Patients with eosinophilic chronic rhinosinusitis (ECRS) respond poorly to many treatment modalities. Overproduction of periostin in the nasal mucosa is reported to contribute to polyp formation. This study examined periostin levels in patients with ECRS in comparison with levels in patients with non-ECRS. Fifty-nine patients with chronic rhinosinusitis were grouped into those with ECRS and those with non-ECRS. We compared the relationships between peripheral blood eosinophil level, serum periostin level, histopathological findings, clinical and laboratory findings, nose findings, diagnostic score of the Japanese Epidemiological Survey of Refractory Eosinophilic Chronic Rhinosinusitis Study, and postoperative recurrence of nasal polyps in each group. In the ECRS group, a positive correlation was found between peripheral blood eosinophil level and serum periostin level (r_s = 0.49, P < 0.01: Spearman's rank correlation coefficient). ROC curve analysis was used to evaluate the serum periostin level that could predict postoperative recurrence of nasal polyps in the ECRS group: the area under the curve (AUC) was 0.95, sensitivity was 92%, and specificity was 100%; the serum periostin cutoff value for postoperative recurrence of nasal polyps was 130 ng/ml. In ROC curve analysis to evaluate peripheral blood eosinophil level, the AUC was 0.73, sensitivity was 69.2%, and specificity was 85.0%; the cutoff value was 8.8%. periostin was implicated in the pathophysiology of ECRS. Periostin shown to be a more useful biomarker than eosinophils in ECRS. Periostin was shown to likely be an important biomarker for pathological severity of ECRS and postoperative recurrence of nasal polyps.

The purpose of this histopathological study is to examine temporal bones of patients with cochlear otosclerosis adjacent to the round window or adjacent to the oval window as compared with healthy controls. It is unclear if the extent and site of otosclerosis affects the extent of damage to cochlear structures and hearing loss. Twelve temporal bones from 10 patients with cochlear otosclerosis adjacent to the round window, 11 temporal bones from 8 patients with cochlear otosclerosis adjacent to the oval window, and 12 bones of healthy age-matched controls were selected for study. We calculated the number of spiral ganglion cells, changes in cochlear structures, the extent and site of cochlear otosclerosis, and audiometric data. The loss of spiral ganglion cells and the absence of outer hair cells in patients with cochlear otosclerosis adjacent to the round window were significantly higher than those in patients with cochlear otosclerosis adjacent to the oval window and healthy controls. The area of the spiral ligament in patients with cochlear otosclerosis adjacent to the oval window was significantly smaller than that in healthy controls. However, no significant difference was found in the spiral ligament of patients with cochlear otosclerosis adjacent to the round window and healthy controls. There was no significant difference between patients with cochlear otosclerosis and age-matched controls in audiometric data. Cochlear otosclerosis adjacent to the round window caused significantly more damage to spiral ganglion cells and outer hair cells than cochlear otosclerosis adjacent to the oval window without loss of spiral ligament.

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