1. Clinical condition in which there is inadequate mineralisation of growing bone. Primarily due to Vit D deficiecy or a disturbance in its metabolism. Rickets children Osteomalacia bones of adults.

2. VIT.D DEFICIENCY decrease absorption of ca. & p from the gut decrease ca. level in blood increase PTH mobilization of ca. & po4 from bones and decrease tubular reabsorption of p in kidneys normal serum ca. & low serum po4 decrease ca. available for bones ca. & po4 will be far below 40 failure of calcification around the mature cart. cells and osteoblasts in the ostoeid tissue. 3. Normal bone growth THERE ARE 4 ZONES : 1.ZONE OF RESTING CARTILAGE : 1 layer 2.ZONE OF PROLIFERATING CART. : 6 layers 3.zone OF PROVISSIONAL CALCIFICATION "epiphyseal line " : the cart. cells in this layer become mature, they containe alkaline phosphatase release the phosphate in the matrix which already contains ca. & po4 in solution increase production of ca. & po4 once the production exceeds 40 precipitation of ca.phosphate in the matrix around the cartilage cells death of the cells. 4.ZONE OF BONE FORMATION : The layer of prov. calc. is invaded by capillaries and osteoblast which deposit a layer of organic bone matrix "osteoid tis. rapidly meniralized and the calcified cartilage ultimitly replaced by bone. 4. PATHOLOGY 1. The mature cartilage cells will not die and the proliferating zone will be formed of many layers and invades the adjacent zone of of provis. calc.- irrIegularity of epiphseal line. 2. The prov. calc. zone and newly formed ost. tis. will fail to calcify or will calcified irregularly. wide irregular frayed zone of non rigid tis. " RACHITIC METAPHSIS " is produced. 3. In the shaft the preformed bone is replaced by uncalcified ost. soft rarified cortical bone bone deformities & green stick fractures. 5. CAUSES Vitamin D deficiency Lack of sunlight exposure Dietry lack of meat & dairy products Malsbsorption Failure of 1,25 vit D synthesis Chronic renal failure Hyperphosphataemia & kidney damage Vit D dependent rickets ( type 1) - AR Inactivating mutation in 1,25,hydroxylase enzyme. 6. Vitamin D receptor defects Vit D dependent rickets type2 (AR) Mutation in vit D receptors Defects in phosphate metabolism Primary hypophosphataemic rickets(XLH) renal phosphate wasting. Fanconi syndromes Proximal renal tubular acidosis. Hypophosphatasia Mutation of bone specific ALP 7. NUTRITIONAL RICKETS VIT D DEFICIENCY 3-18 MONTHS LACK OF SUNLIGHT EXPOSURE & NO DIETARY SUPPLEMENTATION PROLONGED BREAST FEEDING CALCIUM DEFICIENT DIET BOTH VEGETARIANS WHO AVOID DAIRY PRODUCTS 8. GASTROINTESTINAL RICKETS ABSORPTION OF CALCIUM & VITAMIN D PREVENTED GLUTEN SENSITIVE ENTEROPATHY CROHNS DISEASE ULCERATIVE COLITIS SARCOIDOSIS SHORTGUTSYNDROMES LIVERDISEASE 9. X LINKED HYPOPHOSPHATEMIA MOST COMMON INHERITED ETIOLOGY X LINKED DOMONANT DISORDER DEFECT IN PHEX GENE(REGULATE TRANSPORT OF RENAL PHOSPHATES) RENALPHOSPHATE WASTING HYPOPHOSPHATEMIA RICKETS SHORT STATURE DENTAL ABSCESSES 10. McCUNE-ALBRIGHT SYNDROME HYPOPHOSPHATEMIC RICKETS CAF AU LAIT SPOTS PRECOCIOUS PUBERTY FIBROUS DYSPLASIA OF MULTIPLE LONG BONES CONSTITUTIONAL ACTIVATION OF C-AMP-PKA SIGNALING PATHWAY DUE TO GENETIC DEFECTS IN G SIGNALING PROTEINS 11. 1 ALPHA HYDROXYLASE DEFICIENCY VITAMIN D DEPENDENT RICKETS