T. Matsuya

Immunohistochemical localization of epidermal growth factor (EGF) and EGF receptor in human oral mucosa and its malignancy.

The immunohistochemical localizations of human epidermal growth factor (hEGF) and EGF receptor (EGFr) in oral tissues, including normal mucosa, leukoplakia and squamous cell carcinoma were examined by the use of monoclonal antibodies to hEGF and EGFr. In normal mucosa and leukoplakia, immunostaining of hEGF was limited to an underlying layer of connective tissue near the epithelium. The intensity of extracellular staining appeared to increase with the degree of epithelial malignancy and was eventually most striking in the stroma of invasive carcinoma. The epithelial cells in normal mucosa, leukoplakia, and squamous cell carcinoma showed negligible immunoreactivity for hEGF. Expression of EGFr appeared to be associated with the proliferative activity of cells and/or epithelial malignancy. In normal mucosa, anti-EGFr monoclonal antibody reacted only with the basal cell layer. In all sections of leukoplakia, the positive cells for EGFr were found in the prickle cell layer in addition to the basal cell layer. Most tumour cells in squamous cell carcinoma were strongly positive for EGFr. These findings indicate increased expression of hEGF and EGFr with malignancy. The characteristic localization of extracellular hEGF in the underlying connective tissue and in stroma of oral mucosal tumours suggests a possible epithelial-mesenchymal interaction in hEGF secretion.

Infiltrating lipoma of the tongue

A case of an infiltrating lipoma, occurring in the tongue of a 56-year-old Japanese woman, is presented. The relevant literature is discussed.

Measurement of Velopharyngeal Movements Induced by Isolated Stimulation of Levator Veli Palatini and Pharyngeal Constrictor Muscles

The levator veli palatini (LVP) and superior pharyngeal constrictor muscles (PC) close the velopharynx. However, for the velopharyngeal movements to be understood in detail, each muscle contraction must be analyzed precisely. This study was performed to clarify the velopharyngeal movement which was induced by a single muscle contraction, LVP or PC. Using a nasopharyngeal fiberscope, we analyzed the velopharyngeal movement associated with the contraction of the LVP and PC muscles in mongrel dogs. To elicit the maximal contraction of each muscle, we applied repetitive electrical stimulation to each peripheral nerve efferent to the LVP or PC muscle. Stimulation with a frequency of 77 Hz and 83 Hz induced maximal tension in the LVP and PC muscles, respectively, in isometric contraction. In a second series of experiments, fiberscopic views of the velopharyngeal movements associated with each muscles maximal contraction were recorded. The degree of closure was calculated at several sections. The LVP muscle pulled the caudal fourth of the soft palate, while the PC projected the posterior wall at the level of the caudal end of the soft palate. The PC muscle also projected the lateral wall of the velopharynx. The effect of LVP contraction on the lateral wall was very small. These results show that the velopharyngeal movement associated with LVP contraction is very different from that with PC contraction.

Effect of Lung Inflation on Levator Veli Palatini Muscle Activity

Palatal movements play a critical role in regulating oropharyngeal airflow during breathing. We hypothesized that these movements are coordinated with breathing movements via afferent signals from the lung. However, the control of palatal movements in relation to the lung remains unclear. This study was designed to define, by electromyographic techniques, the relationship between palatal movement and lung action during respiration. We performed tracheotomies on 12 mongrel dogs anesthetized with sodium pentobarbital and found that lung inflation augmented the activity of the levator veli palatini muscle (LVP). Two kinds of discharges were recognized during the expiratory pause following lung inflation. One was a continuous, low-amplitude discharge induced during apnea following lung inflation. The other was a transient, high-amplitude discharge which appeared immediately after lung inflation. Both of these response activities were eliminated by bilateral vagotomy. We thus concluded that palatal movements, which can regulate expiratory airflow resistance and cause switching from nasal to oral airflow, are under the control of vagal afferent signals from the lung.