tympanosclerosis It can be evaluated anatomically and clinically as a result of healed inflammation and has been described by many authors as middle ear infections It is defined as a sequela of the recovery period. Calcified hyaline plaques collect in the middle ear, eardrum and rarely in the mastoid cavity (Figure 1). These plaques may disrupt the movements of the eardrum and ossicles, may completely fix the stapes, malleus and incus, or may not affect the movements of the ossicles. tympanosclerosis It is not an invasive process and does not cause damage to the ossicles (Tos)1. Kulak zarındaki kalker birikimleri, Gibb’e göre ilk kez 1734 yılında Cassebohm tarafından “chalky patches” olarak ‘tanımlandı. Middle ear infectionsVon Troltsch was the first to describe the sclerotic changes that occurred afterwards using the term "Taukensklerose" in 1878. Walb first revealed its histological structure in 1878. 2Politzer was the first to use the term tympanosclerosis and define it in its current meaning in 1883. Zollner and Beck described the pathologies caused by tympanosclerosis in the middle ear and ossicular chain using the ear microscope in 1955.2
tympanosclerosis If the plaques are only on the eardrum, this condition is called Myringosclerosis (Doyle 1975) and hearing is generally only slightly affected in these patients.3 Myringosclerosis (MS) is frequently seen in patients with recurrent acute otitis media or otitis media with effusion. Clinically, white plaques may occur in a limited area or cover the entire eardrum, but do not involve the Shrapnel membrane (Tos).1. The incidence of tympanosclerosis was reported as 10% by Plester.4
tympanosclerosis; It is classified by Tos as histological (subclinical) tympanosclerosis, clinical tympanosclerosis and surgical tympanosclerosis. Histological tympanosclerosis; Clinical tympanosclerosis, which is detected by histological examination, can be seen under the operating microscope or visually, and surgical tympanosclerosis can be summarized as tympanosclerosis that causes conductive hearing loss.1
HISTOPATHOLOGY: Light and electron microscopy showed that tympanosclerotic lesions were located in the submucosa. The most common pathological changes are hyalinization, necrosis, calcification, fibrosis and ossification. Electron microscopy studies have shown calcified accumulations and a dense network of typical collagen fibers in the mitochondria and lysosomes of fibrocytes (Friedmann, 1971).5. Sorenson and True (1972) observed that the degenerative process involves not only the connective tissue (lamina propria and submucosa) but also the tympanic membrane epithelium. It may be involved in mastoid cells by tympanosclerosis (Ferlito, 1979)6. Examination of the plaques using an electron microscope showed that they consisted of irregular collagen fibers and calcium phosphate.
ETIOPATHOGENESIS: In otitis with prolonged effusion, Miller (1984) suggested that postinflammatory factors combined with edema and inflammation in the submucosa cause degeneration in the fibrous layer.7. Schiff and Yoo (1985) hypothesized that tympanosclerosis is an immune complex reaction resulting from otitis media in a patient sensitized by previous inflammation.8. . Wielinga et al. (1988) suggested that it develops due to damage caused by hydrolytic enzymes in the serous fluid to the lamina propria of the eardrum.9.. Wielinga et al. (2001) concluded that both sterile and infected effusions lead to irreversible changes in the lamina propria of the pars tensa.9They also stated that mechanical injury and disruption of lamina propria vascularization are important factors in the development of tympanosclerosis.9.. Although the etiopathogenesis of tympanosclerosis is not fully known, it is known that middle ear infections and eardrum traumas initiate tympanosclerosis. However, tympanosclerosis is not seen in every patient who has a middle ear infection or a ventilation tube (VT). This suggests that genetically different molecular causes may also be effective in the formation of tympanosclerosis. In many experimental studies conducted in recent years, different opinions have been put forward for the causes of tympanosclerosis. Tos et al. argue that there will be no myringosclerosis in the normally vibrating eardrum, but events that reduce eardrum movement, such as VT, will increase hyalinization and calcification in the collagen layer.10 Several other studies indicate that bleeding during paracentesis or VT insertion increases the occurrence of MS.11-13 Another study suggests that immunological reactions as a result of an organism previously sensitized to an antigen encountering the antigen again cause the development of MS.14 Many experimental and clinical studies suggest that free oxygen radicals (SOR) produced by inflammatory cells and bacteria during otitis play an important role in the formation of tympanosclerosis.15 Tissue damage due to SOR occurs in many diseases such as cataract, cerebrovascular disease, atherosclerosis, arthritis and ischemia. For tympanosclerosis to occur, tissue damage must occur. Tissue damage occurs in two ways during middle ear infections. One of these is the production of excessive amounts of SOR, the other is the direct effect of neutrophils and bacteria.16. It is known that the most common pathogen causing acute middle ear infection is Streptococcus pneumoniae.17 Streptococcus pneumoniae produces significant amounts of hydrogen peroxide in the infection environment. Hydrogen peroxide is an important mediator of SOR. Since SOR is produced especially by macrophages in the connective tissue, the most significant damage occurs in this region.18 It has been shown that tissue damage and sclerosis can occur in a short period of time, such as 9 hours, during middle ear infections and paracentesis.19 It is known that paracentesis or VT installation during the treatment of otitis media with effusion increases tympanosclerosis. In healthy humans and animals, the O2 concentration in the middle ear is between 5.5-12.1%. With paracentesis or VT insertion, this concentration increases and reaches the normal outdoor air level. This situation causes a relative excess of oxygen in the middle ear.15,16.20 Mattsson and his colleagues kept the paracentesis mice in different O2 concentrations and showed that the development of MS increased as the oxygen concentration increased. These findings support the existence of a significant relationship between tympanosclerosis and the amount of oxidation and SOR formation.21 A study in a mouse model of otitis media caused by Streptococcus pneumoniae showed an increase in macrophages in the middle ear mucosa and parts of the eardrum close to the annulus. In the later period, T, B lymphocytes, giant osteoclasts and osteoblast-like cells increase in the parts of the eardrum adjacent to the bone.22 Another toxic agent whose production increases in tissue during trauma and inflammation is peroxynitrite. Peroxynitrite is formed as a result of the reaction of superoxide (O2-) and nitric oxide (NO) molecules. 23 Nitric oxide is a radical molecule produced by nitric oxide synthetase.24 If the tissue damage caused by reactive molecules such as SOR and Peroxynitrite is mild, it is corrected in a short time by the restorative mechanisms in the body. However, if the damage is irreversible, cell death occurs through necrosis or apoptosis.
It has been reported that tissue damage and, as a result, the development of tympanosclerosis are significantly reduced or prevented by these antioxidant and anti-inflammatory substances.16-18 It has been shown that in mice treated with selenium, N-acetyl cysteine and L-carnitine, these antioxidant agents protect the cell from necrosis and apoptosis by reducing the production of SOR and NO.25,26,27,28. Although antioxidant agents have been experimentally shown to reduce MS or tympanosclerosis, studies on their clinical effectiveness need to be conducted.
CLINIC: Conductive hearing loss may occur as a result of fixation of the head of the malleus and the body of the incus in the epitympanic region or the stapes in the oval window with tympanosclerosis plates. Tympanosclerosis can also affect the otic capsule, causing sensorineural hearing loss. Schuknecht (1974) defined tympanosclerosis as the thickening of collagen fibers and their fusion with intracellular and extracellular calcium and phosphate crystals.29. These masses may be isolated accumulations in the eardrum, or they may be massive, covering the ossicles or filling the middle ear.
Austin (1988) defined clinically significant tympanosclerosis as a condition requiring surgical intervention to restore hearing.30. Plester (1972)29, Kamal (1997)31 ve Wielinga ve ark. (2001)32 They reported that eardrum perforations associated with tympanosclerosis were located in the pars tensa. Asiri et al. In a study of 90 cases, they found involvement of the eardrum only in 50% of patients with tympanosclerosis, involvement of both the eardrum and the middle ear in 20%, and involvement of the middle ear only in 30%.33. Emmett and Shea (1978) found the incidence of incudomalleolar fixation to be higher than isolated stapes fixation.34. While Austin reported mucosal disease in 21% of 320 cases, Asiri et al. reported mucosal disease in 12% of 90 cases. The coexistence of tympanosclerosis and cholesteatoma is controversial. Sheehy and House (1962)35 While they reported a 28% cholesteatoma incidence in their study of 75 cases, Kinney reported a 30% cholesteatoma incidence in 311 cases.36. On the other hand, while Emmett and Shea (1978) reported a 4% cholesteatoma incidence in their series of 45 cases, Austin reported no cases of cholesteatoma in 320 cases. Extreme reported a 2% cholesteatoma incidence.
SURGERY: Surgical treatment of tympanosclerosis Zollner (1963) and Smyth (1972) first worked on the subject and defined tympanosclerosis as the lesion least suitable for surgery among middle ear diseases, but although a long way has come since then, discussions continue.37. Tos (1990) recommended surgery after a surgical series of 73 cases and recommended mobilization first by cleaning the plaques around the incus, malleus and stapes.38. Smyth (1972) recommended 2-stage surgery in the form of stapedectomy 6 months after eardrum repair in cases with stapes fixation.37.
It is not always possible to clean the plaques and surgically correct the resulting ossicular damage. In cleared cases, hearing loss occurs again in the early postoperative period, mostly due to refixation. In cases where the stapes base and legs are involved, hearing repair can be performed by stapedotomy or stapedectomy and placement of a teflon piston (Figure 1). In cases where mobilization is performed, surgery creates a new tissue trauma, and after a while, tympanosclerosis plaque forms again and impairs hearing. Therefore, surgical treatment of tympanosclerosis is controversial. While Austin, Sheehy and House, Tos et al. recommend surgical procedures, some authors argue that surgery is the last solution in the treatment of tympanosclerosis. It is assumed that stapes mobilization carries risks such as refixation, hydraulic trauma to the cochlea, and neurosensory hearing loss as a result of perilymph fistula. Giddings and House (1992) examined the results of various surgical treatment methods in 154 cases with tympanosclerotic stapes fixation after a 10-year postoperative follow-up and reported that they did not find a significant difference between stapedectomy and mobilization and that both treatment modalities were equally effective.39. Albu et al. (2000) reported that they obtained good results with the mobilization of the ossicles in 115 cases with incudomalleolar fixation in the attic.40. They also reported that patients with stapes fixation and stapedectomy achieved good hearing results immediately after surgery, but after a while there was a deterioration in air-bone conduction patency.40. Elpern and Elbrond (1966) concluded in a temporal bone study that removal of the malleus head had minimal acoustic effects.41Plester (1967) stated that even after the most meticulous removal of tympanosclerotic plaques, long-term mobilization of the entire ossicular chain is almost impossible.4. Kinney (1978) stated that removal and reposition of the fixed malleus or incus is an acceptable technique because the anatomy of the posterior wall of the external auditory canal is preserved.36. Wielinga et al. (1995) examined the effects of tympanosclerosis on myringoplasty results and reported that the presence of tympanosclerosis in the eardrum did not have a significant effect on the graft retention rate, but when looking at the postoperative hearing results, if the tympanosclerotic plaques exceeded one-third of the eardrum, their removal provided a gain of 6 dB.32. The success rate of myringoplasty is the same as eardrum repair without tympanosclerosis, but we prefer cartilage as a graft in ears with tympanosclerosis. Although plaque removal is recommended in myringosclerosis, it is not always necessary.
Although surgical treatment of tympanosclerosis is widely used, it is especially Selection of surgical technique, staging of the surgery and surgery regarding stapes There are still controversial issues, including:
Performing stapedotomy, especially in tympanosclerotic stapes fixation, is controversial and there is a widespread belief that it carries a high risk of developing postoperative neurosensory hearing loss. There is no direct relationship between the degree of conductive hearing loss and the extent of tympanosclerosis. Neurosensory hearing loss in tympanosclerosis may be due to involvement of the cochlea by hyaline degeneration of the membranous labyrinth.
Participated et al. In their series of 37 cases, they concluded that postoperative hearing outcomes were worse in tympanosclerosis than in COM cases without tympanosclerosis.42. Bayazıt et al. As a result of their evaluation of 42 tympanosclerosis cases performed in a single stage, they stated that they could not obtain satisfactory results in cases of stapes fixation performed with mobilization in a single stage, and they recommended stapedotomy in the second stage surgery.43. In 117 cases with tympanosclerosis, Stankovic cut off the malleus head and performed incus interposition or applied stapedotomy and Teflon piston, depending on the location of the fixation. As a result of short and long-term (5 years) follow-up, they found a significant improvement in the air-bone conduction gap and pure tone threshold, and the long follow-up results were close to the early period results. They did not find significant neurosensory hearing loss, and reported a mild long-term decrease in hearing threshold in the stapedotomy group.44.Teufert K.B. and De La Cruz A. found an average postoperative air-bone conduction gap of 17.4 dB in 203 cases with tympanosclerosis, 135 of which had ossicular fixation, and an air-bone conduction gap below 20 dB in 65.3% of the cases. They found partial neurosensory hearing loss in 1% of the cases and profound hearing loss in none of the cases. They did not find neurosensory hearing loss. In the long term (1.6 years), they detected a 0.3 dB decrease in the air-bone conduction gap and a 2 dB decrease in the pure tone threshold.45. They concluded that ossicular reconstruction can provide satisfactory long-term results with a low complication rate in patients with tympanosclerosis.45.
Vincent et al. In their study on 65 patients with tympanosclerotic stapes fixation, they placed a vein graft at the base after stapedotomy and used a Teflon piston or total prosthesis, and concluded that good results would be obtained if some rules were observed.46. Considering all these, it can be concluded that good long-term results can be obtained with a good surgery and that patients can be followed by recommending a hearing aid. The options should be discussed with the patient and he/she should be allowed to make his/her own decision.
Important factors that determine the technique to be applied in tympanosclerosis surgery are:
1.The condition of the ossicles (defect etc.) 2.Fixation of the manubrium due to myringosclerosis (fixation between the bone annulus and the manubrium) 3.The presence and extent of fixation between the attic wall and the malleus and/or incus 4.Fixation of the base of the stapes and the extent of tympanosclerosis (ability to reach the base and sufficient distance for surgery) 5. Presence of perforation in the eardrum 6. Presence of accompanying cholesteatoma 7. Presence of active infection
POSSIBLE PATHOLOGIES
In attic fixation of the ossicles or incudomalleolar fixation, instead of mobilization, incision and removal of the malleus head are preferred to prevent re-fixation (Figure -8) and incus interposition or PORP application is preferred after the removal of the incus (Figure -9 and figure -10).
In this case, if there is stapes fixation, a stapedotomy can be performed a few months after the eardrum repair and a Teflon piston of appropriate size can be placed from the manubrium to the base (figure -11). It should be kept in mind that if the malleus head has been cut (to prevent refixation), there may be a stabilization problem of the manubrium. If the stapes base is found to be fixed during the first surgery and a stapedotomy is planned in the second session, this situation should be discussed with the patient and the patient should be allowed to choose between hearing aid and surgery.
It should be noted that in patients for whom tympanoplasty is planned and whose Rhinne is negative (especially tympanosclerosis is seen in the eardrum or middle ear structures through perforation), a second surgery may be required if the stapes base becomes fixed. Otherwise, failure to solve the problem in one session may be interpreted as your failure.
The extent of tympanosclerosis and the critical areas it affects are usually evident during surgery, so the surgeon must be prepared for various pathologies.
RESOURCES
1.Tos M, Lau T, Arndal H, Plate S.Tympanosclerosis of the middle ear: late results and surgical treatment. J Laryngol Otol 1990;104: 685-9.
2.Akyıldız AN. Kronik (süpüratif) otitis media. Akyıldız AN (ed) Kulak hastalıkları ve mikrocerrahisi. Bilimsel TıpYayınevi, Ankara 1998; 1: 337-472.
7.Miller,P. (1984). Tympanosclerosis of the eardrum in secretory otitis media. Acta Otolaryngologica (Suppl 105 : 537-543.
10.Tos M, Bonding P Poulsen G. Tympanosclerosis of the,drum in secretory otitis after insertion of grommets. J Laryngol Otol 1983;97:489-96.
13 . McRae D, Gatland DJ, Youngs R, Cook J. Aspiration of middle ear effusions prior to grommet insertion an etiological factor in tympanosclerosis. J Otolaryngol 1989 18(5):229-31
21.Mattsson C, Magnuson K, Hellström S. Myringosclerosis caused by increased oxygen con-centration in traumatized tympanic membranes. Experimental study. Ann Otol Rhinol Laryngol 1995;104:625-32.
22 . Forseni M, Eriksson A, Bagger-Sjoback D et al. Development of tympanosclerosis: can predicting factors be identified? Am J Otol 1997;18(3):298-303.
24 . Nathan C, Xie Q. Regulation of biosynthesis of nitric oxide. J Biol Chem 1994;269: 13725-8.
26 . Özcan C, Polat G, Görür K et al. The effect of local administration of N-acetylcysteine in perforated rat tympanic membrane: An experimental study in myringosclerosis. Pharmacol Res 2002; 45:5-9.
28 . Akbaş Y, Pata YS, Görür K et al. The effect of L-carnitine on the prevention of experimentally induced myringoscleroosis in rats. Hear Res 2003;184:107-12.
30.Austin DF. Reconstructive techniques for tympanosclerosis. Ann Otol Rhinol Laryngol 1988; 97: 670 674.
31.Kamal SA (1997) Surgery of tympanosclerosis. J Laryngol Otol
111:917–923
45.Teufert KB, De La Cruz A (2002) Tympanosclerosis: long-term hearing results after ossicular reconstruction. Otolaryngol Head Neck Surg 126:264–272.
Tympanosclerosis and Surgical Treatment
Prof.Dr.Burhan Dadaş
SUMMARY: Tympanosclerosis is an irreversible condition in which pathological events in the middle ear result in predominantly conductive hearing loss. In this article, etiopathogenesis and treatment options according to different pathologies are discussed in the light of the literature.
KEYWORDS: tympanoplasty, myringoplasty, otitis media, stapes surgery
ABSTRACT: Tympanosclerosis is an irreversible final stage of pathological process in the middle ear resulting in predominantly conductive hearing loss.In this article etiopathogenesis and therapy modalities were discussed.
KEY WORDS: tympanoplasty, myringoplasty, otitis media, stapes surgery
ENTRANCE: Tympanosclerosis can be evaluated anatomically and clinically as a result of healed inflammation and is defined by many authors as a sequela of middle ear infections during the healing period. Calcified hyaline plaques collect in the middle ear, eardrum and rarely in the mastoid cavity (Figure 1). These plaques may disrupt the movements of the eardrum and ossicles, may completely fix the stapes, malleus and incus, or may not affect the movements of the ossicles. Tympanosclerosis is not an invasive process and does not cause damage to the ossicles (Tos)1. According to Gibb, limestone deposits in the eardrum were first described as "chalky patches" by Cassebohm in 1734. Von Troltsch was the first to describe the sclerotic changes that occur after middle ear infections in 1878, using the term "Taukensklerose". Its histological structure was first revealed by Walb in 1878. 2Politzer was the first to use the term tympanosclerosis and define it in its current meaning in 1883. Zollner and Beck described the pathologies caused by tympanosclerosis in the middle ear and ossicular chain using the ear microscope in 1955.2
If tympanosclerosis plaques are only in the eardrum, this condition is called Myringosclerosis (Doyle 1975), and hearing is generally only slightly affected in these patients.3 Myringosclerosis (MS) is frequently seen in patients with recurrent acute otitis media or otitis media with effusion. Clinically, white plaques may occur in a limited area or cover the entire eardrum, but do not involve the Shrapnel membrane (Tos)1. The incidence of tympanosclerosis was reported as 10% by Plester.4
Timpanoskleroz; It is classified by Tos as histological (subclinical) tympanosclerosis, clinical tympanosclerosis and surgical tympanosclerosis. Histological tympanosclerosis; Clinical tympanosclerosis, which is detected by histological examination, can be seen under the operating microscope or visually, and surgical tympanosclerosis can be summarized as tympanosclerosis, which causes conductive hearing loss.1
HISTOPATHOLOGY: Light and electron microscopy showed that tympanosclerotic lesions were located in the submucosa. The most common pathological changes are hyalinization, necrosis, calcification, fibrosis and ossification. Electron microscopy studies have shown calcified accumulations and a dense network of typical collagen fibers in the mitochondria and lysosomes of fibrocytes (Friedmann, 1971)5. Sorenson and True (1972) observed that the degenerative process involves not only the connective tissue (lamina propria and submucosa) but also the tympanic membrane epithelium. It may be involved in mastoid cells by tympanosclerosis (Ferlito, 1979)6. Examination of the plaques using an electron microscope showed that they consisted of irregular collagen fibers and calcium phosphate.
ETIOPATHOGENESIS: In prolonged otitis media with effusion, Miller (1984) suggested that postinflammatory factors combined with edema and inflammation in the submucosa cause degeneration in the fibrous layer7. Schiff and Yoo (1985) assumed that tympanosclerosis is an immune complex reaction resulting from otitis media in a patient sensitized by previous inflammation8. . Wielinga et al. (1988) suggested that it develops due to damage caused by hydrolytic enzymes in the serous fluid to the lamina propria of the eardrum.9.. Wielinga et al. (2001) concluded that both sterile and infected effusions cause irreversible changes in the lamina propria of the pars tensa9. They also stated that mechanical injury and deterioration in lamina propria vascularity are important factors in the development of tympanosclerosis9. Although the etiopathogenesis of tympanosclerosis is not fully known, tympanosclerosis of middle ear infections and tympanic membrane traumas is the cause. It is known to have started. However, tympanosclerosis is not seen in every patient who has a middle ear infection or a ventilation tube (VT). This suggests that genetically different molecular causes may also be effective in the formation of tympanosclerosis. In many experimental studies conducted in recent years, different opinions have been put forward for the causes of tympanosclerosis. Tos et al. argue that there will be no myringosclerosis in the normally vibrating eardrum, but events that reduce eardrum movement, such as VT insertion, will increase hyalinization and calcification in the collagen layer. 10 In several other studies, it is stated that bleeding during paracentesis or VT insertion increases the occurrence of MS. 11-13 In another study, It is suggested that immunological reactions, as a result of an organism previously sensitized to an antigen, encountering the antigen again, cause the development of MS. 14 Many experimental and clinical studies suggest that free oxygen radicals (SOR) produced by inflammatory cells and bacteria during otitis play an important role in the formation of tympanosclerosis. .15 Tissue damage due to SOR occurs in many diseases such as cataract, cerebrovascular disease, atherosclerosis, arthritis and ischemia. For tympanosclerosis to occur, tissue damage must occur. Tissue damage occurs in two ways during middle ear infections. One of these is the production of excessive amounts of SOR and the other is the direct effect of neutrophils and bacteria16. It is known that the pathogen that most commonly causes acute middle ear infection is Streptococcus pneumoniae.17 Streptococcus pneumoniae produces significant amounts of hydrogen peroxide in the infection environment. Hydrogen peroxide is an important mediator of SOR. Since SOR is produced especially by macrophages in the connective tissue, the most significant damage occurs in this region.18 It has been shown that tissue damage and sclerosis can occur in a short period of time, such as 9 hours, during middle ear infections and paracentesis.19 It is known that paracentesis or VT placement during the treatment of otitis media with effusion increases tympanosclerosis. In healthy humans and animals, the O2 concentration in the middle ear is between 5.5-12.1%. With paracentesis or VT insertion, this concentration increases and reaches the normal outdoor air level. This situation causes a relative excess of oxygen in the middle ear. 15,16,20 Mattsson and his colleagues showed that the development of MS increases as the oxygen concentration increases by keeping the paracentesis mice in different O2 concentrations. These findings support the existence of a significant relationship between tympanosclerosis and the amount of oxidation and SOR formation.21 In a study on a mouse otitis media model caused by Streptococcus pneumoniae, it was shown that there was an increase in macrophages in the middle ear mucosa and parts of the eardrum close to the annulus. In the later period, T, B lymphocytes, giant osteoclasts and osteoblast-like cells increase in the parts of the eardrum adjacent to the bone.22 Another toxic agent whose production increases in the tissue during trauma and inflammation is peroxynitrite. Peroxynitrite reacts with superoxide (O2-) and nitric oxide (NO) molecules. 23 Nitric oxide is a radical molecule and is produced by nitric oxide synthetase. 24 If the tissue damage caused by reactive molecules such as SOR and Peroxynitrite is mild, it is corrected in a short time by the restorative mechanisms in the body. However, if the damage is irreversible, cell death occurs through necrosis or apoptosis.
It has been reported that tissue damage and, as a result, the development of tympanosclerosis are significantly reduced or prevented by these antioxidant and anti-inflammatory substances. It has been shown to protect against necrosis and apoptosis.25,26,27,28. Although antioxidant agents have been experimentally shown to reduce MS or tympanosclerosis, studies on their clinical effectiveness need to be conducted.
CLINIC: Conductive hearing loss may occur as a result of fixation of the head of the malleus and the body of the incus in the epitympanic region or the stapes in the oval window with tympanosclerosis plates. Tympanosclerosis can also affect the otic capsule, causing sensorineural hearing loss. Schuknecht (1974) defined tympanosclerosis as the thickening of collagen fibers and their fusion with intracellular and extracellular calcium and phosphate crystals29. These masses may be isolated accumulations in the eardrum, or they may be massive, covering the ossicles or filling the middle ear.
Austin (1988) defined clinically significant tympanosclerosis as a condition requiring surgical intervention to restore hearing30. Plester (1972)29, Kamal (1997)31 and Wielinga et al. (2001)32 reported that eardrum perforations associated with tympanosclerosis were located in the pars tensa. Asiri et al. In a study of 90 cases, they found involvement of only the eardrum in 50% of patients with tympanosclerosis, involvement of both the eardrum and middle ear in 20%, and involvement of only the middle ear in 30. Emmett and Shea (1978) found the incidence of incudomalleolar fixation to be higher than isolated stapes fixation34. While Austin reported mucosal disease in 21% of 320 cases, Asiri et al. reported mucosal disease in 12% of 90 cases. The coexistence of tympanosclerosis and cholesteatoma is controversial. While Sheehy and House (1962)35 reported a 28% cholesteatoma incidence in their study of 75 cases, Kinney reported a 30% cholesteatoma incidence in 311 cases36. On the other hand, while Emmett and Shea (1978) reported a 4% cholesteatoma incidence in their series of 45 cases, Austin reported no cases of cholesteatoma in 320 cases. Extreme reported a 2% cholesteatoma incidence.
SURGERY: Zollner (1963) and later Smyth (1972) first studied the surgical treatment of tympanosclerosis and defined tympanosclerosis as the lesion least suitable for surgery among middle ear diseases, but although a long way has come since then, discussions continue37. Tos (1990) recommended surgery after a surgical series of 73 cases and recommended mobilization first by cleaning the plaques around the incus, malleus and stapes38. Smyth (1972) recommended 2-stage surgery in the form of stapedectomy 6 months after eardrum repair in cases with stapes fixation37.
It is not always possible to clean the plaques and surgically correct the resulting ossicular damage. In cleared cases, hearing loss occurs again in the early postoperative period, mostly due to refixation. In cases where the stapes base and legs are involved, hearing repair can be performed by stapedotomy or stapedectomy and placement of a teflon piston (Figure 1). In cases where mobilization is performed, surgery creates a new tissue trauma, and after a while, tympanosclerosis plaque forms again and impairs hearing. Therefore, surgical treatment of tympanosclerosis is controversial. While Austin, Sheehy and House, Tos et al. recommend surgical procedures, some authors argue that surgery is the last solution in the treatment of tympanosclerosis. It is assumed that stapes mobilization carries risks such as refixation, hydraulic trauma to the cochlea, and neurosensory hearing loss as a result of perilymph fistula. Giddings and House (1992) examined the results of various surgical treatment modalities in 154 cases with tympanosclerotic stapes fixation after a 10-year postoperative follow-up and reported that they found no significant difference between stapedectomy and mobilization and that both treatment modalities were equally effective39. Albu et al. (2000) reported that they obtained good results with the mobilization of the ossicles in 115 cases with incudomalleolar fixation in the attic40. They also reported that patients with stapes fixation and stapedectomy achieved good hearing results immediately after the surgery, but after a while there was a deterioration in air-bone conduction40. In a temporal bone study, Elpern and Elbrond (1966) concluded that removal of the malleus head had minimal acoustic effect41. Plester (1967) stated that long-term mobilization of the entire ossicular chain was almost impossible even after the most meticulous removal of tympanosclerotic plaques4. Kinney (1978) stated that removal and reposition of the fixed malleus or incus is an acceptable technique because the anatomy of the posterior wall of the external auditory canal is preserved36. Wielinga et al. (1995) examined the effects of tympanosclerosis on myringoplasty results and reported that the presence of tympanosclerosis in the eardrum did not have a significant effect on the graft retention rate, but when looking at the postoperative hearing results, if the tympanosclerotic plaques exceeded one-third of the eardrum, their removal provided a 6 dB gain32. The success rate of myringoplasty is the same as eardrum repair without tympanosclerosis, but we prefer cartilage as a graft in ears with tympanosclerosis. Although plaque removal is recommended in myringosclerosis, it is not always necessary.
Although surgical treatment of tympanosclerosis is widely used, there are still controversial issues, especially the choice of surgical technique, staging of the surgery and surgery regarding the stapes.
Performing stapedotomy, especially in tympanosclerotic stapes fixation, is controversial and there is a widespread belief that it carries a high risk of developing postoperative neurosensory hearing loss. There is no direct relationship between the degree of conductive hearing loss and the extent of tympanosclerosis. Neurosensory hearing loss in tympanosclerosis may be due to involvement of the cochlea by hyaline degeneration of the membranous labyrinth.
Participated et al. In their series of 37 cases, they concluded that postoperative hearing outcomes were worse in tympanosclerosis than in COM cases without tympanosclerosis42. Bayazıt et al. As a result of their evaluation of 42 tympanosclerosis cases performed in a single stage, they stated that they could not obtain satisfactory results in cases of stapes fixation performed with mobilization in a single stage, and they recommended performing stapedotomy in the second stage surgery43. In 117 cases with tympanosclerosis, Stankovic cut off the malleus head and performed incus interposition or applied stapedotomy and Teflon piston, depending on the location of the fixation. As a result of short and long-term (5 years) follow-up, they found a significant improvement in the air-bone conduction gap and pure tone threshold, and the long follow-up results were close to the early period results. They did not find significant neurosensory hearing loss, and reported a mild long-term decrease in hearing threshold in the stapedotomy group44. Teufert K.B. and De La Cruz A. found an average postoperative air-bone conduction gap of 17.4 dB in 203 cases with tympanosclerosis, 135 of which had ossicular fixation, and an air-bone conduction gap below 20 dB in 65.3% of the cases. They found partial neurosensory hearing loss in 1% of the cases and profound hearing loss in none of the cases. They did not find neurosensory hearing loss. They found a 0.3 dB decrease in the air-bone conduction gap and a 2 dB decrease in the pure tone threshold in the long term (1.6 years)45. They concluded that ossicular reconstruction in patients with tympanosclerosis could provide satisfactory long-term results with a low complication rate45.
Vincent et al. In their study on 65 patients with tympanosclerotic stapes fixation, they placed a vein graft at the sole after stapedotomy and used a Teflon piston or total prosthesis, and concluded that good results would be obtained if some rules were observed46. Considering all these, it can be concluded that good long-term results can be obtained with a good surgery and that patients can be followed by recommending a hearing aid. The options should be discussed with the patient and he/she should be allowed to make his/her own decision.
Important factors that determine the technique to be applied in tympanosclerosis surgery are:
1.The condition of the ossicles (defect etc.) 2.Fixation of the manubrium due to myringosclerosis (fixation between the bone annulus and the manubrium) 3.The presence and extent of fixation between the attic wall and the malleus and/or incus 4.Fixation of the base of the stapes and the extent of tympanosclerosis (ability to reach the base and sufficient distance for surgery) 5. Presence of perforation in the eardrum 6. Presence of accompanying cholesteatoma 7. Presence of active infection
POSSIBLE PATHOLOGIES
Myringosclerosis (does not disrupt ossicular movements) (Figure -2)
Myringosclerosis (Fixation between manubrium and bone annulus) (Figure -3)
Fixation between the attic wall and malleus and/or incus (incudomalleolar joint fixed) (Figure -4)
Stapes base is fixed (there is distance for surgery) (Figure -5)
Stapes base is fixed, oval window is completely obliterated (Figure -6)
The incudomalleolar joint is fixed and the stapes base is fixed (Figure -7)
In attic fixation of the ossicles or incudomalleolar fixation, instead of mobilization, incision and removal of the malleus head are preferred to prevent re-fixation (Figure -8) and incus interposition or PORP application is preferred after the removal of the incus (Figure -9 and figure -10).
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