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We reviewed serial radiographs of 22 hips in 20 patients with developmental dislocation of the hip (DDH), who were treated by open reduction and followed without additional surgery until puberty, to identify predictive measures of subsequent acetabular development. The average age at surgery and at final follow-up was 14 (5-26) months and 15 (13-20) years, respectively. Hips with a CE angle above 20 degrees and femoral head coverage above 75 degrees at the final follow-up were classified as "satisfactory outcome". At the final follow-up, 14 hips were classified as satisfactory and 8 hips as unsatisfactory. In the former group, acetabular improvement continued throughout growth, whereas in the unsatisfactory group, the acetabulum did not improve after 3-5 years of age. Unsatisfactory condition at the final follow-up was noted in all hips that had a CE angle less than 0 degrees and head coverage less than 50%, when the patients were 3-5 years old and less than 5 degrees and 60%, respectively, at the age of 6-8 years. These findings should be useful in assessing the need for and the timing of acetabuloplasty after open reduction for DDH.

We examined the intracellular mechanisms of substance P induced oxyradical production in rheumatoid synovial cells by the luminol-dependent chemiluminescence method. After stimulation with substance P (30 microM), single synovial A (macrophage-like) or B (fibroblast-like) cells released oxyradicals such as superoxide anions (O2-) and/or hypochlorous anions (OCl-) under a microscope equipped with an ultrasensitive photonic image intensifier. The substance P induced oxyradical production was blocked by a tachykinin NK1 (NK1) receptor antagonist, GR82334, GTP-binding protein (G-protein) inactivators, GDP beta S and islet-activating protein (IAP), and a phospholipase C (PLC) inhibitor, U-73122. Substance P (30 microM) also induced a transient increase in the intracellular Ca2+ concentration ([Ca2+]i) in both synovial A and B cells as measured by a Ca2+ indicator, fura 2, BAPTA-AM and an inositol-1,4-5-triphosphate (IP3) receptor antagonist, heparin, inhibited the substance P induced increase in [Ca2+]i, but they had no effects on oxyradical production. In contrast to the effects of BAPTA-AM and heparin, protein kinase C (PKC) inhibitors, H-7 and calphostin C, completely inhibited substance P induced oxyradical production without any significant effects on [Ca2+]i increase. These findings suggest that the NK1 receptor/PLC-linked diacylglycerol (DAG) formation with the resulting activation of PKC is the main signal transduction pathway for substance P stimulated oxyradical production in synovial cells.

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