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RICKETS & OSTEOMALACIA Def.: reduction in bone mineralization !
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OSTEOMALACIA and RICKETS Clinical syndromes that result from inadequate bone mineralization
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Vitamin D Deficiency Osteomalacia & Rickets Osteomalacia occurs in adults Rickets occurs in children Defective mineralization of the skeleton
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VITAMIN D DEFICIENCY Vitamin D deficiency leads to decreased absorption of calcium by the GI tract. As serum calcium starts to fall, secondary hyperparathyroidism occurs.
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VITAMIN D DEFICIENCY Elevated Pth levels may maintain serum calcium in the normal range, but at the cost of phosphaturia, hypophosphatemia and increased bone reabsorption Low serum phosphate results in inadequate bone mineralization and osteopenia.
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VITAMIN D DEFICIENCY In severe cases, secondary hyperparathyroidism is not adequate to maintain serum calcium levels, and hypocalcemia occurs.
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OSTEOMALACIA,RICKETS Normal bone metabolism CALCIUM 99% in bone. Main functions- muscle /nerve function, clotting. Plasma calcium- 50% free, 50% bound to albumin. Dietary needs- Kids- 600mg/day, Adolesc.-1300mg/day, Adult-750mg/day, Pregnancy-1500mg/day, Breastfeeding-2g/day, Fractures- 1500mg/day Absorbed in duodenum (active transport) and jejunum (diffusion), 98% reabsorbed in kidney prox. tubule, may be excreted in stool.
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OSTEOMALACIA,RICKETS Normal bone metabolism PHOSPHATE 85% in bone. Functions-metabolite and buffer in enzyme systems. Plasma phosphate mainly unbound. Daily requ. 1-1.5g/day
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OSTEOMALACIA,RICKETS Regulation of Calcium & Phosphate Metabolism: Peak bone mass at 16-25 years. Bone loss 0.3- 0.5% per year (2-3% per year after 6th decade). Parathyroid Hormone (PTH) Vitamin D3 Calcitonin Other Hormones: Estrogen: Prevents bone loss Corticosteroids: Increases bone loss Thyroid hormones: Leads to osteoporosis Growth hormones: Cause positive calcium balance Growth factors
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Vitamin D RDA Range Adult males: 5 – 10 mg/day Adult females: 5 – 10 mg/day Primary source of Vitamin D Sunlight Dietary source of Vitamin D Fortified milk
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Sources of Vitamin D Cod liver oil Egg yolk
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Biochemistry of Vitamin D3 – Brief Review Vitamin D3 (cholecalciferol) is synthesized in the skin, with UV light, from 7-dehydrocholesterol Vitamin D3 is hydroxylated twice – first in the liver, to 25-hydroxycholecalciferol, then in the kidney, to 1, 25-dihydroxycholecalciferol, the most potent form of Vitamin D
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Vitamin D metabolism
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Vitamin D Metabolism
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Vitamin D (cont’) Primary role of Vitamin D Increase calcium and phosphate absorption from the intestines Other tissues that Vitamin D acts on Parathyroid glands Bone, Kidneys Skin, Brain, Pituitary Lymphocytes,Tumors D
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Vitamin D Deficiency Secondary to Insufficient sun exposure Malabsorption, Malnutrition Liver disease Renal disease, nephrotic syndrome Anticonvulsants (generics Phenytoin, Carbamazepine, Valproate, Phenobarbital) can inhibit hepatic hydroxylation of Vitamin D
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Other conditions that can cause Osteomalacia Hereditary or acquired disorders of vitamin D metabolism Kidney failure and acidosis Phosphate depletion associated with not enough phosphates in the diet Cancer Side effects of medications used to treat seizures (Dilantin) Liver disease
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RICKETS, OSTEOMALACIA PATHOLOGY: Sufficient osteoid, poor mineralization (Rickets is found only in children prior to the closure of the growth plates, while OSTEOMALACIA occurs in persons of any age. Any child with rickets also has osteomalacia, while the reverse is not necessarily true).
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RICKETS, OSTEOMALACIA CAUSES: Nutritional deficiency Vit D chelators of calcium- phytates, oxalates, phosphorous Antacid abuse, causing reduced dietary phosphate binding GI Absorption defects Post gastrectomy Biliary disease (reduced absorption of Vitamins ) Small bowel disease liver disease Renal tubular defects Renal osteodystrophy Miscellaneous causes
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Vitamin D Deficiency Osteomalacia & Rickets (cont’) Secondary to many things, including Vitamin D deficiency as discussed above Dietary calcium deficiency Phosphorus deficiency Aluminum toxicity Hypophosphatasia Fibrogenesis imperfecta ossium
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Clinical features Osteomalacia in adults starts insidiously as aches and pains in the lumbar (lower back) region and thighs, spreading later to the arms and ribs. Pain is non-radiating, symmetrical, and accompanied by tenderness in the involved bones. Proximal muscles are weak, and there is difficulty in climbing up stairs and getting up from a squatting position. Physical signs include deformities like and lordosis. Pathologic fractures due to weight bearing may develop. Most of the time, the only alleged symptom is chronic and bone aches are not spontaneous but only revealed by pressure or shocks.
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RICKETS, OSTEOMALACIA CLINICAL FEATURES: Rickets - Tetany , convulsions, failure to thrive, restlessness, muscular flaccidity. Flattening of skull (craniotabes), Thickening of wrists from epiphyseal overgrowth, Stunted growth, Rickety rosary, spinal curvature, Coxa vara, bowing, # of long bones Osteomalacia, - Aches and pains, muscle weakness loss of height, stress #s.
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Manifestations of Osteomalacia Localized bone pain Difficulty walking Low back pain Fractures are common, and delayed healing occurs Muscular weakness Weight loss Progressive deformities of the spine (kyphosis)
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Kyphosis
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Rickets, clinical manifestations Skeletal findings: Delay in closure of the fontanelles. Parietal & frontal bossing. Craniotabes ( soft skull bones). Enlargement of the costochondral junction (rachitic rosary). The development of Harrison sulcus ( caused by pull of the diaphragmatic attachments to the lower ribs). Enlargement of the wrist & bowing of the distal radius & ulna. Progressive lateral bowing of the femur & tibia.
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RICKETS, OSTEOMALACIA XRAY FINDINGS: RICKETS Thickening and widening of physes, Cupping of metaphysis, Wide metaphysis, Bowing of diaphysis, Blurred trabeculae.
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RICKETS, OSTEOMALACIA XRAY FINDINGS: OSTEOMALACIA Loosers zones - incomplete stress # with healing lacking calcium, on compression side of long bones. Codfish vertebrae due to pressure of discs Trefoil pelvis, due to indentation of acetabulae stress #s
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Source Undetermined
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Source Undetermined
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Osteomalacia & Rickets – Clinical Manifestations Asymptomatic at onset Muscle weakness, especially of pelvic girdle Bone pain Atraumatic fractures X-rays assist in diagnosis
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Vitamin D Deficiency (cont’) Vitamin D deficiency can cause Osteoporosis Osteomalacia and Rickets
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Source Undetermined
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Extra skeletal findings in Rickets Extraskeletal manifestation of rickets vary depending upon the 1ry mineral deficiency. Hypoplasia of the dental enamel is typical for hypocalcemic rickets, whereas abscesses of the teeth occur more often in phosphopenic rickets. Hypocalcemic seizures, decreased muscle tone leading to delayed motor milestones, recurrent infections, increased sweating.
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RICKETS, OSTEOMALACIA INVESTIGATIONS: BLOOD TESTS Calcium Reduced, Phosphate reduced Alkalline Phosphatase increased Urinary excretion of calcium diminished Calcium phosphate products (= serum [Ca] x serum [PO4]) normally 30. In rickets and osteomalacia is less than 24
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Osteomalacia & Rickets - Diagnosis Other laboratory abnormalities may include Hypocalcemia Hypophosphatemia Elevated serum alkaline phosphatase
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Biochemical findings in rickets Alkaline phosphatase usually is ↑in all forms of rickets. Serum phosphorus concentrations usually are↓ in both hypocalcemic and hypophosphatemic rickets. Serum Ca is ↓only in hypocalcemic rickets. Serum parathyroid hormone typically is ↑in hypocalcemic rickets, in contrast it is N in hypophosphatemic rickets. 25-OH vitamin D reflect the amount of vitamin D stored in the body, and is ↓in vit D deficiency. 1,25-OH2 vitamin D can be↓, N or ↑in hypocalcemic rickets and usually is N or slightly ↑in hypophosphatemic rickets.
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Osteomalacia & Rickets - Diagnosis Bone biopsy is diagnostic Serum 25-hydroxycholecalciferol <50nmol/L indicates Vitamin D deficiency
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OSTEOMALACIA: EVALUATION Careful diet and sunlight history Renal function Fecal fat determination Anti IgA tissue transglutaminase antibodies. Small bowel biopsy
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RICKETS, OSTEOMALACIA MANAGEMENT: Depends on the cause Nutritional Vitamin D deficiency Dietary chelators of calcium Phytates Oxalates Phosphorus deficiency (unusual) Antacid abuse Treatment- vitamin D (50000u/w`/up to 3-12 w) and Calcium (1.5-2g/day)
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RICKETS, OSTEOMALACIA MANAGEMENT: Depends on the cause Gastro-intestinal absorption defects Post-gastrectomy Biliary disease Enteric absorption defects Short bowel syndrome Rapid onset (gluten-sensitive enteropathy) Inflammatory bowel disease Crohns Celiac
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RICKETS, OSTEOMALACIA MANAGEMENT: Depends on the cause Renal tubular defects Vitamin D dependant type I type II Treatment; High levels of vit D Vitamin D resistant (familial hypophosphatemic rickets) Treatment; Phosphate 1-3 gm daily, Vit D3 high dose Fanconi syndrome I, II, III Renal tubular acidosis
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Collaborative Care of Osteomalacia Correction of the vitamin D deficiency Vitamin D3 and vitamin D2 can be supplemented (patient shows dramatic response) Calcium salts or phosphorus supplements may also be prescribed Encourage dietary ingestion of eggs, low-fat milk, fish and vegetables Exposure to sunlight is valuable Encourage weight bearing exercises
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RICKETS, OSTEOMALACIA MANAGEMENT: Depends on the cause Renal Osteodystrophy – in chronic renal failure Miscellaneous Hypophosphatasia Anticonvulsant therapy SURGERY For deformities
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Vitamin D Deficiency - Treatment 50,000 IU of oral Vitamin D2, once or twice weekly for 6 – 12 w, followed by 1000 IU/day Appropriate exposure to sunlight Phosphate and Calcium replacement, if needed
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OSTEOMALACIA: ETIOLOGY Vitamin D deficiency or resistance Inadequate intake and sunlight Malabsorption Severe liver disease Renal failure Hereditary syndromes
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OSTEOMALACIA: ETIOLOGY Phosphate deficiency Renal tubular disorders Tumor associated osteomalacia X-linked hypophosphatemia Phosphate binders
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OSTEOMALACIA: ETIOLOGY Inhibitors of mineralization Aluminum Fluoride
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OSTEOMALACIA: CLINICAL MANIFESTATIONS Bone pain and pathologic fractures Decreased bone density Hypophosphatemia, increased alkaline phosphatase, and increased PTH
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OSTEOMALACIA: CLINICAL MANIFESTATIONS Late hypocalcemia Pseudofractures In children, bowing of the legs and rachitic rosary, short stature
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OSTEOMALACIA: DIAGNOSIS Low levels of 25-hydroxyvitamin D Elevated parathyroid hormone and alkaline phosphatase Bone biopsy
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Osteomalacia (adult bone disease) Vitamin D deficiency resulting in decalcification and softening of the bone Same as Ricketts in children
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Etiology (osteomalacia) Not enough vitamin D in the diet Not enough exposure to sunlight, which produces vitamin D in the body Malabsorption of vitamin D by the intestines
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Osteomalacia Clinical features? In child In adult Investign Ca/PO4 decr, alk ph incr, Ca excr decr Ca x PO4 <2.4 Bone biopsy
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Laboratory findings in Osteomalacia Decreased serum calcium levels Decreased serum phosphorus levels Elevated serum alkaline phosphatase Xrays show bone demineralization
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Laboratory findings in Osteomalacia Decreased serum calcium levels Decreased serum phosphorus levels Elevated serum alkaline phosphatase Xrays show bone demineralization
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Classification of metabolic bone disease 1.Calcium deficiency disease. Any factor that impairs intestinal calcium absorption, including deficient dietary intake, results in calcium deficiency 2.Phosphate deficiency disease. On the other hand, except for dietary phosphate depletion, phosphate deficiency is the result of inappropriate excessive renal excretion of this ion. 3. If these deficiencies are severe enough, both osteomalacia and rickets will result 4. Rickets is the disorder wherein chondrocytes do not undergo mineralization, & the provisional zone of calcification does not form.
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Hypocalcemic disorders of childhood Hypoparathyroidism ( post surgery, infiltration, idiopathic as congenital) Pseudohypoparathyroidism. Hypomagnesemia( impaired absorption, excess renal wasting, diarrhea). Vitamin D abnormalities( ↓intake, ↓sunlight exposure, ↓absorption, hepatocellular disorders, that impair 25(OH)D synthesis, ↓ production of calcitriol- renal disease or AR vit D- dependant rickets, End-organ unresponsiveness to calcitriol with rickets).
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Hypophosphatemic disorders of childhood Primary hypophosphatemic rickets. Oncogenous rickets with phosphaturia ( neurofibromatosis). Complex proximal tubulopathy ( Fanconi syndrome either 1ry or 2ry to Wilson’s tyrosinosis, galactosemia, fructose intolerance). 2ry to ↑ iPTH secretion ( vit D ↓rickets, vit D dependency rickets, rickets unresponsive to calcitriol with receptor defect, Fanconi with vit D ↓).
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Introduction Normal bone growth & mineralization require adequate availability of calcium & phosphate. Deficient mineralization can result in rickets and/or osteomalacia. Rickets refers to the changes caused by deficient mineralization at the growth plate. Osteomalacia refers to impaired mineralization of the bone matrix. Rickets & osteomalacia usually occur together as long as the growth plates are open; only osteomalacia occurs after the growth plates have fused.
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Rickets , introduction Mineralization defect are classified according to the mineral deficiency. Calcipenic rickets ( vit D↓, 1-alpha hydroxylase defect, vit D receptor dysfunction, dietary Ca ↓, CRF) . Phosphopenic ricket: Inadequate intake (Premature infants (rickets of prematurity) , Aluminum-containing antacids).
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Rickets, Etiology Deficient Intake: Ca, Ph, Vit D. Poor absorption: vit D ↓, pseudo vit D↓, vit D resistance, high phytin content( soy formula), antacids, anticonvulsants, renal insufficiency, Fanconi syndrome, hepatic insufficiency, fat malabsorption (cystic fibrosis). Increased excretion: furosemide, renal tubular dysfunction( phosphaturia, RTA with hypercalciuria), renal tubular damage e.g. cystinosis, tyrosinosis, galactosemia, fructose intolerance, wilson disease. Local effect on bone matrix: hypophosphatasia(alp↓)
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Causes of Rickets VITAMIN D DISORDERS Nutritional vitamin D deficiency; Congenital vitamin D deficiency; Secondary vitamin D deficiency; Malabsorption ; Increased degradation; Decreased liver 25-hydroxylase; Vitamin D-dependent rickets type 1; Vitamin D-dependent rickets type 2 ;Chronic renal failure. CALCIUM DEFICIENCY Low intake Diet Premature infants (rickets of prematurity) Malabsorption Primary disease Dietary inhibitors of calcium absorption PHOSPHORUS DEFICIENCY Inadequate intake Premature infants (rickets of prematurity) Aluminum-containing antacids RENAL LOSSES X-linked hypophosphatemic rickets; Autosomal dominant hypophosphatemic rickets; Hereditary hypophosphatemic rickets with hypercalciuria; Overproduction of phosphatonin ( Tumor-induced rickets, McCune-Albright syndrome’ Epidermal nevus syndrome, Neurofibromatosis) ,Fanconi syndrome, Dent disease DISTAL RENAL TUBULAR ACIDOSIS
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Rickets, clinical manifestations Skeletal findings: Delay in closure of the fontanelles. Parietal & frontal bossing. Craniotabes ( soft skull bones). Enlargement of the costochondral junction (rachitic rosary). The development of Harrison sulcus ( caused by pull of the diaphragmatic attachments to the lower ribs). Enlargement of the wrist & bowing of the distal radius & ulna. Progressive lateral bowing of the femur & tibia.
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Treatment of Rickets Vitamin D. stoss therapy: 300,000-600,000 iu orally or IM in 2-4 divided doses over one day. High dose vit D 2000-5000 iu orally for 4-6wks followed by 400iu daily orally as maintenance. Adequate dietary Calcium & phosphorus provided by milk, formula & other dairy products. Symptomatic hypocalcaemia need IV cacl as 20mg/kg or ca gluconate as 100mg/kg as a bolus, followed by oral calcium tapered over 2-6 weeks.
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Osteomalacia Disorder of mineralisation of newly formed bone matrix Vitamin D deficiency Hypophosphatemia (Fanconi syndrome, X-linked hypophosphatemic rickets) Bone matrix disorders (Fibrogenesis imperfecta, Hypophosphatasia) Aluminium
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Osteomalacia Skeletal pain, proximal muscle weakness X-ray – Looser’s zones Laboratory – low PO4-, (vitamin D deficiency: low Ca2+, increased alkaline phosphatase) Treat underlying deficiency
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Osteomalacia Skeletal pain, proximal muscle weakness X-ray – Looser’s zones Laboratory – low PO4-, (vitamin D deficiency: low Ca2+, increased alkaline phosphatase) Treat underlying deficiency
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Osteomalacia Definition? Rickets - growth plates affected, children Osteomalacia - incomplete mineralisation of osteoid, adults Types - vit D def, vit-D resist (fam hypophos) Aetiology? Decr intake/production(sun/diet/malabs) Decreased processing (liver/kidney) Increased excretion (kidney)
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Osteomalacia Types Vitamin D deficient Hypophosphataemic growth decr +++ and severe deformity with wide epiphyses x-linked dominant decreased tubular reabs of PO4 Ca normal but low PO4 Rx PO4 and vit D
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Osteomalacia vs osteoporosis Osteomal Osteopor Ageing fem, #, decreased bone dens Ill Not ill General ache Asympt till # Weak muscles normal Loosers nil Alk ph incr normal PO4 decr normal Ca x PO4 <2.4 Ca x PO4 >2.4
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What are osteomalacia / Rickets Osteomalacia Disorder of mature bone in which mineralisation of new osteoid bone is inadequate or delayed Rickets Disease of growing bones in which defective mineralisation occurs in both bone and cartilage of epiphyseal growth plate, associated with: Growth retardation Skeletal deformities
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Rickets The primary pathology is defective mineralisation of bone matrix The primary bone matrix mineral = hydroxyapatite = Ca10(Po4)6(OH)2 Any disease that limit the availability of calcium or phosphate will lead to rickets 2 main categories Hypocalcaemia rickets Disorders of vitamin D metabolism or action Hypophosphatemic rickets Disorders of phosphate metabolism
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Causes Nutritional: commonest cause in the developing countries Malabsorption Drugs that increases metabolism of vitamin D in the liver Chronic liver disease Renal rickets Chronic renal failure RTA Hereditary rickets Vitamin D dependent rickets ( Type 1& 2) Vitamin D resistant rickets
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Celiac disease Pancreatic insufficiency Cystic fibrosis Hepato-biliary disease Biliary Artesia Cirrhosis neonatal hepatitis Drugs Anti-convulsants Phenobartbitone Phenytoin Diet Excess of phytate in diet with impaired calcium absorption (chapati flour)
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Chronic liver disease Cirrhosis reduces 25-hydroxylation of vitamin D Biliary obstruction: prevents absorption of fat soluble vit D Interrupts its enterohepatic circulation
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Chronic renal failure Reduces 1  hydroxylation of 25 hydroxy vitamin D leads to low concentration of 1,25-di hydroxy vitamin D Consequently impair calcium absorption from the gut Renal osteodystrophy Osteitis fibrosa cystica due to long standing secondary hyperparathyroidism When GFR falls below 30 ml/min/1.73m2 Impaired growth Osteitis fibrosa results Sub-periosteal resorption at middle and distal phalanges Bone pain Muscle weakness
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Hereditary Rickets Hypophosphatemic rickets (Vit D resistant) Vitamin D dependent rickets
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Vitamin D dependent rickets Type 1 Rare, autosomal recessive Lack of 1  hydroxylase enzyme Clinically and Biochemically similar to nutritional rickets except it appears early at 3-4 months Type 2 Rare autosomal recessive disorder 1  hydroxylase enzyme is present Lack of Calcitriol receptors Common in Arabs Baldness Severely affected individuals Unresponsive to treatment
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Hypophosphatemic rickets Nutritional phosphate deficiency Prematurity Decreased intestinal absorption of phosphate Ingestion of phosphate binders (aluminum hydroxide) Renal phosphate wasting RTA Vitamin D resistant rickets Tumor induced osteomalacia (oncogenic osteomalacia)
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Hypophosphatemic Rickets X-linked dominant / Autosomal dominant Males affected more than females Commonest inherited form of rickets Prevalence 1: 25000 Phosphate wasting by renal tubules leads to: Low serum phosphate Normal calcium In-appropriate low or normal 1,25-di hydroxy vitamin D phosphate is the major stimulus for 1 hydroxylase Severe rickets and short stature by 1-2 years
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Clinical features The earliest sign of rickets in infant is craniotabes (abnormal softness of skull) Delayed closure of anterior fontanel Widening of the forearm at the wrist (widened metaphysis= area between epiphysis and diaphysis) Rachitic rosary Swelling of the costo-chondral junction Harrison’s groove Lateral indentation of the chest wall at the site of attachment of diaphragm Bowing of tibia and fibula may be observed at any age Growth retardation due to impaired calcification of bone epiphysis (epiphysis= area of growth plates) Hypocalcaemic manifestations hypotonia Seizure, tetany,muscle weakness, paraesthesia, numbness
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Biochemical findings of rickets Vitamin D deficiency rickets Low- normal serum calcium level Increased secretion of PTH (secondary hyperparathyroidism) to compensate for low calcium Hyperparathyroidism will increase renal excretion of phosphate, leads to low serum phosphate level Elevated alkaline phosphatase enzyme Reduced urinary calcium level Low level of both 25 and 1,25- di hydroxy vitamin D Elevated parathyroid hormone level
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Biochemical findings of rickets Hypophosphatemic rickets Low serum phosphate level Normal calcium level Normal parathyroid hormone level High alkaline phosphatase level In-appropriate low or normal 1,25-di hydroxy vitamin D phosphate is the major stimulus for 1 hydroxylase
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Radiological findings of rickets Generalized osteopenia Widening of the unmineralised epiphyseal growth plates Fraying of metaphysis of long bones Bowing of legs Pseudo-fractures (also called loozer zone) Transverse radio lucent band, usually perpendicular to bone surface Complete fractures Features of long standing secondary hyperparathyroidism (Osteitis fibrosa cystica) Sub-periosteal resorption of phalanges Presence of bony cyst (brown Tumor)
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Therapy Administration of vitamin D preparation Vit D2 = ergocalciferol 25-hydroxy vitamin D = calcifedol 1 hydroxy vitamin D = one alpha 1, 25 Di hydroxy Vitamin D = Calcitriol Calcium supplement initially in severe disease To avoid hungry bone hypocalcaemia Phosphate supplements in Hypophosphatemic rickets
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Osteomalacia Osteomalacia is the general term for the softening of the bones due to defective bone mineralization. Osteomalacia in children is known as rickets, and because of this, osteomalacia is often restricted to the milder, adult form of the disease. It may show signs as diffuse body pains, muscle weakness, and fragility of the bones.
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General characteristics Osteomalacia is derived from Greek: osteo refers to bone, and malacia means softness. Osteomalacia in the adult is most commonly found in confined, dark-skinned, or diet-disbalanced subjects. Many of the effects of the disease overlap with the more common osteoporosis, but the two diseases are significantly different. Osteomalacia is specifically a defect in mineralization of the protein framework known as osteoid. This defective mineralization is mainly caused by lack in vitamin D.
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Physiology Serum Ca & Phosphate in equilibrium with Ca , Phosphate in bone. There is relation:.( Ca X Phosphate) =constant product. Important of this relation to keeping Ca , Phosphate cross product constant. So, more ppt. in vascular system or soft tissue, there is no metastasis calcification.
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PATHO PHYSIOLOGY
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PATHO PHYSIOLOGY
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Treatment Nutritional osteomalacia responds well to administration of 200,000 IU weekly of vitamin D for 4 to 6 weeks, followed by a maintenance dose of 1600 IU daily or 200,000 IU every 4 to 6 months. Natural sources cheese, sardines, salmon, dark leafy vegetables & sesame seeds.