Upper respiratory tract infections are one of the most common infectious diseases in man and are characterized by relatively mild symptoms. However, complications of bacterial superinfection or asthma exacerbations are not seldomly seen. Most upper respiratory tract infections are caused by rhinoviruses. The rhinovirus is a non-enveloped 30nm RNA-virus with over 100 serotypes that belongs to the Picornaviridae family and only replicates in primates. It is characterized by a single positive stranded genome acting not only as a template for RNA synthesis, but also encoding for a single polypeptide necessary for viral replication. The viral capsid has an icosahedral symmetry and demonstrates deep canyons, with a receptor-binding domain. Rhinoviruses are transmitted mainly via direct-or indirect contact with infected secretions and invade their host by binding to the ICAM-1 receptor on the nasal epithelium. Typical for rhinovirus upper respiratory tract infections are isolated scattered foci of infected epithelium, not showing any striking damage or cytopathic alterations, between large areas of normal epithelium.
Today there is still little detailed knowledge on the pathophysiology of common cold, especially on the aspect of cellular migration and defense. A better understanding in mechanisms underlying this cellular response would not only have therapeutical consequences, but may also explain the relationship between viral infectious rhinitis and asthma or atopy.
During a rhinovirus infection, a selective neutrophil and monocyte recruitment is observed. In vitro and in vivo data have demonstrated a time-limited, rhinovirus-induced increase in bradykinin, cytokine, chemokine and sICAM-1 concentrations. Epithelial derived proinflammatory cytokines initiate an adhesion cascade and activate T lymphocytes that create a Till-type cytokine environment within the infected tissue, necessary to eradicate the viral infection. The selective recruitment of neutrophils seems linked to increased concentrations of the chemokine IL-8 and common cold symptoms. It is doubtful that the cytokine-regulated-production of specific neutralising immunoglobulins is necessary for recovery from viral illnesses and presumably only contributes to a late and temporary protection against rhinovirus reinfection.
These observations confirm the crucial role that cytokines and mediators play in the pathogenesis of a rhinovirus infection by mediating chemotaxis, transmigration and activation of inflammatory-and immunocompetent cells.

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The clinical effects of Clarithromycin (CAM), S-carboxymethylcysteine (S-CMC) and anti-allergy agents were investigated in children with maxillary sinusitis and nasal allergies. The subjects were 95 children, 14 years or younger. The maxillary sinusitis was diagnosed by X-ray examinations. The pataients were classified into two treatment groups. Patients in group A received both 5-7mg/kg per day of CAM and 30mg/kg per day of S-CMC for 12 weeks, and those in group B received only 30mg/kg per day of S-CMC for 12 weeks. All patients in the study were also treated with anti-allergy agents. Moreover, the nasal treatment were given once a week locally.
On the fourth month after beginning treatment, X-ray examinations of the maxillary sinus showed 63.9% and 62.7% of cure rates in group A and B, respectively. There was no significant difference in cure rates between group A and B. These results suggest that the efficacy of treatment of maxillary sinusitis in children with nasal allergy is related to a regimen of S-CMC and anti-allergy agents and that CAM provides no added benefit to S-CMC and anti-allergy agents. The study also found an age-related decline in cure rates in goup A. This suggests that there may be pathological changes in their sinusitis as patients grow older.

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In 48 cases of perennial nasal allergy resistant to pharmacotherapy, we performed laser surgery and studied clinical nasal symptoms. The cases ranged in age from 14 to 46 years (mean: 22.6 years), —and consisted of 33 male and 15 female patients. By severity, there were 3 moderate cases and 45 severe cases. According to the postoperative questionnair, over all clinical results were good, with clinical symptoms either disappearing or mild for 80% in sneeze, 80% in rhinorrhea and 90% in nasal obstruction two years after operation. In the regenerated nasal mucosa after laser operation, unlike the edematous morphology before surgery, the whole lamina propria mucosa was replaced by collagen fiber, indicating a condition not conducive to the development of various allergic symptoms. We believe these results demonstrate that laser conchotomy is one of the useful therapies for patients with refractory nasal allergy resistant to pharmacotherapy. The application of laser surgery to nasal allergy is expected to increase in the future.

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Nasal polyps resected from 20 children with chronic sinusitis were analyzed in this study. For comparison, nasal polyps from 26 responders and 11 non-responders to macrolide therapy among adult patients with chronic sinusitis were similarly studied. Paraffin sections of the nasal polyps were stained immunohistologically with antibodies against IgA, IgE, CD68 (a macrophage marker antigen) and HLA-DR, in addition to hematoxylin and eosin staining. The number of immunopositive cells in the submucosa was counted under a light microscope.
A significantly greater number of eosinophils was observed in the submucosa of nasal polyps of the adult non-responders to macrolide therapy, compared to those of adult responders or children. Neutrophilic infiltration was more frequently seen in the nasal polyps of children compared to those of adults. The number of IgA-positive cells was the greatest in the nasal polyps of children, while the smallest number of the cells was noted in adult non-responders. In the nasal polyps of children, numerous CD68-positive cells were noted, however, the expression of HLA-DR was minimal in children compared to adult responders and non-responders.
The present study suggests that chronic sinusitis in children is characterized mainly by nonallergic inflammation and infection. In children, the CD68-positive macrophages act may predominantly as phagocytes rather than as antigen-presenting cells. Nasal polyps in adult responders to macrolide therapy also showed non-allergic type of inflammation. Therefore, macrolide therapy may be effective for the treatment of chronic sinusitis in children.

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We seldom encounter primary paranasal sinus cysts in clinical practice, and a maxillary sinus cyst is a rare occurrence indeed. Clinical symptoms usually include cheek swelling, nasal obstruction, and rhinorrhea, whereas ophthalmological symptoms are very rare.
Here, we present a maxillary sinus cyst accompanied by exophthalmus and double vision in a 66-year-old woman. Computed tomography revealed a cystic lesion in the right maxillary sinus. Surgery to remove the cyst was performed under general anesthesia. Occlusive change of the maxillary sinus ostium is the general pathogenesis of a primary maxillary sinus cyst. In this case, occlusive change in the left maxillary sinus ostium was not observed at the time of surgery, however, there was a past histroy of chronic sinusitis. We surmise, therefore, that this left maxillary sinus cyst was triggered by cystic change of the maxillary sinus mucosa accompanying maxillary sinusitis.

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The air flow through the nose during quiet breathing is composed mainly of transitional and turbulent flow conditions. However, the nasal resistance is calculated from the equation R=ΔP/∨, which describes the relationship between differential pressure and flow under laminar flow conditions. The discrepancy between empirical measurements and the equation is still unresolved. Values of nasal resistance at ΔP150Pa have been recommended by the International Standardization Committee for clinical use, but this point seems somewhat high for quiet nasal breathing, especially for Japanese. Thus, in an attempt to avoid the above stated problem, we measured actual nasal resistance at ΔP100Pa and ΔP150Pa and calculated nasal resistance from Röhrer's equation at the same predetermined point and compared results in 76 patients (60 males and 16 females with a mean age of 46.2 years), and 152 nostrils, to determine the usefulness of calculated nasal resistance at ΔP100Pa and ΔP150Pa from Röhrer's equation when transnasal pressure fails to reach the predetermined point. The values at ΔP100Pa and ΔP150Pa calculated from the method were compared with actual measured nasal resistance at ΔP100Pa and ΔP150Pa by an active anterior rhinomanometry with a nasal nozzle during quiet nasal breathing in this study.
We fixed the measured nasal resistance at “y” and the calculated one at “x” on the x-y coordinates. Correlation lines between measured and calculated nasal resistances were y=0.98x+0.01 (r=0.9950, P<0.0001) on expiration and y=1.02x+0.01 (r=0.9901, P<0.0001) on inspiration at ΔP100Pa, and y=0.99x+0.01 (r=0.9928, P<0.0001) on expiration and y=0.93x+0.02 (r=0.9944, P<0.0001) on inspiration at ΔP150Pa, and these resistances were almost identical, respectively. Calculated nasal resistance at ΔP100Pa and ΔP150Pa from Röhrer's equation may be suitable for evaluation when transnasal pressure fails to attain the predetermined points.

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Nitric Oxide (NO) has been idetified recently as a multifunctional mediator. TO evaluate the function of NO in the pathophisiology of nasal allergy, the distribution of nitric oxide synthase i. e. neuronal NOS (nNOS), endotherial NOS (eNOS) and, inducible NOS (iNOS) was investigated in the nasal mucosa exposed to Compound 48/80 (C48/80). They were histochemically studied and compared with those in the normal nasal mucosa. The nasal mucusa was obtained from rats in this study. Type 1-like allergic inflammation was induced by C48/80. C48/80 is an inhibitor of phosphatidylinositol-specific-phospholipase C, It induces degranulation of mast cells. Then type 1-like allergic infllammatory model was obtained. In the nasal mucosa of rats exposed to C48/80, allergic inflammatory microscopic findings appered, that is, eosinocytes, macrophages, bleeding and, edematous changes appeared.
The immunoreactivity to iNOS was shown in macrophages, not in eosinocytes in the nasal mucosa with C48/80. In contrast, the iNOS immunoreactivity was negative in normal rats. The immunoreactivity to iNOS in macrophages is suspected to relate to the pathogenesis and toxic actions on the nasal membrane in nasal allergy.

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Eosinophil infiltration of tissue is a hallmark of nasal polyps in both atopic and nonatopic patients. Structural cells like airway fibroblasts are a rich source of cytokines and inflammatory mediators. To verify whether nasal fibroblasts play a role in eosinophilic infiltration, we investigated the release of eotaxin from nasal polyp fibroblasts when stimulated with lipopolysaccharide (LPS), interleukin-1β and tumor necrosis factor-α. We demonstrated that LPS, proinflammatory cytokines (IL-1β and TNF-α) could induce the gene expression and production of eotaxin in nasal polyp fibroblasts. These findings suggest that nasal polyp fibroblasts may play an important role in the recruitment of eosinophils through the release of eotaxin.

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This paper assesses the effectiveness of our laser surgical technique for chronic paranasal sinusitis retrospectively. Forty-one adult patients with chronic paranasal sinusitis and bilateral nasal polyposis underwent laser surgery. After local anesthesia was administered, nasal polyps were resected and the diseased mucous membrane of the middle meatus and middle turbinate were vaporized with a CO₂ laser, without opening the paranasal sinuses. Relief or improvement of symptoms was achieved in patients with nasal obstruction (100%), amount of nasal discharge (97.4%), and anosmia (85.8%). The degree of opacity of the maxillary and ethmoid sinuses on x-ray films improved in 95% and 93. 8% of sinuses, respectively. The laser surgical technique that we have developed for chronic paranasal sinusitis is noninvasive and appears to be a good alternative to the Caldwell-Luc operation or endoscopic sinus surgery.

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45 cases with chronic sinusitis were studied. Patients with chronic sinusitis accompanied by eosinophil infiltration and goblet-cell hyperplasia in the sinus mucosa often had a poor post operative course. We hypothesized that eosinophil-dominant sinusitis might have a different pathogenesis than narrowing of the ostiomeatal unit, which is believed to be the main cause of mononuclear-cell-dominant, ordinary chronic sinusitis. Cases of eosinophil-dominant sinusitis were often accompanied by bronchial asthma, but not by nasal allergy. Immunohistological studies revealed that most of the eosinophils in the sinus mucosa were EG2-positive and TGF-β-positive. These results indicate that eosinophils may play an important role both in the injury and repair of the sinus mucosa in chronic sinusitis.
Some fibrosis was observed in the sinus mucosa, with no correlation with either inflammatory cell infiltration or the post operative course. However, in one patient, almost the entire area of the lamina propria of the sinus mucosa was replaced by fibrosis, and the post operative course of this patient was poor.
It was concluded that it is clinically worthwhile to classify chronic sinusitis into four histological types, namely, the eosinophilic type, the mononuclear-cell type, the fibrosis type (only one patient in this study), and the edematous type.

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