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![25
Decreased vitamin D synthesis Skin pigmentation, physical agents
blocking UVR exposure, clothing,
latitude, season, air pollution, cloud
cover, altitude
Decreased 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]](https://image.slidesharecdn.com/3-180510133625/85/vitamin-D-dental-applications-25-320.jpg)
![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
26
Vitamin D Status in Relation to 25 (OH) D Levels](https://image.slidesharecdn.com/3-180510133625/85/vitamin-D-dental-applications-26-320.jpg)
![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.
91](https://image.slidesharecdn.com/3-180510133625/85/vitamin-D-dental-applications-91-320.jpg)
Uploaded bySohail Mohammed
vitamin D - dental applications
This document provides information on vitamin D, including its history, forms, sources, functions, deficiency, testing, and role in dental health. It discusses the key points that vitamin D is important for calcium absorption and bone mineralization, sources include exposure to sunlight and dietary intake of oily fish, eggs, and fortified foods. Vitamin D deficiency can lead to metabolic bone diseases like rickets in children and osteomalacia in adults, causing bone pain and deformities. Biomarkers and tests are used to diagnose and monitor vitamin D levels.
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vitamin D - dental applications
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- 5. Contents History Whatis 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 5
- 6. History 1600 1stdescription 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 6
- 7. What is VitaminD..?? Fat Soluble Vitamin Known as calciferol Absorbed through sunlight exposure Converted to hormone form through liver and kidney 7
- 8. Two Major Formsof Vitamin D Vitamin D2, ergocalciferol Vitamin D3, cholecalciferol 8
- 9. Other Forms ofVitamin D Vitamin D1: molecular compound of ergocalciferol with lumisterol, 1:1 Vitamin D4: 22-dihydroergocalciferol Vitamin D5: sitocalciferol (made from 7- dehydrosisterol) 9
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- 15. What are thesources? Fish (salmon,tuna,mackerel) Cod liver oil Milk, cheese. (vitamin D fortified) Margarine, Dry cereal (Vitamin D fortified) Liver, meat Egg 15
- 16. Exposure to sunlight Important source of vitamin D Season, latitude, time of day 16
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- 19. What does VitaminD 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 19
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- 22. Amount of vitaminD 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) 22
- 23. 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 23
- 24. Vitamin Ddeficiency 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
- 25. 25 Decreased vitamin Dsynthesis Skin pigmentation, physical agents blocking UVR exposure, clothing, latitude, season, air pollution, cloud cover, altitude Decreased 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]
- 26. Vitamin D statusLevels 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 26 Vitamin D Status in Relation to 25 (OH) D Levels
- 27. Biomarkers for VitaminD 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. 27
- 28. When is itordered? 25 OH Vitamin D test 1,25 di OH Vitamin D test 28
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- 30. What does thetest 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 30
- 31. Vitamin D Measurements InterpretationVit D Level 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 31
- 32. Causes of VitaminD 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 32
- 33. DISORDERS DUE TODEFICIENCY 33
- 34. BONE Vitamin D increasescalcium absorption in the gut and encourages new bone formation. Deficiency Rickets and osteoporosis 34
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- 36. Osteomalacia Decalcification andsoftening 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. 36
- 37. 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 37
- 38. 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 38
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- 40. RICKETS Rickets is consequenceof 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. 40
- 41. 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. 41
- 42. Biochemical stages ofrickets 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. 42
- 43. Biochemical stages ofrickets 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. 43
- 44. Biochemical stages ofrickets 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. 44
- 45. CLASSIFICATION Calcium deficiency ricketscan be classified in to 3 grades Depending on the duration, evolution and the complication: 1. I, evolution acute 2. II, subacute 3. III; recidivant. 45
- 46. Vitamin-D dependent rickets typeII (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 46
- 47. Vitamin D resistantrickets 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 47
- 48. Hypophosphatemic resistant rickets Severehypophosphatemia 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 48
- 49. International journalof pediatric dentistry Dental co-relations with hypophosphatemic resistant rickets Volume 8, Issue 1, pages 19–28, March 1998 49
- 50. Objective. Toreview 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. 50
- 51. Pseudo deficiency rickets Severe hypocalcemia with secondary hypothyroidism Charecterized by – Bone deformities, muscular hypotonia, enamel hypoplasia. Mode of inheritance is autosomal recessive. 51
- 52. COMPLICATIONS Rickets tetany Convulsions Respiratory disorders Cardiac disorders Skeletal deformation Frequent illness 52
- 53. CLINICAL MANIFESTATIONS Rickets maydevelop 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). 53
- 54. 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. 54
- 55. SUBACUTE SIGNS Subacutesigns 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. 55
- 56. Knowing how ricketsaffects 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. 56
- 57. Radiological findings Only indifficult 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. 57
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- 59. 59 Osteopenia (Rickets) of Prematurity Staging: 1.Hypodensity of bones 2. Abnormalities of metaphyses Fraying and cupping Dense line (healing) 3. Above findings and fractures
- 60. 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. 60
- 61. SPECIFIC TREATMENT INRICKETS 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. 61
- 62. Osteoporosis * Normal mineralization *Decrease bone mass (amount of bone per unit volume) * Age related * Associated or manifestation of other conditions 62
- 63. Osteoporosis Causes * Idiopathic * Nutritional *Endocrine disorders * Drug induced * Malignant diseases * Miscellaneous 63
- 64. Osteoporosis Symptoms & Signs -Bony aches - Easy fractures spine - lower radius - femoral neck - Rib fracture , chest pain - Normal biochemistry 64
- 65. Osteoporosis X-rays - Decrease bonedensity - Wedging or biconcave vertebrae - Thin cortex and deformities 65
- 66. Osteoporosis Treatment - Treat underlyingcause - Idiopathic , extremely difficult - Calcium and vitamin D - Fluoride and triple therapy - Calcitonin , Diphosphonate - Treat fractures 66
- 67. Osteoporosis Prevention * Good diet *Exposure to sun light * Ca and vitamin D supplement * Hormone therapy 67
- 68. 68Vitamin D andthe 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
- 69. 69 Vitamin D andCritical 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
- 70. 70Vitamin D andMS 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).
- 71. 71Vitamin D andCancer 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.
- 72. 72Vitamin D andthe 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.
- 73. 73Vitamin D andthe 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
- 74. 74Vitamin D andDementia 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
- 75. Vitamin D andObesity Seasons Altitude Calcium Link between other diseases Treatable 75
- 76. Vitamin D andDiabetes Low serum levels at greater risk Lack of Vitamin D interferes with insulin secretion 76
- 77. Vitamin D anddepression SAD (seasonal affective disorder) 130 patients 600 or 4,000 IU supplements Re-evaluated 1 year later 77
- 78. 78Vitamin D ControlsGenes 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 andDentistry 79
- 80. Vitamin D andperiodontal 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. 80
- 81. What is thelink 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. 81
- 82. Vitamin Dreceptors 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. 82
- 83. 83 • Mothers ofchildren 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
- 84.
- 85. Should children andadolescents be supplemented with Vitamin D? 200 IU, 400 IU, 600 IU or 1000 IU daily? Vitamin D2 or D3? 85 Pediatrics 122:1142, 2008
- 86.
- 87. Group Daily regimen (8-12 weeks) Weeklyregimen (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 IU 1 lakh -6 lakhs units over 1-5 days 400- 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
- 88. What can wedo? 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 88
- 89.
- 90. Deficiency (<25 nmol/lor 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. 90
- 91. Insufficiency (25-50 nmol/lor 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. 91
- 92. 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. 92
- 93. Alfacalcidol/Calcitriol Alfacalcidol (1alpha- 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. 93
- 94. 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. 94
- 95. Nutritional Strategies to ImproveVitamin 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 95
- 96.
- 97. Maternal Vitamin DSupplementation 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 97
- 98. Does Supplementation During PregnancyWork? 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 98
- 99. Who may needextra 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 99
- 100. Who is atrisk 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. 10 0
- 101. What is thehealth risk of too much vitamin D? nausea vomiting poor appetite constipation weakness weight loss 101
- 102. 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 102
- 103. 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) 103
- 104. Previous questions onthis 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) 104