We aimed to assess whether patients with hemifacial microsomia can be quantitatively identified using bone mineral density information. Mandibular bone mineral density was studied using computer assisted analysis between the nonaffected (r) and the affected (l) sides with an orthopantomograph in a patient with hemifacial microsomia with median mandibular cleft, and four patients who suffered from hemifacial microsomia in the left side. Fifty controls without bone diseases were randomly selected. Bone mineral density r/l ratios in the controls ranged from 0.479 to 2.064, and those in two patients that were associated with and without median mandibular cleft were higher than those in the controls, with a maximum of 8.622 in a particular male with median mandibular cleft after bone graft, whereas the r/l ratios in the other three cases were similar to the controls. Our findings indicate that the quantitative character in the case with median mandibular cleft reveals a large discrepancy of bone mineral density between the nonaffected and the affected sides. This may suggest a compensatory mechanism for bone hypertrophy from regulated bone mineral density with underdevelopment in hemifacial microsomia.

The aim of the present study was to clarify whether ATP binding cassette transporters are refractory factors in head and neck cancer chemotherapy. For in vitro and in vivo chemotherapeutic studies, we employed a human salivary gland adenocarcinoma cell line (HSY) and a human oral squamous cell carcinoma cell line (SCCSK) with vincristine (VCR) at clinically equivalent doses. Western blot analysis, reverse transcription-polymerase chain reaction, in vivo evaluation in xenograft models inoculated with cultured carcinoma cell line and drug efflux analysis were performed. VCR-treated SCCSK and HSY cells, as well as xenografted SCCSK and HSY cells in tumor-bearing nude mice, were found to express MDR1/ABCB1 and MRP1/ ABCC1. In addition to MDR1 and MRP1 mRNA, HSY/VCR and its cloned cells expressed MRP7/ABCC10 mRNA, but SCCSK/VCR did not express MRP7. Furthermore, drug resistance to VCR and docetaxel decreased in HSY/VCR in the presence of a competitive MRP7 inhibitor, 17-beta-estradiol-(17-beta-D-glucuronide). These results indicate that MDR1 and MRP1 expression are refractory factors in head and neck cancer chemotherapy and suggest that induction of MRP7 expression is involved in drug resistance in salivary gland adenocarcinomas.