Bone infarction

Myocardial ischemic bone death refers to the cellular elements of bone and marrow. Today the term is used and osteonecrosis.Bone infarction generally refers to lesions that occur in metaphysics and the bone shaft. Necrosa lesions are called avascular epiphysis.Osteonecrosis can be idiopathic or secondary to a number of conditions that reduce the intake of blood to the bone, such conditions include abnormal intraluminal, extrinsic compression or a combination of both. Tomographic scans, bone scans magnetic resonance plays an important role in diagnosing disease at an early stage and thus reduce the severity of complications and associated morbidity.
The clinical picture of heart disease in bone depends on the stage and location. Patients with medullary infarcts are usually asymptomatic. If present, symptoms are nonspecific in early stages of the disease. Patients with juxta-articular lesions shows instability. Localized pain is the most common symptom of heart attack and the juxta-articular bone marrow. These shows joint pain and limiting movement. Untreated affected bone will disintegrate with increasing pain and disability.
Several measures are available nonchirurgicale to treat symptoms caused by osteonecrosis. It manages or other anti-inflammatory analgesic, decrease physical activity and stress, we recommend a special physical therapy to relieve symptoms. These measures are indicated for the treatment of shoulder damage, small areas of osteonecrosis of the knee and thigh. Treatments and surgical options include vascularized bone grafting or nonvascularizat, prosthesis, rotational osteotomy, joint fusion, total arthroplasty.
Pathogenesis of bone infarction
Ischemic cell death and necrosis are the result of reducing intake of blood to the bone by a bone abnormality vasculaturii intrinsic, extrinsic abnormality or a combination. Rapidity of cell death depends on cell type and the degree and duration anoxiei.Hematopoietic cells are sensitive to anoxia and are the first to die in 12 hours. Osteocite composed of bone cells, osteoblasts and osteoclasts die within 12-48 hours and adipoasele marrow in 5 days. Death does not affect bone radiographic opacity.Osteoporotic bone is living as a result of osteoclastic resorption by hyperemia. Dead bone resorption and therefore do not suffer appears opaque.
Ischemic bone repair:It occurs in two phases. First, when the dead bone support bone marrow, the capillaries and undifferentiated mesenchymal cells alive, while dead cells, macrophages degrade. Second, mesenchymal cells differentiate into osteoblasts or fibroblasts. In favorable conditions, new bone is formed on the surface layers of dead bone trabeculelor.Histologically dead bone marrow is yellow with calcium deposits.The area of ​​necrosis is surrounded by a gray capsule collagen.Granulation tissue or collagen vascular gray dead bone separates the living dead. Trabecular fractures occur in dead bone just below the subchondral plate. Later cracks and wrinkles on the edge of the articular cartilage backlash, followed by fractures that lead to structure collapse.
Causes of osteonecrosis include:-Trauma, renal transplantation, Cushing's syndromeLupus erythematosus, rheumatoid arthritis, scleroderma, collagen vascular disease-Thalassemia or sickle cell hemoglobinopathies,-Hemoflia, Fabry disease, Gaucher infection-Pancreatitis, pregnancy, gout and hyperuricemia-Diabetes, alcohol abuse, radiation.