УДК: 616.284-002.3-004-053.2
THE DEVELOPMENT OF TYMPANOSCLEROSIS IN CHILDREN WITH CHRONIC SUPPURATIVE OTITIS MEDIA
Shavkat Ergashevich AMONOV1, Fazliddin Nuriddinovich NAZIROV2
1Tashkent Pediatric Medical Institute, Tashkent, Uzbekistan
2Republican Specialized Scientific and Practical Medical Center for Pediatrics, Tashkent, Uzbekistan
РАЗВИТИЕ ТИМПАНОСКЛЕРОЗА У ДЕТЕЙ С ХРОНИЧЕСКИМ ГНОЙНЫМ СРЕДНИМ ОТИТОМ
Шавкат Эргашевич АМОНОВ1, Фазлиддин Нуриддинович НАЗИРОВ2
1Ташкентский педиатрический медицинский институт, Ташкент, Узбекистан
2Республиканский специализированный научно-практический медицинский центр педиатрии, Ташкент, Узбекистан
СУРУНКАЛИ ЙИРИНГЛИ ЎРТА ОТИТ БИЛАН КАСАЛЛАНГАН БОЛАЛАРДА ТИМПАНОСКЛЕРОЗНИНГ РИВОЖЛАНИШИ
Шавкат Эргашевич АМОНОВ1, Фазлиддин Нуриддинович НАЗИРОВ2
1Тошкент педиатрия тиббиёт институти, Тошкент, Ўзбекистон
2Республика педиатрия ихтисослаштирилган илмий-амалий тиббиёт маркази, Тошкент, Ўзбекистон
ABSTRACT
This review presents a variety of views on development of tympanosclerosis in children with chronic suppurative otitis media (CSOM). The review showed that all of the above indicates the need for in-depth studies of the mechanisms of development of tympanosclerosis in children with CSOM in order to develop effective methods for diagnosing, treating and preventing the disease.
Key words: chronic suppurative otitis media, tympanosclerosis, children, hearing loss.
АННОТАЦИЯ
Данный обзор посвящён развитию тимпаносклероза у детей с хроническим гнойным средним отитом (ХГСО). Обзор показал, что все вышеуказанное свидетельствует о необходимости проведения углубленных исследований механизмов развития тимпаносклероза у детей с ХГСО целью разработки эффективных методов диагностики, лечения и профилактики заболевания.
Ключевые слова: хронический гнойный средний отит, тимпаносклероз, дети, тугоухость.
АННОТАЦИЯ
Ушбу шарҳ сурункали йирингли ўрта отит (СЙЎО) билан касалланган болаларда тимпаносклерознинг ривожланишига бағишланган. Шарҳ шуни кўрсатдики, юқоридагиларнинг барчаси касалликни ташхислаш, даволаш ва олдини олишнинг самарали усулларини ишлаб чиқиш учун СЙЎО билан оғриган болаларда тимпаносклерознинг ривожланиш механизмларини чуқур ўрганиш зарурлигини кўрсатади.
Калит сўзлар: сурункали йирингли ўрта отит, тимпаносклероз, болалар, эшитиш қобилияти йўқлиги.
Exacerbation of chronic inflammation of the middle ear for many years remains one of the most common and dangerous conditions encountered in the practice of pediatric otolaryngologists and pediatricians, due to the risk of severe intracranial otogenic complications that threaten the life of a child [1, 4, 12, 15]. The incidence of chronic suppurative otitis media (CSOM), despite significant progress in prevention, diagnosis and treatment, has an alarming tendency to increase in the structure of pathologies of the ear, nose and throat. Many medical and social causes that cause the current state of this problem are described in the world scientific literature, and a number of studies are devoted to such an unfavorable consequence of the disease as hearing loss, which, in turn, together with the frequent recurrence of the inflammatory process, directly affects the deterioration in the quality of life of people suffering from this disease [2, 7, 13].
According to various authors, the prevalence of tympanosclerosis ranges from 3,3% to 33% among all patients with chronic otitis media and, thus, can be considered a common disease [12].
There is an opinion that the incidence of tympanosclerosis is only increasing [3, 6]. One of the possible reasons for this trend is considered to be irrational antibiotic therapy, leading to a change in the clinical course of chronic otitis media, and, as a result, to the formation of tympanosclerosis [5, 10].
Purpose: To study the development of tympanosclerosis in children with chronic suppurative otitis media.
Material and methods of research: Scientific publications on this subject, published over the past 10 years in the E-library and PubMed databases, were studied.
Results: The course of CSOM in children currently has a number of features: the disease began to occur at an earlier age, the actual pathological process has noticeably changed, it has become more stubborn and aggressive, with a high risk of exacerbations that are life-threatening for the child, causing intracranial complications. In a number of studies, the reason for this trend is considered to be the ineffective treatment of the most chronic pathology of the middle ear [14]. Mortality in complications of CSOM caused by exacerbations of the disease reaches 16,1% [15]. There are well-known general factors that influence the development of the disease: social status, material well-being, culture of the population, the level of medical care and the commercial component in the provision of medical services.
The development of microbial invasion and the maintenance of a chronic inflammatory infectious process in the middle ear cavity are facilitated by the peculiarities of the anatomy in children. The younger the child, the more pronounced they are. So, in newborns and infants, the auditory tube mainly consists of fibrocartilaginous tissue. Later, its bone part begins to form. In children, it is more extensible, wider and shorter than in adults, directed horizontally and cylindrical in shape. The isthmus of the auditory tube is rarely expressed, the pharyngeal mouth is bordered by a cartilaginous ring, often gaping and located low in the nasopharynx. All this contributes to stagnation and reflux into the middle ear of the discharge from the nasal cavity and nasopharynx [1, 9]. The inflammatory process of the auditory tube is maintained due to the presence of many depressions and bays in its bone section [8]. Such features of the auditory tube in children are one of the factors of recurrence of acute inflammation of the middle ear, sclerosis of the structures of the mastoid process and chronicity of the process with the possible development of cholesteatoma [4].
In addition to the anatomical features of the child's body, the development of CSOM is affected by various pathological conditions of the upper respiratory tract: hypertrophy of adenoid vegetations and adenoiditis, deviated nasal septum, chronic sinusitis, hypertrophic, vasomotor and allergic rhinitis [5]. All of the above types of pathology cause a violation of the ventilation and drainage function of the auditory (Eustachian) tube, congestion in the nasopharynx, which in turn leads to impaired aeration of the temporal bone cavities, difficulty in evacuating the contents from the middle ear cavity and persistence of various microflora. The pathology of the auditory tube is widely covered in the publications of domestic and foreign authors as a key moment in the development of chronic otitis media [12].
Many authors pay attention to the widely occurring diseases in the practice of an ENT doctor, which can lead to the development of CSOM. It has long been an axiom that acute purulent otitis media (APOM), especially with a recurrent nature of the course, is the cause of permanent perforation of the tympanic membrane. It is possible to develop CSOM as a consequence of exudative otitis media, in which suppuration of the exudate occurred. Thus, the aggressive destruction of injured tissues by a purulent process in acute otitis media leads to a significant increase in the size of the perforation of the tympanic membrane and the formation of a mesotympanic defect. An increase in the vacuum state in the middle ear leads to the appearance of epitympanic perforation. This is especially pronounced in exudative otitis, when there is not only an increase in the block of the auditory tube, but also a blockade in the tympanic cavity between the epi- and mesotympanum. This is facilitated by the features of the anatomy of the ligamentous apparatus of the auditory ossicles, folds and pockets of the mucous membrane of the middle ear in the projection of the loose part of the tympanic membrane. Under conditions of edema, these structures almost completely block the communication between the upper and middle floors of the tympanic cavity, leaving only separate slit-like canals. In this connection, pars flaccida is subjected to vacuum retraction in the direction of the epitympanum and the epidermis of the tympanic membrane is immersed in the folds and pockets of the mucous membrane, which can lead to the formation of cholesteatoma in this area [6]. The process of formation of such retraction pockets is often observed with prolonged dysfunction of the auditory tube, exudative and adhesive otitis media [1]. In addition, such architectonics of the structures of the tympanic cavity, in the presence of transudate, exudate or pus in the middle ear, can lead to the appearance of an isolated and difficult-to-treat focus of inflammation in the epitympanum.
Despite many studies, not only clinical and morphological, but also immunological, histochemical, and electron microscopy, the pathogenesis of this disease has not been fully studied [3]. Inflammation is considered as an etiological factor in the development of tympanosclerosis, and ectopic calcification is considered the main mechanism for the formation of tympanosclerotic changes [12]. A number of researchers consider tympanosclerosis to be the final and static outcome of various inflammatory processes in the middle ear, while others consider it to be a slowly progressive destructive process [14].
Most authors agree that tympanosclerosis, as a rule, begins to form in childhood or adolescence, and any inflammatory disease in the middle ear is the initiating moment. It has been established that tympanosclerotic changes occur as a result of various acute and chronic diseases of the middle ear, and are a manifestation of a degenerative lesion of the mucoperiost [12].
It is noteworthy that in some patients tympanosclerosis is actively formed after a single otitis media, in others, despite frequent otitis media, signs of tympanosclerosis never appear [7].
It has already been proven that some factors are likely to influence the development of the tympanosclerotic process. So, a significant role is assigned to genetic predisposition. Based on the results obtained, it was established that the serum levels of HLA-B35 and -DR3 in patients with diagnosed tympanosclerosis are significantly higher than in healthy people, and attention was focused on a possible immunogenetic predisposition to the development of tympanosclerosis [4]. When studying the expression levels of genes encoding type I, II, III and IV collagen (COL1A1, COL2A1, COL3A1, COL4A1), as well as osteopontin. The revealed correlation between the expression of type I, II, IV collagen, as well as osteopontin, and the severity of clinical manifestations of tympanosclerosis indicates the involvement of these proteins in excessive fibrosis and pathological sclerotic remodeling of the tympanic membrane [14].
It has been proven that an important role in the occurrence of tympanosclerosis is played by free radicals, which are formed, in particular, during hyperoxia associated with long-term perforation of the tympanic membrane [9]. A relationship was found between a decrease in the levels of cellular antioxidants - superoxide dismutase and catalase, and the development of tympanosclerosis [11]. In an experiment on rats, it was found that the local application of acetylcysteine, a mucolytic drug with antioxidant and antitoxic properties, prevents the development of tympanosclerosis after myringotomy [14]. In other experiments on laboratory animals, a similar effect was observed with the systemic use of a number of antioxidants, including caffeic acid phenyl ester contained in propolis, L-carnitine, and selenium [15].
There is information about the development of the tympanosclerotic process as a result of an injury to the tympanic membrane [5]. According to many authors, myringotomy with the installation of a tympanoventilation tube in the treatment of exudative otitis media in children contributes to the formation of myringosclerosis [2]. The results of clinical studies indicate an increase in the occurrence of tympanosclerotic lesions in the thickness of the tympanic membrane after bypass surgery of the tympanic cavity [8]. The effectiveness of the use of vitamin E for the prevention of the development of tympanosclerosis after the installation of tympanoventilation tubes has been proven [12].
Currently, one of the promising areas for studying the pathogenesis of tympanosclerosis is the study of the features of calcium metabolism in patients with tympanosclerosis [11]. Studies have proven the effectiveness of the use of calcium channel blockers to prevent the development of tympanosclerosis [15].
It was shown that the concentration of parathyroid hormone in the middle ear in patients with CSOM with tympanosclerosis compared with patients with CSOM without tympanosclerosis, as well as healthy people, is higher by 21,5%. When tympanosclerosis is combined with other pathological processes in the middle ear (cholesteatoma, caries), the concentration of parathyroid hormone is increased by 38,3% [12].
The role of matrix metalloproteinases involved in the degradation of extracellular matrix structures has been studied [7]. To date, it has been established that in patients with severe atherosclerotic changes, tympanosclerosis occurs significantly more often than in patients without manifestations of atherosclerosis, and therefore, studies are ongoing aimed at identifying common mechanisms for the development of these diseases [13].
Conclusion: Thus, it follows that all of the above indicates the need for in-depth studies of the mechanisms of development of tympanosclerosis in children with CSOM in order to develop effective methods for diagnosing, treating and preventing the disease.
