Occult osteochondral lesions after anterior cruciate ligament rupture. Six-year magnetic resonance imaging follow-up study.

Twenty-three patients with acute anterior cruciate ligament injuries, normal radiographs, and occult osteochondral lesions revealed by magnetic resonance imaging were reviewed 6 years after initial injury and anterior cruciate ligament hamstring autograft reconstruction. Each patient completed the Mohtadi Quality of Life outcome measure for anterior cruciate ligament deficiency, underwent clinical examination, and had a repeat magnetic resonance imaging scan. The index and follow-up magnetic resonance imaging scans were compared with respect to cartilage thinning and marrow signal. A significant number of patients had evidence of cartilage thinning adjacent to the site of the initial osteochondral lesion. Marrow signal changes persisted in 15 (65%) of the patients. Clinical comparison of patients with normal cartilage with those who had cartilage thinning revealed similar results on both KT-1000 arthrometry and on the Mohtadi outcome measure. This suggests that the initial injury resulted in irreversible changes in the knee. Injuries causing marrow signal changes may result in an alteration in the load-bearing properties of subchondral bone, which in turn allow for changes in the overlying cartilage. Further follow-up will determine the clinical significance of changes detected by magnetic resonance imaging.

Cellular immunity to a lung homogenate in asymptomatic cigarette smokers.

Leucocyte migration in the presence and absence of a soluble lung homogenate has been studied in a group of asymptomatic cigarette smokers. Results were expressed as migration indices. Controls consisted of age-matched subjects who had never smoked and had no past history of any pulmonary disease. The migration indices, the number of pack-years smoked and the results of pulmonary function studies were tested for correlation. The mean leucocyte migration index of the test group of sixteen smokers was significantly less than was that of the control group (P less than 0.001). Inhibition of leucocyte migration in the presence of the lung homogenate was not observed in any of the control subjects. Six of the sixteen asymptomatic cigarette smokers, however, were identified by inhibition of leucocyte migration in the presence of the lung homogenate. The number of pack-years which had been smoked did not correlate with the migration indices (r = -0.06); however, inhibition of leucocyte migration was not observed in subjects who had smoked less than 6 pack-years.