Discussion
To our best of knowledge, this is the first study radiologically assessing the association of the paranasal sinus volumes and mastoid, petrous apex, and perilabyrinthine pneumatization in patients with COM. A study 11 investigating the association of the length, height, and weight of the paranasal sinuses and mastoid pneumatization in COM patients was published while we were in the data-gathering stage of our study. We included only the patients with unilateral middle ear disease, creating an internal control group while they included both unilateral and bilateral disease and an external control group, including healthy participants. Although the methodology of the studies was different, both have reached similar outcomes. In our study, the volumes of sphenoid sinus were significantly smaller in COM (with isolated tympanic membrane and with cholesteatoma/retraction pocket) side than the contralateral healthy side. There was no difference in volumes of other sinuses. Similarly, Arai et al.11 found that the anterior-posterior length of the sphenoid sinus was smaller in cholesteatoma patients than control subjects. However, there was no difference in width. In contrast, while the width was smaller in patients with COM without cholesteatoma, no difference was seen in the length. Both studies also agreed to that poor mastoid cell pneumatization is associated with lower sphenoid sinus in patients with cholesteatoma. The pneumatization of the sphenoid sinus might be restricted more than other sinuses by childhood chronic rhinosinusitis, as it needs a longer time to complete its development16. Arai et al.11 hypothesized that childhood chronic rhinosinusitis might play an essential role in the etiopathogenesis of the acquired cholesteatoma based on their results. However, it is logical to expect that bilateral COM and bilateral smaller sphenoid sinus length should have been observed, considering the chronic rhinosinusitis is a disease that generally affects all mucosa of the nasal cavity and paranasal sinuses. However, they observed smaller sphenoid sinus only in patients with unilateral cholesteatoma. The outcome of our study seems to support their hypothesis. However, we included patients with unilateral COM. The reduced volume of sphenoid sinus on both sides would be expected if the cholesteatoma was caused by childhood chronic rhinosinusitis in these patients. Therefore, we propose another hypothesis suggesting that long-standing childhood COM and middle ear ventilation problems might restrict to pneumatization of the same sided sphenoid sinus. This restriction might be explained the changing of the bone resistance against pneumatization due to the inflammatory mediators triggered by adjacent chronic inflammatory tissue. Unfortunately, our study did not have enough data to prove both hypotheses.
Mastoid pneumatization starts primarily in the mastoid antrum at 21st-22nd weeks during the embryogenesis, and by the 34th week, the pneumatization of the antrum is nearly completed 17. The development of the mastoid bone continues until puberty, thus influenced by genetic and environmental factors 18. For more than half a century, clinicians have been exploring the association between mastoid aeration and middle ear disease. In a cadaveric study in 1940 by Diamant19, the mastoid cell system of the sides with COM was determined to be smaller and underdeveloped. In 1959, Tumarkin suggested that mastoid bone hypocellularity is one of the most important risk factors for COM 20. After that, many studies have been done on this subject. The study of Tos et al.7 with 79 patients between the ages of 2-7 in 1985; and Sade and Fuch’s study8 in 325 patients with cholesteatoma in 1994 are the striking ones which state the insufficient mastoid aeration increases the risk of otitis. Aria et al. 11 and our study showed that mastoid aeration is reduced in cholesteatoma patients, comparable to literatüre 7,8. However, the mastoid pneumatization was normal in COM without cholesteatoma in both studies. This can be explained by the possible presence of a single attack of acute otitis media-related perforation and traumatic tympanic membrane perforation in this group. Besides, effects on COM with or without cholesteatoma to adjacent structures may vary at the molecular level. Also, mastoid bones with low pneumatization are thought to have limited ability to buffer pressure changes, resulting in atelectasis, retraction pocket, or a cholesteatoma 21.
The development of the mastoid cells and paranasal sinuses are affected by environmental factors, genetic diseases, and previous infections. The interplay of mastoid cell and paranasal sinus development can be explained as 3,5,10:
The connection between sinonasal diseases and ear diseases has been interest. The first large scale study has been published by Van Cauwenberge et al. 7 in 1983, which stated that in children with septum deviation and allergic rhinitis, the risk for otitis media with effusion is increased. In the following years, studies indicating that septum deviation increases the risks of COM have been published. Gopalakrishnan and Kumar 22 observed that in patients with COM between 18-49 of age, septum deviation is present in 73%. Moreover, in the study of Sajitha et al.10, at least one sinonasal pathology was found in 82 of 100 patients with COM; thus, routine endoscopic nasal cavity examination was suggested. One possible explanation for sinonasal diseases and increased COM incidence is secondary eustachian tube dysfunction and consecutive mastoid aeration disruption.
The relation between the mastoid and paranasal sinus pneumatization has also been investigated. In 2005 Karaskas and Kavaklı23 published their study showing the strong correlation between the right, left, and total paranasal sinus volume and right, left, and total mastoid volume, respectively. However, no correlation between any specific sinus and the mastoid bone was determined. Lee et al.4 described the correlation between age and the development of the mastoid cells and paranasal sinuses in their study in 62 pediatric patients with an age average of 13.4. Similarly, they also failed to show any correlation between any specific sinus and the mastoid bone. On the other hand, Kim et al.24 and Hindi et al. 25 found a correlation between the sphenoid sinus and mastoid pneumatization.
In our study, unlike the above studies, the relation between mastoid aeration and paranasal sinus volumes was investigated on patients with suffering unilateral COM. This can be explained by the close neighborhood of the mastoid cells and the sphenoid sinus and mucosal lining contiguity. Also, delayed development of the sphenoid sinus in comparison with other sinuses may increase exposure to various pathological conditions. Both Aria et al. 11 and us suggested it could be the reason for the developmental insufficiency of the sphenoid sinus in patients with COM. However, in our study, reliable history of childhood sinonasal and middle ear diseases were not present. Besides, no molecular and histopathological data of affected structures were available to prove these hypotheses. Therefore, further prospective cohort studies with a large population, and animal studies, modeling COM and chronic rhinosinusitis, should investigate these diseases’ effect on the related anatomical structures.
Conclusion
There are studies in the literature investigating the relationship between mastoid cell pneumatizion and paranasal sinus volumes, but none of them investigate the relation between mastoid pneumatizion and paranasal sinus volumes in patients with unilateral COM. Our study’s attractive finding is that although there is no statistically significant difference in the maxillary and frontal sinus volumes, sphenoid sinus volumes were significantly lower at the affected side of patients with unilateral COM.
Further studies with larger groups are needed to obtain more information about the relation between sphenoid sinus pneumatization and COM.