MORPHOLOGICAL STUDIES OF THE OESOPHAGUS

Abstract

F26 Oesophagitis is a common diagnosis in childhood, yet oesophageal structure is poorly studied. The aim was to establish the pattern of normal epithelial development and to ascertain how this changed in pathological conditions. Oesophageal appearance was studied in normal (n= 12, 7M:5F; median age 75 months, range 10-148 Mo) and abnormal (n=19; 14M:5F; median age 48 months, range 3-223 Mo) endoscopic biopsies, as defined by routine histological evaluation of H&E stained sections. Samples were studied using "Per-iodic acid Schiff" staining, quantitative morphometry, electron microscopy, and glycosaminoglycan [GAG] staining. Proceeding from basal to functional layers - in the normal specimens the basal cell layer was thin and mitoses were rarely seen. Lower prickle cells increased in size and desmosomal junctions became more complex and organised. Upper prickle cells grew further, glycogen deposition occurred, and membrane coating granules were seen. Mitochoiidria were few in number and rough endoplasmic reticulum was scanty. Cell size decreased in the functional layer where desmosomes were reduced in frequency and tonofilaments were increased. In the abnormal samples absolute and relative basal cell hyperplasia and increased papillary length were seen; mitotic figures were observed in several basal cell layers, cell growth was significantly reduced, glycogen deposition and membrane coating granules were not so noticeable, and desmosomal junctions were less complex. GAG staining showed peripheral membrane staining in prickle cells in controls and a variable increase in cytoplasmic and nuclear staining of basal and prickle cells in abnormal samples. Thus, changes in cell growth and organelle content can be identified as epithelial cells develop in histologically normal controls. The organelle pattern suggests a limited role in protein synthesis for export, indicating that endogenous requirements predominate, and the assumption that the cells' main function is exclusion of potentially harmful luminal contents is probably correct. This pattern is disrupted in abnormal samples where, although cell hyperplasia is seen, cell growth is reduced, cell junctions become less organised and GAG metabolism is altered.