1. Metabolic bone diseases 1

2. Bones…. What do they need to be strong? Calcium/ PO4 Vit D PTH calcitonin 2

3. Sources of Vitamin D and importance 3

4. * VIT D LEVEL IN SERUM: 25 (OH) D3 level ng/ml DEFICIENT < 10 INSUFFICIENT10 - 20 OPTIMAL 20 - 60 HIGH60 - 90 TOXIC>90 4

5. Vitamin D Deficiency in Saudi Arabia Group mostly affected are: Breast- Fed infants because Human milk contains little vitamin D, Age < 2 years Darked –skin children because darkly pigmented skin, which blocks penetration of ultraviolet light necessary for formation of cholecalciferol (Vit. D3) from cholesterol in the skin. Low socio-economic Class Urban > Rural 5

6. PARATHYROID HORMONE (PTH) PTH increases the blood calcium level by: 1.Promoting bone resorption process. 2.Increasing calcium absorption from intestine by increasing the synthesis of active vit D 3. PTH also stimulates the excretion of phosphates by the kidneys. 6

7. CALCITONIN It is produced by para follicular c cells of thyroid. It is a calcium lowering hormone in serum by inhibiting bone resorption by decreasing the number & activity of osteoclasts. 7

8. Metabolic bone Diseases 8

9. Rickets Osteomalacia osteoporosis 9

10. Rickets: Disease of growing bones of children(epiphyseal plate not closed )in which defective mineralization occurs in both bone and cartilage of epiphyseal growth plate.Osteomalacia: Disorder of mature bones in adult (after epiphyseal plate closure )in which mineralization of new osteoid bone is inadequate or delayed 10

11. * Causes of rickets: 1.Nutritional deficiency: - Excess of phytate in diet which form insoluble compounds with calcium so prevent its absorption (chapati flour) 2. Malabsorption: as in Celiac disease, Pancreatic insufficiency 3. Hepato-biliary diseases: – Biliary Atresia. – Cirrhosis. – neonatal hepatitis. 11

12. 4. Drugs: – Anti-convulsants. – Phenobartbitone. – Phenytoin 5. Chronic renal causes : -Renal osteodystrophy 12

13. * Types of Rickets: (1). Vitamin D deficient rickets: there is decrease in vitamin D inside body. (2). Vitamin D dependent rickets: there is defect in the process of vitamin D activation. (3). Vit D resistant rickets: either -Hypophosphatemic rickets. - End organ resistance to 1,25 Dihydroxy Vit D3. 13

14. Vitamin D deficient rickets The predominant cause of rickets is a deficiency in vitamin D, which is required for normal calcium absorption from the gut. Malabsorption leads to low levels of calcium in the blood. This not only prevents proper bone growth, but can also lead to calcium being released form the bones to increase its blood level. 14

15. Hypophosphatemic rickets Nutritional phosphate deficiency. Prematurity. Decreased intestinal absorption of phosphate – Ingestion of phosphate binders (aluminum hydroxide). Renal phosphate wasting. 15

16. Diagnosis of rickets A. Clinical features of rickets: (1). Skeletal manifestations (2). Extr-askeletal manifestations B. Investigations. 16

17. (1). Skeletal manifestations Craniotabes: The earliest sign of rickets in infant, is (abnormal softness of skull) Delayed closure of anterior fontanel. Frontal and parietal bossing: Rounded prominence of the frontal and parietal bones in an infant’s cranial vault Delayed eruption of primary teeth. Enamel defects and caries teeth. Rachitic rosary – Swelling of the costo-chondral junctions. 17

18. Harrison’s groove: – Lateral indentation of the chest wall at the site of attachment of diaphragm. Enlargement of long bones around wrists and ankles Bow legs knock knees Green stick fractures Deformities of spine, pelvis and leg – rachitic dwarfism Growth retardation due to impaired calcification of bone epiphysis. 18

19. Frontal and parietal bossing 19

20. Rachitic Rosary beads due to Swelling of the costo-chondral junctions 20

21. Rachitic Rosary beads due to Swelling of the costo-chondral junctions 21

22. Harrison’s groove Lateral indentation of the chest wall at the site of attachment of diaphragm 22

23. Wrist enlargement 23

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29. Wide ankle 29

30. (2). Extra – skeletal manifestations: HYPOTONIA AND DELAYED MOTOR DEVELOPMENT Muscle weakness PROTUBERANT ABDOMEN, BONE PAIN, WADDLING GAIT AND FATIGUE. 30

31. B. Investigations * BASIC INVESTIGATIONS TO CONFIRM RICKETS: Serum Ca, P: Hypocalcemia if serum Calcium less than 9 mg/dl X rays of ends of long bones at knees or wrists: Widening and cupping of the distal ends of shaft. 31

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33. Osteoporosis & Osteomalacia 33

34. Difference Between Osteoporosis & Osteomalacia Osteoporosis refers to the degeneration of already constructed bone, making them brittle, while osteomalacia is an abnormality in the building process of bone, making them soft. 34

35. Osteoporosis  The word osteoporosis literally means porous bones. It occurs when rate of degeneration of already constructed bone is rapid and exceed rate of bone building.  This leads to loss of an excessive amount of their protein and mineral content.  An osteoporotic bone characterized by: – Thinning of bone trabecula – low bone mass and volume. – Enhanced bone fragility and increase in fracture risk even with any trivial trauma. 35

36. Osteoporotic Vertebra 36

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39. * Types of osteoporosis: A.Idiopathic type: - which is subclassified into  Post menopause (Type I).  Senile type (Type II). B. Secondary type: B. Secondary type: which occur secondary to any other disease, or drug intake. 39

40. Idiopathic Osteoporosis: Postmenopausal osteoporosis (type I) Postmenopausal osteoporosis (type I) – Caused by lack of estrogen. – Estrogen loss triggers increases in InterLeukin-1, IL-6, and Tumor Necrosis factor lead to increased osteoclast development and lifespan. – Also estrogen loss stimulate parathormone hormone. Senile osteoporosis (type II): Senile osteoporosis (type II): as a result of aging 40

41. Normal vs. Osteoporotic Bone 41

42. Commonest sites affected by osteoporosis 42

43. Osteoporosis in vertebra 43

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46. Investigations: DEXA - The primary method of testing is DEXA or dual energy X-ray absorptiometry,This can detect the density of bones. - Sometimes, ultrasound or CT scans are also used to make a diagnosis. 46

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