GOOD MORNING

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Contents

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

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History

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

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What is Vitamin D..??

Fat Soluble Vitamin

Known as calciferol

Absorbed through sunlight exposure

Converted to hormone form through liver and

kidney

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Two Major Forms of Vitamin D

Vitamin D2, ergocalciferol

Vitamin D3, cholecalciferol

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Other Forms of Vitamin D

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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10Production and metabolism

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SOURCES

What are the sources?

Fish (salmon,tuna,mackerel)

Cod liver oil

Milk, cheese. (vitamin D fortified)

Margarine,

Dry cereal (Vitamin D fortified)

Liver, meat

Egg

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Exposure to sunlight

Important source of vitamin D

Season, latitude, time of day

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Functions 18

What does Vitamin D do?

Maintain normal blood levels of Calcium and

Phosphorus

Aids in absorption of calcium

Promotes bone mineralization

Prevents rickets in children and Osteomalacia in

adults

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Amount of vitamin D in foods…

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)

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Role in immunomodulation

Binds to nuclear Vitamin D receptors (VDR)

Immune enhancing and immunosuppressive

effects

Increase activity of NKCs

Increased production of cathelicidin

Therepeutic Clinical Applications

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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

24Vitamin D in INDIA

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Decreased vitamin D synthesis Skin pigmentation, physical agents

blocking UVR exposure, clothing,

latitude, season, air pollution, cloud

cover, altitudeDecreased nutritional intake of

vitamin

Strict vegan diet

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.

TABLE I Etiology of Vitamin D Deficiency [19]

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

26Vitamin D Status in Relation to 25 (OH) D Levels

Biomarkers for Vitamin D Sufficiency

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.

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When is it ordered?

25 OH Vitamin D test

1,25 di OH Vitamin D test

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Testing 29

What does the test result 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

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Vitamin D MeasurementsInterpretation 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 calciumStop treatment

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Causes of Vitamin D Deficiency

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

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DISORDERS DUE TO DEFICIENCY

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BONE

Vitamin D increases calcium absorption in the gut and

encourages new bone formation.

Deficiency Rickets and osteoporosis

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Osteomalacia

METABOLIC BONE DISEASE

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Osteomalacia

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.

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Osteomalacia Signs & Symptoms

Most Common

Difficulty rising from a chair

Difficulty walking

Additional Signs and Symptoms

Low back pain, muscle weakness

Weight loss, progressive deformities

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Diagnosis

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

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Rickets 39

RICKETS

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.

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History

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.

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Biochemical stages of rickets

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.

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Biochemical stages of rickets

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.

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Biochemical stages of rickets

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.

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CLASSIFICATION

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.

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Vitamin-D dependent rickets 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

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Vitamin D resistant rickets

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

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Hypophosphatemic resistant 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

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International journal of pediatric dentistry

Dental co-relations with hypophosphatemic resistant rickets

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

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Objective. To review a series of cases of hypophosphataemic vitamin D

resistant rickets.

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.

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Pseudo deficiency rickets

Severe hypocalcemia with secondary

hypothyroidism

Charecterized by – Bone deformities, muscular

hypotonia, enamel hypoplasia.

Mode of inheritance is autosomal recessive.

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COMPLICATIONS

Rickets tetany

Convulsions

Respiratory disorders

Cardiac disorders

Skeletal deformation

Frequent illness

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CLINICAL MANIFESTATIONS

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).

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ACUTE SIGNS

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.

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SUBACUTE SIGNS

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.

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Knowing how rickets affects 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.

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Radiological findings

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.

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Osteopenia (Rickets) of Prematurity

Staging:1. Hypodensity of bones2. Abnormalities of metaphyses

Fraying and cuppingDense line (healing)

3. Above findings and fractures

PROPHYLAXIS IN RICKETS

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.

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SPECIFIC TREATMENT IN RICKETS

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.

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Osteoporosis

* Normal mineralization

* Decrease bone mass

(amount of bone per unit volume)

* Age related

* Associated or manifestation of other conditions

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Osteoporosis

Causes

* Idiopathic

* Nutritional

* Endocrine disorders

* Drug induced

* Malignant diseases

* Miscellaneous

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Osteoporosis

Symptoms & Signs

- Bony aches

- Easy fractures

spine - lower radius - femoral neck

- Rib fracture , chest pain

- Normal biochemistry

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Osteoporosis

X-rays

- Decrease bone density

- Wedging or biconcave vertebrae

- Thin cortex and deformities

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Osteoporosis

Treatment

- Treat underlying cause

- Idiopathic , extremely difficult

- Calcium and vitamin D

- Fluoride and triple therapy

- Calcitonin , Diphosphonate

- Treat fractures

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Osteoporosis

Prevention

* Good diet

* Exposure to sun light

* Ca and vitamin D supplement

* Hormone therapy

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68Vitamin D and the Heart

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

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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

70Vitamin D and MS

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).

71Vitamin D and Cancer

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.

1000 IU/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.

72Vitamin D and the Lungs

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.

73Vitamin D and the Lungs

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

74Vitamin D and Dementia

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

Seasons

Altitude

Calcium

Link between other

diseases

Treatable

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Vitamin D and Diabetes

Low serum levels at greater risk

Lack of Vitamin D interferes with insulin secretion

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Vitamin D and depression

SAD (seasonal affective disorder)

130 patients

600 or 4,000 IU supplements

Re-evaluated 1 year later

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78Vitamin D Controls Genes

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

Vitamin D and Dentistry

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Vitamin D and periodontal 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.

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What is the link between vitamin D and dental caries?

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.

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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.

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• 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

ECC AND VITAMIN D

VITAMIN D SUPPLEMENTATION84

Should children and adolescents be supplemented with Vitamin D?

200 IU, 400 IU, 600 IU or 1000 IU daily?

Vitamin D2 or D3?

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Pediatrics 122:1142, 2008

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GroupDaily regimen

(8-12 weeks)

Weekly regimen

(8-12 weeks)Stoss therapy (oral or IM)

Maintenance

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

1-12 mo old 1,000-5000 IU 50,000 IU1 lakh -6 lakhs units over 1-5

days400- 1,000 IU

(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.

87Treatment Regimens for Vitamin D Deficiency

What can we do?

Rule out systemic disease, endocrinopathybone 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

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89Vitamin D Supplementation

Deficiency (<25 nmol/l or 10 mcg/l)

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.

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Insufficiency (25-50 nmol/l or 10-20 mcg/l) or for long-term

maintenance following rx of deficiency

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.

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Combined calcium & vitamin D supplements

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.

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Alfacalcidol/Calcitriol

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.

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Monitoring

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.

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Nutritional Strategies to Improve Vitamin D Status Effective strategies in infants (current recs)

200 IU vitamin D/day

1/2 dose 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

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v

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Maternal Vitamin D Supplementation During Pregnancy

IOM (2001) determines

AI as 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

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Does Supplementation 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

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Who may need extra vitamin D to prevent a deficiency?

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

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Who is at risk to overdose on 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.

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0

What is the health risk of too much vitamin D?

nausea

vomiting

poor appetite

constipation

weakness

weight loss

101

Take Home Points

Vitamin D deficiency is common

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

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References

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)

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Previous questions on this topic: 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)

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