Osteomalacia is the term used to describe the mineralization of bone softening of the bones TROUBLE. Osteomalacia in children is known as rickets. The term osteomalacia is used only moderate form of the adult. Osteomalacia is most often found in people with dietary imbalances, with dark skin. Many of the effects of this disease overlap with those of osteoporosis, but the two entities are significantly different. Osteomalacia is primarily a protein-osteoid mineralization defect, caused mainly by lack viteminei D.
Osteomalacia causes vary: insufficient exposure to sunlight, insufficient amounts of vitamin D supply, malnutrition during pregnancy, renal tubular acidosis, malabsorption syndromes, tumor-induced osteomalacia. Osteomalacia in adults begins insidiously with cramps and pain in the lumbar region and thighs, extending the arms and ribs. Pain does not radiate, accompanied by sensitivity is symmetric and bones involved. Proximal muscles are weak, who presented a difficulty in climbing stairs and lifting the pelvic position. By etching the bones become less rigid, physical signs including deformations and triradiar pelvis and lordosis. The patient has a "roll" characteristic. However, these symptoms may be the result of a previous episode of osteomalacia, because bones no longer regain its original shape after deformation. It develops pathological fractures. Most often the symptom is accused muscle fatigue and cramps caused by pressure or mechanical shock.
Clinical osteomalacia is a moderate form of rickets. Affected patients may present moderate bone pain and tenderness with weakness. Severely affected patients have difficulty in ambulatiei and waddle. Syndrome "milkman" is a condition in which the patient shows bilateral and symmetrical multiple fractures.Common localizations include the femoral neck, axillary side of the scapula, ribs and pubic ram. Skeletal deformities may occur in the corpus vertebral and basilar skull with intussusception, with fractures of the vertebrae and long bones.
Renal osteodystrophy is a consequence of osteomalacia which shows weakness, bone pain and skeletal deformities. Clinic varies with age. adults may present evidence of osteomalacia, while children show retardation of growth. The most common complication of renal osteodystrophy is insufficient or pathological fracture through the depositaries of amyloid or tumors.Treatment for osteomalacia depends on the underlying cause of disease and includes pain control and orthopedic surgery, when indicated. Health surveillance of renal osteodystrophy include maintaining normal serum calcium and phosphorus, vitamin D and phosphate therapy, reducing excessive exposure to aluminum and iron or aluminum chelation treatments to reduce toxicity.Nutritional Osteomalacia administration responds well to a 10.000UI of vitamin D weekly for 4-6 weeks. Osteomalacia in malabsorption requiring parenteral treatment or daily dose.
Osteomalacia - PathogenesisVitamin D metabolism in the body:Vitamin D is a prohormone. It can be synthesized in the skin in response to exposure to sunlight or ultraviolet obtained from specific diet. Dietary sources of vitamin D: oily fish, egg whites only supplements a part of daily needs, such sun exposure is necessary to maintain adequate vitamin D levels in people under 70 years, even limited exposure to sunlight is adequate though after 70 years in the skin convert the hormone is less effective at predisppozind deficiency.Once formed in the skin or ingested vitamin D is hydroxylated in the icat to 25-hydroxyvitamin D, calcidiol, which is normally present in high concentrations in traffic and connected by a transport protein. Final activation of vitamin D to active hormone 1, 25-hydroxyvitamin D, calcitriol occurs in the kidney. Vitamin D stimulates the active absorption of calcium and phosphorus in the intestine favoring bone mineralization.Resorption of bone in osteomalacia:It is classified as subchondral, trabecular, endosteal, intracorticala, subperiosteala, and subtendinoasa subligamentoasa. Effect on the hands and feet is typical subperiosteala resorption along the edges and middle phalanges of the radial cortical bone on the distal phalanges. Subperiosteala resorption resembles joint marginal erosions of rheumatoid arthritis. Trabecular resorption of the skull is affected by forming one aspect of bone calvarine salt and pepper.Subtendinoasa subligamentara resorption and appears in ligementele coracoclaviculare clavicle, the calcaneal attachment of the plantar aponeurosis, the triceps insertion on the olecranon, humerus tuberosity, femoral trochanter and the tuberosity ischiadic.Subchondral bone resorption occurs in the distal clavicle, sacroiliac joints and pubic symphysis.
Causes and risk factors for osteomalaciaOsteomalacia causes may include:-Insufficient exposure to sunlight, the dark peopleFood-insufficient amounts of vitamin D deficiency or vitamin D metabolism and phosphorusRenal tubular acidosis,-Malnutrition during pregnancy-Malabsorption syndromes-Chronic renal failureTumor-induced osteomalaciaFumaderm-therapy, anticonvulsantsVegetarian-only diet, people over 65 years-Chronic liver disease, lack of phosphate in the dietCeliac-disease.
Osteomalacia result from moderate or severe deficiency of vitamin D-deficient patients usually present with moderate or slight osteoporosis. Vitamin D deficiency may be caused by inadequate synthesis of vitamin in the skin by sun exposure limited to patients with darker skin or living at northern latitudes. Impaired intestinal absorption of the old vitamin in the diet with fat malabsorption or hypothyroidism may also contribute to osteomalacia. Damage occurs in the liver vitamin hidroxilarii apcientii with severe liver disease and those who have drugs that affect hepatic hydroxylation: anticonvulsants-phenytoin, barbiturates, carbamazepine. Hidroxilarii renal impairment occurs in kidney failure.Causes hypocalcemia:Vitamin D deficiency lead to hypocalcemia, which stimulates parathyroid hormone in hyperparathyroidism. Hyperparathyroidism cause increased bone resorption and decreased urinary excretion of calcium. On the other hand, PTH increases urinary excretion of phosphorus which combined with low intestinal absorption cause hypophosphatemia.Causes of hypophosphataemia:Cause phosphate deficiency osteomalacia by affecting bone mineralization. Hypophosphatemia occurs rarely but appears inadequate aliemntar by contribution by malabsorption or vitamin D intake can result hypophosphatemia large amounts of aluminum hydroxide. A form of hypophosphatemia with osteomalacia, the oncogene is associated with neoplasia or mesenchymal tunorile.Osteomalacia induced by aluminum:Aluminum-induced bone disease is a cause of osteomalacia.Aluminium negatively affects bone formation through inhibition of osteoblast activity, and the formation of hydroxyapatite crystals.Aluminum can be inserted through the dialysis solution, binding agents, antacids or aluminum phosphate used to combat hyperphosphataemia in renal failure.
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