st expansion and the ability to effectively breath deeply and cough (Loeb, 755). Patients are also more susceptible to infection.In assessing a patient data is needed about the genetic history and birth of the child, as well as a complete development assessment from birth. Vital signs are taken, and periods of increased heart and respiratory rate and elevated body temperature are noteworthy. Skin should be examined for color, elasticity, translucency, and signs of edema and bruising. A description of position and appearance of a child's trunk and extremities and facial characteristics should be noted. The height of the child in terms of expected growth, signs of scoliosis or laxity of ligaments and range of motion of the joints are all important. Sight and hearing should be tested since there are sensory problems associated with OI. The appearance of the sclerae and tympanic membranes and defects of primary teeth and gums are important (Jackson, 1699). X-rays usually reveal a decrease in bone density. "There is no consensus, however, as to whether the diagnosis can be made by microscopy of bone specimens." (Isselbacher, 2112) DNA sequencing and incubating skin fiboblasts are two ways help diagnose OI. Prenatal ultrasonography is used to detect severely affected fetuses at about 16 weeks of pregnancy. Diagnosis of the lethal type II by ultrasound during the second trimester of pregnancy is by the identification of fractures of the long bones. Compression of the fetal head is seen by ultrasound probe, and low echogeneity of the cranium can be signs of skeletal dysplasia (faulty development of the tissues). Diagnosis is confirmed by postmortem examination including biochemical studies of cultivated fibroblasts from the fetus (Berge, 321). Diagnosis by analyzing DNA sequencing can be carried out in chronic villa biopsies at 8-12 weeks. There is no known treatment of OI at this time. Treatment therefore is predominantly supportive and e...