [19]
25
Decreased vitamin D synthesis Skin pigmentation, physical agents
blocking UVR exposure, clothing,
latitude, season, air pollution, cloud
cover, altitude
Decreased nutritional intake of Strict vegan diet
vitamin
Age and physiology related Elderly, obese and institutionalised

Decreased maternal vitamin D stores Exclusive breast feeding

Malabsorption Celiac disease, pancreatic

insufficiency (cystic fibrosis), biliary
obstruction (biliary atresia)
Decreased synthesis Chronic liver disease

Increased degradation of 25 (OH) D Drugs such as rifampicin, isoniazid,

anticonvulsants, glucocorticoids.
Vitamin D Status in Relation to 25 (OH) D Levels
26
Vitamin D status Levels
US IOM classification [17]
Severe deficiency <5 ng/mL
Deficiency <15 ng/mL
Sufficiency >20 ng/mL
Risk of toxicity >50 ng/mL
US Endocrine Society classification [8]
Deficiency <20 ng/mL (50 nmol/L)
Insufficiency 21-29 ng/mL (52.5–72.5) nmol/liter
Sufficiency >30 ng/mL
Toxicity >150 ng/mL
1mcg = 40IU; 0.025 mcg is 1 IU
Biomarkers for Vitamin D Sufficiency
27
 25(OH)D
 PTH
 Bone mineral density (BMD)
 Fracture + falls
 Intestinal calcium absorption
 Blood pressure
 Dental health
 Insulin sensitivity
 Beta cell function
 Immune function
 Respiratory disease, wheezing.
When is it ordered? 28

 25 OH Vitamin D test
 1,25 di OH Vitamin D test
Testing 29
What does the test result 30
mean?
 25 OH Vitamin D test
Low blood levels = not getting enough vitamin d,
problem with absorption from the intestines
High levels = supplementation from vitamin pills
or other nutritional supplements
Vitamin D Measurements 31
Interpretation Vit D Level (nmol/l) Action

Deficiency < 25 Replace Vit D

Loading dose followed by

maintenance
Insufficient 25-50 Consider replacement if:
• Glucocorticoids
• Osteopenia/osteoporosis
• 2° HPTH
• Hypocalcaemia
• CKD

Maintenance dose
Replete >50 No need for replacement or continue
dose
Toxic >150 Check calcium
Stop treatment
Causes of Vitamin D Deficiency
32

1.Reduced Skin Synthesis Sunscreen, Veel, Aging,

Season, Skin Pigment
2. Decreased Availability Malabsorption, Obesity
3. Increased Catabolism / Loss Anticonvulsants,
HAART, Nephrotic Syndrom
4. Decreased 25-OH-D Synthesis Liver Failure
5. Decreased 1,25-(OH)2-D Synthesis CKD,
Vitamin D-dependent Rickets X-Linked
Hypophosphatemia, AD Hypophosphatemia,
Oncogenic Osteomalacia
 33

DISORDERS DUE TO DEFICIENCY

BONE
34
Vitamin D increases calcium absorption in the gut and
encourages new bone formation.

Deficiency  Rickets and osteoporosis

 35

Osteomalacia
METABOLIC BONE DISEASE
Osteomalacia
36

 Decalcification and softening of the bone

 Caused mainly by: vitamin D deficiency

 **Vitamin D is required for the absorption of calcium

from the intestine and calcium is responsible for
mineralization of bone

 Etiology
 Lack of exposure to sun
 GI malabsorption, extensive burns, chronic diarrhea, pregnancy,
drugs such as Dilantin.
Osteomalacia 37
Signs & Symptoms

 Most Common
 Difficulty rising from a chair
 Difficulty walking

 Additional Signs and Symptoms

 Low back pain, muscle weakness
 Weight loss, progressive deformities
Diagnosis 38

 Blood tests
 Decreased serum calcium or phosphorus
 Decreased serum 25-hydroxyvitamin D
 Elevated alkaline phosphatase

 X-Rays
 Show loose’rs transformation zone –
 ribbons of decalcification in bone
Rickets 39
RICKETS 40

Rickets is consequence of the vitamin D deficit and

may occur due to calcium and phosphorus
metabolic disorders.

 Blood analysis shows hypocalcemia and

hypophosphatemia.
 Histology- Failure in mineralisation of the bone
and cartilaginous tissues .
 Clinical- manifests as skeletal growth disorder.
 History
41
 Rickets ( from Greek word meaning spinal column )
 It was described by Soran Efess (A.D) and by Galen
(134-211 A.D).
 Described in detail by a British anatomist and
orthopedician, Glisson in 1650.
 Incidence:
Rickets is frequently in premature children and the
children fed only wheat floor.
Biochemical stages of rickets 42

 Stage 1: Low serum Ca level,

 normal serum P;
 normal serum PTH,
 little raise AP Ca and P tubular reabsorption are
normal,
 no amino acid loss in the urine.
Biochemical stages of rickets 43

 Stage 2. Raised PTH in the serum, serum Ca

is normalized by bone demineralization.
 Change in the ratio of Ca : P ( N=2:1), in this
stage become 3:1 or 4:1, high serum AP.
 Raised Ca tubular re-absorption and decrease
phosphate tubular re-absorption.
 As a result => hyper-aminoaciduria.
Phosphates are lost in the urine, Ph alkaline.
 X-ray findings: Osteoporosis and meaphis-
epiphesial changes.
Biochemical stages of rickets 44

 Stage 3. Severe deficiency of vit.D for a long

duration.

 Laboratory reports:

 Hypocalcemia, hypophosphatemia, serum

elevated of AP, PTH; hyperaminoaciduria,
 Radiological changes more expressive.
CLASSIFICATION 45

Calcium deficiency rickets can be classified in to 3 grades

Depending on the duration, evolution and the complication:

1. I, evolution acute

2. II, subacute

3. III; recidivant.
Vitamin-D dependent rickets 46
type II (VDDRII)
 Hereditary 1,25-dihydroxy vitamin D3 resistant
rickets.
 Autosomal recessive inheritable disorder,
resulting from a failure of target organs to respond
to hormonal form of vitamin D i.e. 1,25-
dihydroxy vitamin D3 (1,25(OH)2D3)(1).
 Characterised by an early onset refractory rickets,
hypocalcemia, hypophosphatemia, growth
retardation, hyper-parathyroidism, and elevated
circulating levels of 1,25- (OH)2D3 and total
scalp and body alopecia
Vitamin D resistant rickets 47

 Resistance to vitamin D treatment used in deficiency

 Signs- observed in first months of life

 Radiological signs of defective mineralization on

cartilage growth (rickets) and bones (osteomalacia)

 Alterations in phosphocalcic homeostasis inspite of

good vitamin D status
Hypophosphatemic resistant 48
rickets
 Severe hypophosphatemia

 Absence of radiological or biological signs of

secondary hyperthyroidism

 Caused mainly due to alteration in x linked gene

 Treatment with phosphates and derivates of

vitamin D prevents bone deformities
 49

 International journal of pediatric dentistry

 Dental co-relations with hypophosphatemic resistant

rickets

 Volume 8, Issue 1, pages 19–28, March 1998

 Objective. To review a series of cases of hypophosphataemic vitamin D
resistant rickets. 50
 Subjects included: Seventeen cases, aged between 2 years 1 month and 15 years 9
months at first referral, and with an established diagnosis of vitamin D resistant
rickets from twelve families were included in the review. Information was drawn
from patient records for follow-up periods between 9 months and 20 years 4
months.
 Setting. All subjects had been referred to the Eastman Dental Hospital between
1973 and 1997.
 Findings. Abscessed non-carious primary and/or permanent teeth were a presenting
feature in eleven of the seventeen cases. Although attrition and exposure of the
abnormally formed dentine accounted for the route of infection in primary teeth, the
route for microbial invasion of pulpal tissues in permanent teeth remained
unexplained in a number of patients. The possible part played by infractures of the
enamel as a portal of entry for infection is discussed. Enamel defects were observed
in only six patients, in three of whom these changes were limited to the primary
dentition. Taurodontism of permanent molar teeth was confirmed as a feature of the
condition in the more severely affected male subjects.
Pseudo deficiency rickets 51

 Severe hypocalcemia with secondary

hypothyroidism

 Charecterized by – Bone deformities, muscular

hypotonia, enamel hypoplasia.

 Mode of inheritance is autosomal recessive.

COMPLICATIONS 52

 Rickets tetany
 Convulsions
 Respiratory disorders
 Cardiac disorders
 Skeletal deformation
 Frequent illness
CLINICAL MANIFESTATIONS 53

Rickets may develop in any age of an infant, more frequent at

3-6mo, early in prematures.
 The first signs of hypocalcaemia are CNS changes-
excitation, restlessness, excessive sweated during sleep and
feeding, tremors of the chin and extremities.
 Skin and muscle changes- pallor, occipital alopecia, fragile
nails and hair, muscular hypotony,motor retardation.
 Complications- apnoea, stridor, low calcium level with
neuromuscular irritability (tetany).
ACUTE SIGNS 54

 Craniotabes – acute sign of rickets,

 Osteolyses detected by pressing firmly over the
occipital or posterior parietal bones, ping-pong
ball sensation will be felt.
 Large anterior fontanellae with hyperflexible
borders,
 Cranial deformation with asymmetric occipital
flattening.
SUBACUTE SIGNS 55

 Subacute signs are all the following: frontal and temporal

bossing
 False closure of sutures (increase protein matrix), in the X-ray
craniostenosis is absent.
 Maxilla in the form of trapezium, abnormal dentition.
 Late dental evolution, enamel defects in the temporary and
permanent dentition.
 Enlargement of costo-chondral junctions-“rickets rosary”
 Thorax, sternum deformation, softened lower rib cage at the site
of attachment of the diaphragm- Harrison groove.
Knowing how rickets affects 56
teeth
 Rickets, a condition resulting from inadequate mineralization of all the bones,
can have a negative effect at every stage of the development of teeth. The
primary effects of rickets include the following:
 Delayed formation: The baby teeth may not erupt until after one year. When
they erupt, they may be smaller than normal.
 Periodontal disease: Calcitriol helps regulate the immune system and protect
against inflammation so some have suggested that low vitamin D status
increases periodontal disease by increasing gingivitis. Regardless of the
cause, when the teeth become loose in the mouth they may fall out.
 Dental caries: Because the teeth don’t mineralize sufficiently in rickets
caused by low vitamin D status, this may increase a person’s chances of
getting cavities. In the absence of vitamin D, infection is established on the
tooth, leading to further loss of enamel and cavitation.
Radiological findings 57

Only in difficult diagnostic cases.

1. X-ray of the distal ulna and radius: concave (cupping)

ends; normally sharply,
2. Fraying rachitic metaphyses and a widened epiphyseal
plate.
3. Osteoporosis of clavicle, costal bones, humerus.
4. Greenstick fractures.
5. Thinning of the cortex, diaphysis and the cranial bones.
58
Osteopenia (Rickets) of
Prematurity 59
Staging:
1. Hypodensity of bones
2. Abnormalities of metaphyses
Fraying and cupping
Dense line (healing)
3. Above findings and fractures
PROPHYLAXIS IN RICKETS 60

 WHO recommendation for rickets

prophylaxis in a children coming from
unfavorable conditions and who have
difficult access to hospitals is 2 lac IU
vitamin D2 i/m
 On the 7th day, 2nd , 4th , 6th month- total
dose 8 lac IU.
 In case of the necessary prolongation
700IU/day till 24mo are given.
SPECIFIC TREATMENT IN RICKETS 61

 The treatment is with vitamin D3 depending on

the grade.

 In grade I- 2000-4000IU/day for 4-6weeks, totally

120000-180000IU.
 In grade II- 4000-6000IU/day for 4-6 weeks,
totally 180000-230000IU.
 In grade III- 8000-12000IU/day for 6-8 weeks,
totally 400000-700000IU.
 Osteoporosis 62

* Normal mineralization
* Decrease bone mass
(amount of bone per unit volume)
* Age related
* Associated or manifestation of other conditions
 Osteoporosis 63

Causes
* Idiopathic
* Nutritional
* Endocrine disorders
* Drug induced
* Malignant diseases
* Miscellaneous
 Osteoporosis 64

Symptoms & Signs

- Bony aches
- Easy fractures
spine - lower radius - femoral neck
- Rib fracture , chest pain
- Normal biochemistry
 Osteoporosis 65

X-rays
- Decrease bone density
- Wedging or biconcave vertebrae
- Thin cortex and deformities
 Osteoporosis 66

Treatment
- Treat underlying cause
- Idiopathic , extremely difficult
- Calcium and vitamin D
- Fluoride and triple therapy
- Calcitonin , Diphosphonate
- Treat fractures
 Osteoporosis 67

Prevention
* Good diet
* Exposure to sun light
* Ca and vitamin D supplement
* Hormone therapy
 Vitamin D and the Heart 68

 Low levels of vitamin D associated with increased

risk of cardiovascular disease and mortality.
 One study: Low vitamin D risk increase of
 Coronary Artery Disease - 45%
 Stroke - 78%
 Heart attack - 50%
 25-57% adults may be deficient
 69
Vitamin D and Critical Illness
For critically ill patients in the hospital, low vitamin D
levels have been found to be related to

Organ malfunction

Length of stay

Infection rates
 Vitamin D and MS 70

Multiple Sclerosis: Vitamin D levels of 40 ng/ml or higher

may confer some protection against MS.

 Patients receiving Magnesium, Calcium and 5000 IU

vitamin D significantly reduced MS exacerbations (14 vs
32).
Vitamin D and Cancer 71

Inverse correlation between incidence, mortality and or

survival rates for many cancers including breast,
colorectal, ovarian, and prostate cancers.
Emerging evidence that more than 17 cancers are
likely to be vitamin D sensitive.
1000IU/day could reduce cancers 7% for men, 9% for
women in US.
25(OH)D level of 52 ng/ml reduced breast cancer by
50%
25(OH)D level increase from 29 to 39 reduced cancer
risk by 60% after 4 years.
Vitamin D and the Lungs 72

 Lower respiratory tract infections are more

frequent in those with low 25(OH)D levels.

 2000 IU Vitamin D abolished the seasonality of

influenza and dramatically reduced the self-
reported incidence.

 Vitamin D reduces inflammation and viral

pathogens.
Vitamin D and the Lungs 73

One Vitamin D Influenza study showed:

334 children 6-15 years

50% -1200 D3 4 months vs placebo
Flu: 10.8% (with D) vs 18.6%
Asthma children – 93% reduced attacks
Low vitamin D adults: double risk of viral infections
Vitamin D and Dementia 74

Vitamin D may be primarily associated with cognitive

domains other than memory , such as executive cognitive
functions, depression, bipolar disorders, and schizophrenia.

Low 25(OH)D may be a risk factor for cognitive impairment

(41-60%).

Receptors for Vitamin D are present in brain cells.

Increased Vitamin D may improve cognitive function in
patients with Alzheimer's
Vitamin D and Obesity 75

 Seasons
 Altitude
 Calcium
 Link between other
diseases
 Treatable
Vitamin D and Diabetes 76

 Low serum levels at greater risk

 Lack of Vitamin D interferes with insulin secretion
Vitamin D and depression 77

 SAD (seasonal affective disorder)

 130 patients
 600 or 4,000 IU supplements
 Re-evaluated 1 year later
Vitamin D Controls Genes 78

 Gene direct or indirect control by vitamin D

 Regulate cell growth and prevent malignancy

 Enhance immune system (multiple mechanisms)

 Improve insulin production and sensitivity

 Heart contraction

 Maximize bone health

 79

Vitamin D and Dentistry

Vitamin D and periodontal 80
disease
 People with lower vitamin D levels had more
attachment loss than people with higher vitamin D
levels.
 African-Americans had a greater risk of PD than
white Americans. African-Americans had average
vitamin D blood levels of about 16 ng/mL (40
nmol/L) compared to 26 ng/mL (65 nmol/L) for
white Americans.
 Pregnant women with PD had lower vitamin D
levels and were twice as likely to have vitamin D
insufficiency.
What is the link between
vitamin D and dental caries? 81

 Enamel is the most mineralized substance in the

human body. It is made up of mostly calcium and
phosphate.
 Vitamin D is important for increasing the
absorption of calcium and phosphate
 Increasing the absorption of calcium and
phosphate can improve the strength of teeth and
their ability to fight demineralization from
bacteria.
 82

 Vitamin D receptors are found on cells in immune

system and teeth. Vitamin D can bind to these
receptors and increase the amount of antimicrobial
proteins in your body which help to fight the
bacteria that cause dental caries.

 In addition, the cells in the teeth that form dentin

and enamel contain vitamin D receptors, meaning
that vitamin D may play a role in their
functioning.
ECC AND VITAMIN D
83

• Mothers of children with ECC have lower vitamin D

levels during pregnancy than mothers whose children
don’t have caries.

• Children with ECC tend to have lower vitamin D levels

than healthy children.

. Children with ECC tend to have lower vitamin D

levels than healthy children
VITAMIN D SUPPLEMENTATION
84
Should children and adolescents be 85
supplemented with Vitamin D?
 200 IU, 400 IU, 600 IU or 1000 IU daily?
 Vitamin D2 or D3?

Pediatrics 122:1142, 2008

86
Treatment Regimens for Vitamin D Deficiency 87
Daily regimen Weekly regimen Maintenance
Group Stoss therapy (oral or IM)
(8-12 weeks) (8-12 weeks)

< 1 mo old 1,000 IU 50,000 IU - 400-1,000 IU

1 lakh -6 lakhs units over 1-5

1-12 mo old 1,000-5000 IU 50,000 IU 400- 1,000 IU
days

(Preferably 3 lakh)

1-18 y old 5,000 IU 50,000 IU 3-6 lakh units over 1-5 days 600-1,000 IU

>18 y old 6,000 IU 50,000 IU 3-6 lakh units over 1-5 days 1,500-2,000 IU

Obese patients, patients 6,000-10,000 3,000-6,000 IU

with malabsorption IU/ day

syndrome, or on

medications affecting

vitamin D
* To convert (IU) to mcg of calciferol divide by 40.
What can we do? 88

 Rule out systemic disease, endocrinopathy 

bone loss
 Amenorrhea in young woman  be concerned!
 Consider BMD measurement in at risk patients
and ones with strong family history
• Recall role of genetics in BMD determination

 Encourage:
• Good nutrition, with adequate calcium and vitamin D
Vitamin D Supplementation 89
Deficiency (<25 nmol/l or 10 mcg/l)
90

 Oral Therapy
 1st line agent:
Fultium-D3 (Cholecalciferol) 800 iu capsules x4/d (licensed product)
- 3200 iu daily for 8-12 weeks.
 2nd line:
Dekristol (Cholecalciferol) capsules 20,000 units. Prescribe 1 capsule
(20,000 units) once per week for 8-12 weeks.
 Where oral therapy not appropriate (e.g. malabsorption states)
 Ergocalciferol 300,000 (or 600,000) iu single dose by
intramuscular injection. The injection is gelatin free and may be
preferred for some populations.
Insufficiency (25-50 nmol/l or 10-20 mcg/l) or for long-term
maintenance following rx of deficiency
91

 1st line therapy

 Fultium-D3 800iu capsules x2/d (licensed) - 1600iu per day (a dose between
1000 – 2000 units daily is appropriate).

 2nd line:
 Dekristol capsules 20 000 units [unlicensed import]. Prescribe 1 capsule
(20,000 units) once per fortnight.

 Alternatively where oral therapy not appropriate

 Ergocalciferol 300,000 international units single dose by intramuscular injection
once or twice a YEAR.
Combined calcium & vitamin
D supplements 92

 Calcium component usually unnecessary in

primary vitamin D deficiency

 Dual replacement required where there is severe

deficiency accompanied by hypocalcaemia
leading to secondary hyperparathyroidism

 Appropriate for the management of osteoporosis

and in the frail elderly.
Alfacalcidol/Calcitriol 93

 Alfacalcidol (1 alpha- vitamin D) and Calcitriol

have no routine place in the management of
primary vitamin D deficiency
 Reserved for use in renal disease, liver disease and
hypoparathyroidism.
Monitoring 94

 1 month
 Bone and renal profile
 3 months
 Bone and renal profile, vitamin D, and plasma
parathyroid hormone.
 Once vitamin D replacement is optimised no
further measurement of vitamin D is necessary.
Nutritional Strategies to 95
Improve Vitamin D Status
 Effective strategies in infants (current recs)
 200 IU vitamin D/day
 1/2dose tri-vitamin (ADC) prep
 500 ml of fortified infant formula
 5 mcg calcitriol

 Recent strategies (experimental)

 Supplementing the pregnant mother
 Supplementing the nursing mother
 Single high dose therapy
 96

 v
Maternal Vitamin D Supplementation
97
During Pregnancy

 IOM (2001) determines

 AIas 200 IU/day
 UL as 2,000 IU/day

 FNB data: 50% women of reproductive age have

low vitamin D level
 Infants born to Vitamin D deficient mothers have
lower vitamin D stores
Does Supplementation 98
During Pregnancy Work?
 Supplementation of pregnant women
 Improves neonatal calcium handling
 Improves 9 year bone status
 Improves maternal vit D levels if she was
deficient
 Does not alter already sufficient maternal D
status
Who may need extra vitamin D to prevent
a deficiency? 99

 Older age people (greater than age 50)

 individuals with limited sun exposure
 occupations that prevent exposure to sunlight
 reduced ability to absorb dietary fat
 exclusively breast-fed infants
 10
Who is at risk to overdose on 0
Vitamin D?

 Anyone who takes Vitamin D supplements CAN take too

much Vitamin D. But the majority of documented
overdose on vitamin D are from:

• Children whose parents accidentally give them massive

doses of vitamin D
• Elderly people who incorrectly take massive vitamin D
dosages
• Adults who take more than 10,000 IU's per day for long
periods of time.
• 'Industrial Accidents' where massive quantities of vitamin D
are put into fortified foods in error

 These categories comprise nearly all people who have had

an overdose on Vitamin D.
What is the health risk of too much
101
vitamin D?

 nausea
 vomiting
 poor appetite
 constipation
 weakness
 weight loss
Take Home Points
 Vitamin D deficiency is common 102
 25 OH vitamin D is a predictor of bone health in terms of fracture risk
and risk of falls
 25 OH vitamin D is also potentially an independent predictor of risk
of cardiovascular disease, hypertension, cancer, diabetes, all cause
mortality, and URI
 At least 600 IU of vitamin D3 per day is needed to maintain vitamin
D sufficiency
 Sensible sun exposure is a great way to maintain vitamin D
sufficiency
References
103
 LEHNINGER – principles of biochemistry (3rd edition)
 Biochemistry – BERG, TYMOCZK, STRYER (5TH edition)
 Practical biochemistry- WILSON AND WALKER
 SHAFER’S TEXTBOOK OF ORAL PATHOLOGY- (7TH edition)
 NELSON’S BOOK OF PEDIATRICS
 Dentistry for child and adolescents (McDONALD AND AVERY)- 8th
edition
 FINN- clinical pedodontics (4th edition)
 Pediatric dentistry- CASAMASSIMO,NOWAK- (5th edition)
 SCULLY- oral and maxillofacial medicine (3rd edition)
 TYLDESLY’S oral medicine- FIELD AND LONGMAN (5th edition)
 BURKETTS ORAL MEDICINE (11th edition)
Previous questions on this
topic: 104

 How is vitamin D formed and activated in the body? How does it regulate body
calcium levels? Write a note on hypo and hypervitaminosis D in growing child?
(April 2015)
 Role of vitamins in oral health (October 2012)
 Vitamin D and calcium haemostasis (April 2011)
 1,25 dihydroxy cholecalciferol (1989)
 Role of vitamin D (1981)
 Write a short notes on vitamin D (1980)
 Describe in brief about calcium metabolism (June 1977)
 Describe the process of calcification in body and the role of vitamin D (June 1977)
 Concept of bone resorption and calcium phosphorous blood levels in rickets
(October 1966)