Paget's disease of bone Diagnosis

Paget's disease of bone

    * Introduction
    * Pathogenesis and causes
    * Signs and symptoms
    * Diagnosis
    * Treatment

Diagnosis
Laboratory studies: Alkaline phosphatase isoenzyme-analysis helps to identify the total level of liver alkaline phosphatase Monostotic-disease patients with alkaline phosphatase levels may be normal Urinary hydroxyproline-level is high because it reflects increased osteoclast activity and bone resorption, hydroxyproline is a collagen destruction Telopeptidul and alpha-N-C-telopeptidul are sensitive markers for bone resorption Total serum acid-phosphatase enzyme is an increased osteoclast in Paget's disease but little clinical value Serum-calcium and phosphate are normal -Normal urinary excretion of calcium -Hypercalcemia and hypercalciuria develops in patients with hyperparathyroidism associated or immobilized -Secondary hyperparathyroidism occurs in 15% of patients with Paget's disease with increased calcium intake from low demand -IN-terminal peptide procolagenic is a new sensitive marker for bone formation.
Imaging studies. Include as elements of X-rays: In the skull, lithic stage frontal and occipital bones are affected and mixed model with seals progressing multifocal sclerotic disease in the intermediate stage of wadded-looking. Vertebral corpora become prominent cortical edge marry or become densely sclerotic mimind lymphoma or metastatic disease, ivory vertebra. Thickening in the pelvis include the items described in the early stages iliopectineale line, focal sclerosis and progressive to shine in the late stages. Weakening of the bone leading to protrusion of the acetabulum and acetabular fracture failure. In early impairment of long bones consists subarticular bone lysis, which advances along the shaft with the characteristic appearance of the grass strips. Long bones are affected first in the epiphyseal region, except where the disease begins tibia tubercle. Advanced stages of development of bone disease show deformed large sclerotic with thin trabeculae. Weakened femur and tibia are bent under the weight stress. Insufficiency fractures occur involving convex cortical surface characteristic. Osteomalacia occurs in concave surfaces.
Computed tomography evaluates the development of Paget's sarcomas and bone deformities characteristic. Radionuclide bone scintigraphy with more sensitive X-ray scans. It shows a high absorption of the radionuclide in the affected and circumscribed osteoporosis. scintigraphy follow disease activity and response to treatment. Polyostotic Paget's disease of bone metastases can be distinguished.
Histological examination. Initial osteolytic phase is marked by areas of bone resorption with increased number of osteoclasts. These abnormal osteoclasts contain up to 100 nuclei. Phase abnormal osteoblastic bone formation secondary look porous. Repeated episodes of bone formation of bone fragments have the appearance of irregular, abnormally arranged as a mosaic. Paget's bone is fibrous, avid for calcium and phosphorus. Marrow space is filled with vascularized connective tissue. Paget's bone or haversian centralization model shows no vascularization. The new bone is poorly mineralized and no structural integrity. The differential diagnosis is made with the following conditions: osteomalacia, aosteoartrita, bone metastases, osteoporosis.