-Context -Only a few studies evaluated the digestive alterations caused by low frequency noise (LFN) and most focused only on mucosal alterations. Objectives -To investigate the morphological injury of LFN-exposed gastric wall, beyond the epithelial layer. Methods -Wistar rats were exposed to low frequency noise (LFN), during increasing periods, 1 to 13 weeks. A control group was kept in silence. Gastric specimens were studied using: (i) light microscopy with hematoxylin-eosin and immunostaining for collagens; (ii) transmission electron microscopy; (iii) morphometry allowing statistical analysis. Results -Submucosa of all LFN-exposed animals exhibit increased thickness with fibrous proliferation. Transmission electron microscopy showed massive collagen deposition. Immunostaining identified collagen IV as responsible for the increased thickness. Morphometry allowed the demonstration of a significant difference of thickness between control and exposed groups. Vascular alterations included: i) intima proliferation and thickening, rupture of the internal elastic lamina, thrombotic changes; ii) thickening of the media; iii) after 9 weeks of LFN-exposure, we found new formed vessel presenting tortuous and twisted. There is a significant difference of arterial wall thickness between control and exposed groups. Conclusions -Deeper layers of gastric wall undergo alterations, including fibrosis of the submucosa caused by collagen IV deposition, an early marker of neoangiogenesis. Vascular alterations included thickening and thrombotic phenomena, but also images of newly formed vessels. This study suggests that, at least in the stomach, LFN-induced fibrosis could be linked with neoangiogenesis.

These results suggest that the parotid gland is a target for LFN-induced lesions with an impairment of its function.

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Prolonged tracheal intubation of patients often leads to tracheal stenosis (TS), which may require surgical removal of the narrowed portion of the airway. We studied 20 patients with TS who underwent surgical ablation of the stenotic portion of trachea. The morphology of the tracheal segments was characterized and compared with clinical data and with the prognosis for the disease. We found that TS was usually due to an increase in the width of the mucosa as a result of the fibrosis associated with the chronic inflammation. Plasma cells were the predominant leukocyte type seen in the inflammatory infiltrates of the surgically removed portions of narrowed trachea. In the majority of TS samples, the epithelial surface was intact and presented cilia; in contrast, cilia disappeared when the tracheal lumen was completely obliterated. Mucosal cells and glands were also well preserved in TS samples. The need to remove TS segments was often related to previous tracheal surgery, which was also associated with closing of the tracheal lumen and ossification of cartilage rings. We conclude that (a). chronic inflammation and fibrosis are responsible for the narrowing of trachea in TS patients, (b). metaplastic ossification of cartilage rings only occurs after complete obliteration of the tracheal lumen, and (c). loss of cilia and presence of metaplastic bone tissue are indicators of a poor prognosis for TS.