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The palatal forms in 20 infants with a complete unilateral cleft lip, and palate (12 with a Hotz plate and 8 without, selected at random) were studied from birth until 18 months of age. Using techniques developed previously, the degree of curvature In the palate and the magnitude of migration of the maxillary segments were measured three-dimensionally. Furthermore, using a newly developed method to approximate a set of the points on the alveolar ridge to a circle in a plane, the form of the alveolar arch was evaluated. Results from the group with a Hotz plate revealed that the plate possesses four effects not seen in the group without a Hotz plate. The size of the palate was larger, and the sagittal gap between the two segments of the maxilla was smaller. These results suggest that the appliance could stimulate the growth of the segments and could prevent collapse of the maxillary arch from the force of lip closure. Third, the steepness of the segments toward the nasal cavity was smaller, possibly occurring because the appliance prevents tongue intrusion into the cleft. Fourth, the magnitude of migration of the lesser segment toward the cleft edge of the major segment was larger. This result suggests that the appliance could guide the growth of the maxillary segments to narrow the cleft width until 18 months of age.

A fourth patient suspected of having Pai syndrome is described. The female baby had a median cleft of the upper lip, a polypoid skin mass in the right nostril, and a conjunctival lipoma in the right eye. A median alveolar cleft was in the oral cavity. The polypoid skin mass was attached to the nasal septum, and a histologic examination disclosed mature adipose tissue with normal skin and no cartilaginous tissue. A computed tomographic scan revealed a lipoma of the corpus callosum. However, the patient was neurologically normal, and her electroencephalogram was also normal. Her growth and development have been within normal limits, and no convulsions have occurred.

There have been a number of reports over the last 15 years of patients with cancer who develop both leukocytosis and hypercalcemia, particularly in patients with cancers of the oral cavity. In this study, the authors report the frequency of hypercalcemia and leukocytosis in 225 patients with oral malignancies. Ten patients (4.4%) had hypercalcemia, 11 patients (4.9%) had leukocytosis, and five (2.2%) had both hypercalcemia and leukocytosis. The occurrence of these two distinct paraneoplastic syndromes in the same patients was greater than could have been expected from chance alone (chi-square = 45.8, P less than 0.0001). This study demonstrates that although hypercalcemia and leukocytosis are relatively uncommon in oral cancers, when they do occur they are frequently associated. To the knowledge of the authors, this is the first report in which the frequency of the association hypercalcemia and leukocytosis is studied in detail in large numbers of patients with oral cancer.

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Summary Invasive potentials of malignant cancer cells are regulated by cell motility factors. To examine the regulation of motility and invasiveness in oral squamous carcinoma, we investigated autocrine-and/or paracrine-acting cell motility factors, using a newly established human cell line (IF cells) from oral squamous cell carcinoma, which has highly invasive and metastatic characteristics. Conditioned medium derived from IF cells stimulated cell scattering and migration of GB-d1 gallbladder carcinoma cells, indicating that IF cells secreted cell motility factors. Using antibodies, IF-derived cell motility factors proved to be transforming growth factor (TGF)-α and TGF-β1. Antibodies against TGF-α and TGF-β1 inhibited autonomous migration of the IF cells. On the other hand, in vitro invasion of IF cells was strongly enhanced by hepatocyte growth factor (HGF) but only slightly by TGF-α and TGF-β1. The conditioned medium from fibroblasts enhanced in vitro invasion of IF cells, an event abrogated by anti-HGF antibody, but not by antibodies against TGF-α and TGF-β1. Importantly, IF cells secreted a factor inducing HGF production in fibroblasts and the factor was identified as interleukin-1, which means that a mutual interaction exists between tumour cells and fibroblasts, as mediated by the HGF/HGF-inducer loop. These results indicate that IF cells utilize TGF-α and TGF-β1 as autocrine-acting motility factors and HGF as a paracrine-acting motility factor, and that invasiveness of IF cells is particularly stimulated by HGF derived from stromal fibroblasts. Utilization of multiple cell motility/invasion factors that act in distinct pathways may confer highly invasive and metastatic potentials in IF oral squamous carcinoma cells.