The causes of disutrbance of respiration associated with chronic sinusitis are discussed. The influence of chronic sinusitis on the function of respiration is not only due to the obstruction of the upper respiratory tract that disturbs sound sleep but also to aspiration of postnasal drips during the patient is asleep. The aspirated postnasal discharge would reach as far as bronchioles causing obstruction of the peripheral respiratory system which might be a pathogenesis of sinobronchial syndrome. It is shown that succesful treatments of chronic sinusitis often improved objective as well as the subjective findings of the respiratory function. Chronic sinusitis, in this respect, is considered to have an important bearing when associated with infectious pulmonary diseases.
This paper summarizes pathology, diagnostic technique and therapy of dental sinusitis. The case of dental sinusitis is not rare in our field. Pathology of dental sinusitis is similar to that of acute paranasal sinusitis, however, is different from that of unstable stage of chronic paranasal sinusitis. Evaluation of its pathological condition is the most important in the management of dental sinusitis. Although dental sinusitis is usually treated by rhinologists, dental lesion have to be evaluated by rhinologists in close cooperation withdentists. We classified dental sinusitis into 4 types and each type had characteristic pathology which required special treatment. Type 1: An independent pathology of the maxillary sinus which is not apparently related to a dental disease. Type 2: Dental maxillary sinusitis in a narrow sense, that is, a dental lesion followed by maxillary sinusitis. Type 3: Maxillary sinusitis which is followed by dental diseases. Type 4: Those cases with advanced pathology of both maxillary sinusitis and dental disease where time of onset is not known as to which disease preceded the other. Even with severe inflammatory condition, most cases in type 1 to 3 usually improve by conservative treatments while the cases in type 4 are necessary to be treated surgically.
This study was designed to localize colagenase in the resorbing bone and adjacent tissue by immunocytochmical method. A granulation tissue was produced in various ways in the rat scalp. Three different types of granulations, one produced in an open wound, one produced in response to 1% suspension of carrageenan, and the one produced in response to 1% suspension of epithelial debris were compared one another. The animals were killed two weeks after injection. The scalp bone with adjacent granulation tissue was removed and placed in 1% paraformaldehyde in 0.1M sodium phosphate buffer for fixation at 4°C for 4 hours and the tissue was decalcified in 7% to 1% EDTA at 4°C for 3 weeks. Decalcified bones were frozen and sectioned for immunocytochemistry, using anti-collagenase antisera and the antibody which had been labeled with fluorescein isothiocyanate. Inflammatory mononulear cells were seen at the resorbing margin while areas within the bone were undergoing destruction suggesting osteocytic osteolysis. The epithelium did not contain collagenase. The specific collagenase was concentrated around mononuclear cells and at the irregular bone resorption margins. Within the bone, collagenase staining was found at theperiphery osteocyte lacunae. Collagenase staining of osteocytes was primarily limited to cells adjacent to resorbing margins. No collagenase staining was observed with the nonimmune serum. The finding of increased staining either in inflammatory connective tissue and in bone cells adjacent to the inflammation suggests that inflammatory products may turn on a collagenase in mononuclear cells and in osteocytes.
Two sisters, 34 and 44 years of age, with Morquio's syndrome are described. The two patients were characterized by dwarfism, deformity of various bones and chondroitin sulfate in the urine. Audiometry revealed bilateral sensorineural hearing loss with TTS showing Jerger Type 1 in the ears both cases, while their tympanograms showed type C in both cases. Stapedial reflex was absent in the elder sister because of a severe hearing defect. It was confirmed that the hearing defect in MPS IV was sensorineural in type due to an inner ear disease.
Although the causes of inner ear hearing defect are versatile, disturbances in the microcirculation and metabolism of the hair cells have been considered to be the major factors. Because of the effective barrier system in the inner ear, which appears primarily due to tight junction of the endoethlial cells, drugs are usually unable to gain access to the inner ear. Loop diuretics have been known to affect the striae vascularis and open up the inner ear barrier allowing, though trasiently, the circulation of drugs into the inner ear. The authors report his experience with treatments of sensory hearing loss by Nakai's method. Results were fairly good.
The authors studied operative findings of aural cholesteatomas and classified the pathogenesis of the cholesteatoma into two types, one that originated from the pars tensa and the other from pars flaccida. Recent experience with an extensive aural cholesteatoma in a child revealed such pathology that could not be explained by either type. This case appeared to be an infected case of a congenital cholesteatoma. The authors report the operative findings in this case and discussed the various pathogeneses of aural cholestertoma.
The results of a clinical study of 40 cases of mucoceles in the frontal, ethmoidal and sphenoidal sinuses are summarized as follows: 1. of the 40 mucoceles 12 located in the frontal, 14in the fronto-ethmoidal, 12 in the ethmoidal and 2 in the ethmosphenoidal sinuses. 2.thirtytwo of the 40 cases had a history of sinus operation, of which the maxillary sinus was the most frequent, 3. many mucoceles were considered to be secondary in its pathogenesis, where tissue reaction due to postoperative changes played a greater role. 4. steps in intranasal ethmoidectomy for removal of the mucocele are discussed.