THE ROLE OF CHOLESTEATOMA ON THE BONE CONDUCTION THRESHOLDS IN CHRONIC SUPPURATIVE OTITIS MEDIA
Introduction
Chronic suppurative otitis media (CSOM) is still one of the diseases with high incidence in Indonesia. CSOM incidence based on data from the Ministry of Health in Indonesia in 1994–1996 was 3.8%.1 The most frequent complication of CSOM is hearing loss.1,2 There are three types of hearing loss: conductive, sensorineural and mixed hearing loss with degrees ranging from mild to very severe.1,3 The increasing of the air conduction threshold with a normal bone conduction threshold are the signs of hearing loss in CSOM. In contrast, some researchers reported sensorineural hearing loss (SNHL) in CSOM as a result of a decrease of the cochlear function.4
The correlation between SNHL and CSOM still is relatively unknown.4,5 Gardenghi cited by Kaur4 reported that 22 (44%) from 50 CSOM patients had a SNHL. Bluvstein reported that 37,5% patients CSOM had a SNHL, and Paparella et al. cited by Kaur4 reported there is increase of SNHL prevalence in 232 CSOM patients. Cusimano et al., Levine et al. and Paparella et al. cited by Tuz6 reported that the SNHL degree was associated with the duration of the disease, inflammation or the histopathological change of the middle-ear mucosa and cholesteatoma.
The purpose of this study is to determine the effect of cholesteatoma on bone-conduction thresholds in CSOM patients. It will clarify the effect of cholesteatoma on cochlear damage in CSOM patients.
Methods
The design of this study is cross sectional, using the medical record of CSOM patients. The subjects of this study are CSOM patients with and without cholesteatoma who visited the Dr. Saiful Anwar hospital in Malang from January 2006 to December 2009. All subjects underwent mastoidectomy surgery.
The variables measured included pre-operative bone conduction in four frequencies as dependent variables. Data of duration of otorrhea, the destruction of ossicles (incus, maleus, stapes) and the types of CSOM (with and without CSOM) were collected as independent variables. The difference of bone conduction in the types of CSOM and the destruction of ossicles were tested using an independent t-test. A correlation test was used to analyze the correlation between the duration of otorrhea and the mean of bone conduction for all types of CSOM and for each type of CSOM separately.
This study involved 82 CSOM patients: 56% with and 44% without cholesteatoma. The sex ratio in CSOM patients with and without cholesteatoma showed no significant difference (p = 0.83), neither did the mean age in both of types CSOM.
The mean duration of otorrhea complaints in CSOM with cholesteatoma was significantly longer (p < 0.001) than in CSOM without cholesteatoma. The ossicle destruction (maleus, incus, stapes) in CSOM with cholesteatoma was significantly higher (p < 0.001) than in CSOM without cholesteatoma. Bone conduction in patients with CSOM with cholesteatoma was higher in all frequencies and the highest in 4 KHz. The unpaired t-test showed that the mean bone conduction of CSOM with cholesteatoma (mean = 32) was significantly higher (p = 0.003) than without choleasteatoma (mean = 20). (Table 1.)
Table 1. Clinical characteristics.
The mean bone conduction was higher in CSOM with destruction of ossicles in maleus (p < 0.001), incus (p = 0.03) and stapes (p = 0.04) than without destruction of ossicles. These results indicate there was correlation between ossicles destruction (maleus, incus, stapes) with the risk of hearing loss as showed by the increasing of the mean bone conduction.
The correlation test also showed that a longer duration of otorrhea meant that a higher bone conduction was found (r = 0.36; p = 0.01). In another analysis, there was no correlation between the duration of otorrhea and bone conduction in CSOM without cholesteatoma (r = -0.14; p = 0.4). A significant correlation between duration of otorrhea and bone conduction was found only in CSOM with cholesteatoma (r = 0.4; p = 0.01).
Discussion
This study identify bone conduction thresholds differences between CSOM patient with (46) and without (36) cholesteatoma. The group of CSOM with cholestatoma had a mean 7.6 years of duration of otorrhea, the group of CSOM without cholestatoma had a mean 2.2 years. In the study conducted by Kaur,4 the duration of otorrhea in most CSOM patients was less than five years. Cholesteatoma is a medium or good environment of bacterial growth and CSOM with cholestatoma would mean a persistent bacterial infection. On the other hand, the bacterial infection will stimulate the cholesteatoma to secrete several cytokines, such as IL-1α, IL-1ß, IL-6, TNF-α and GM-CSF. These cytokines, particularly TNF-α, play a role in keratinocyte proliferation and differentiation, so that the cholesteatoma will grow faster. The presence of these cytokines will also enhance the inflammatory process resulting in chronic infection which is characterized by an increasing uration of otorrhea.7–9
The cholesteatoma and infection have a synergistic effect. Cholesteatoma is a good medium for bacterial growth so the infection becomes persistent. The persistence of bacterial infection stimulates the cholesteatoma to secrete several cytokines that can enhance the growth of cholesteatoma.7–9 Cytokines TNF-α and IL-1ß, which increase in the chronic infection, can increase the permeability of the round-window membrane. It increases the absorption of toxic inflammatory mediators or materials to the cochlea. The biochemical changes in perilymph and endolymph will damage the outer and inner hair cells in the cochlea that cause SNHL.9
Cytokines secreted by cholesteatoma can increase the osteolysis process; which increases the destruction of ossicles. The results of this study also show that the destruction of ossicles in the group of CSOM with cholesteatoma was higher than in the group of CSOM without cholesteatoma. Cholesteatoma can increase osteoclasts through several cytokines. TNF-α causes damage to the bone through the differentiation and maturation of osteoclasts directly and through exposure of the bone matrix indirectly. Other cytokines, such as IL-1, IL-6 and RANKL (receptor activation of NF-κ B ligand), are also found in areas of inflammation and are associated with bone destruction. These cytokines can stimulate differentiation and activation of osteo-clast synergistically, thereby increasing the ossicle destruction.7,10 Cholesteatoma can also damage the lateral semicircular canal and extend into the cochlea. Inflammatory mediators may enter into the cochlea through the opening of the semicircular canal. They can damage outer and inner hair cells and lead to SNHL.7,8
The duration of otorrhea in the group with CSOM with cholesteatoma was longer than in those without cholesteatoma. In the study conducted by Kaur4 they found that the duration of otorrhea was proportional to the increasing incidence of SNHL in CSOM. SNHL in CSOM is due to an increase of biochemical materials in the cochlea through the round window. The structure of the round-window semi-permeable membrane allows the toxic substances to enter into the cochlea. The round window has a groove with a depth of one mm and a diameter of two mm. The surface of this window does not have a ciliated cell. This condition causes the secretion to pile up, restrain, and to be absorbed into the perilymph. There is a significant histological change in the middle ear with otitis media with purulence secretion compared to those without it.4 This is consistent with the results of this study that show increasing bone conduction is proportional to the duration of otorrhea, especially in CSOM with cholesteatoma.
The conclusion of this study is that CSOM with cholesteatoma increases the bone conduction thresholds. The destruction of ossicles and duration of otorrhea may affect the relationship between cholesteatoma with an increase of the bone conduction thresholds.
References
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9.Juhn SK, et al. The role of inflamatory mediators in the pathogenesis of otitis media and sequel. Clin Exp Otorhinolaryngol 1(3):117–138, 2008
10.Chole RA, Nason R. Chronic otitis media and cholesteatoma. In: Snow JB, Wackym PA (eds.), pp. 217–227. Ballenger’s Oto-rhinolaryngology Head and Neck Surgery. 17 ed. Philadelphia: BC Decker Inc: 2009
Address for correspondence: Ahmad Dian Wahyudiono, Otorhinolaryngology Department of Medical Faculty of Brawijaya University, Malang, East Java, Indonesia. dian_punk@yahoo.com
Cholesteatoma and Ear Surgery – An Update, pp. 321–323
Edited by Haruo Takahashi
2013 © Kugler Publications, Amsterdam, The Netherlands