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Inflammatory diseases of the paranasal sinuses (sinusitis) are among the most common diseases of the upper respiratory tract. According to the literature, patients with sinusitis make up about 1/3 of the total number of hospitals hospitalized in ENT (Kozlov M.Ya., 1985; Soldatov IB, 1990; Piskunov GZ et al., 1992; Aref'eva N.A. , 1994). The foci of inflammation in the paranasal sinuses can be a source of infectious sensitization of the underlying respiratory tract and lungs, as well as cause severe orbital and intracranial complications.

Most authors on the frequency of involvement in the inflammatory process put in the first place the maxillary sinus (maxillary sinusitis), then the ethmoid labyrinth (ethmoiditis), frontal (frontal sinusitis) and sphenoid (sphenoiditis). However, this provision cannot be considered completely flawless. In the inflammatory process, not one, but several sinuses (polysynitis) are often involved. In this case, in case of damage to the sinuses of one side, they speak of hemisinitis, and in case of damage to all sinuses - about pansinitis.

Often the sinus is susceptible to the inflammatory process. Clinicians know the expression: "inflammation loves the sinuses."

In children, taking into account the age-related development of sinuses, up to 3 years of age, inflammation of the ethmoid labyrinth predominates (up to 80 - 90%), and from 3 to 7 years of age, combined lesions of the ethmoid labyrinth and maxillary sinuses predominate (Soldatov IB, 1990).

In the etiology of both acute and chronic sinusitis, the penetration of the infection into the paranasal sinuses is of primary importance. The most common route is through natural anastomoses that communicate with the sinus to the nasal cavity. In acute infectious diseases (typhoid, diphtheria, scarlet fever, measles), sinus infection is possible through the hematogenous route. In the etiology of maxillary sinusitis, purulent foci of the dento-maxillary system, especially large and small molars adjacent to the lower wall of the sinus, also play a role. The most common cause of odontogenic maxillary sinusitis is foreign bodies that enter the sinus from the oral cavity: filling material, fragments of broken dental instruments, failed tooth roots, and turunds. Granulomas at the root of the tooth, subperiosteal abscesses, periodontal disease can also lead to the occurrence of odontogenic maxillary sinusitis (Ovchinnikov Yu.M., 1995). It is possible that the infection will be brought in when the sinuses are wounded with a gun or other weapon.

The most common cause of acute sinusitis is acute respiratory, including viral diseases. Significant importance, along with influenza and parainfluenza viruses, is given to rhinoviruses and adenoviruses, as well as staphylococci, streptococci, pneumococci, gram-negative and gram-positive bacilli. In some cases, crops from the sinuses in acute sinusitis turn out to be sterile, which is explained by the presence of viral as well as anaerobic flora detected only by special research methods.

Monoflora is characteristic of acute sinuites, and polyflora is chronic.

In chronic sinusitis, along with coccal flora, Pseudomonas aeruginosa, Escherichia coli and various strains of the vulgar protea are found.

Significantly more often than in acute sinuitis, especially in targeted searches, anaerobic flora is found (Lushnikova T.A., 1992, Dainyak LB, 1994). In recent years, fungal infection of the paranasal sinuses has become relevant.
Not being the primary etiological factor in the development of sinusitis, fungal flora due to dysbiosis caused by irrational antibiotic therapy may be the dominant or even the only factor supporting the persistent chronic inflammatory process in the sinuses. It can be the cause of further dangerous development of the disease in the form of deep mycosis (Stammberger H., 1982; Dainiak LB, 1994). The most commonly sown mushrooms of the genus Aspergillus, Penicillum and Candida (Kunelskaya V.Ya., 1989). In the pathogenesis of acute and especially chronic sinusitis, impaired ventilation (aeration) of the paranasal sinuses caused by anatomical defects of the nasal cavity (pronounced curvature of the nasal septum, hypertrophy of the middle nasal concha, the presence of abnormal bulla ethmoidalis), as well as congenital narrowness of the nose (leptorinia) is important.

When the sinus anastomosis is closed by the edematous mucosa, the oxygen content in the sinus will decrease, and the carbon dioxide content will increase. The oxygen content is especially reduced if pus is produced in the sinus (Drettner B., 1984). In the presence of pus, the oxygen content in the sinus approaches zero, the carbon dioxide content increases significantly, and the pH decreases - (Carentfeld C., Lundberg S., 1977). Oxygen is absorbed not only by the mucous membrane, but also by bacteria and leukocytes (Drettner B., 1984). All this contributes to the development of anaerobic infections in chronic sinusitis.

A significant role in the development of acute and chronic sinusitis is played by allergic processes (auto- and bacterial allergies), as well as a known determinism associated with congenital or acquired immunological deficiency. Currently, it has been established that one of the main reasons for the development of recurrent inflammatory diseases of the upper respiratory tract, including paranasal sinuses, there is a deficiency of immunoglobulins, in particular, secretory Ig A. The clinical expression of Ig A deficiency in the mucous membrane of the upper respiratory tract is manifested in the form of chronic rhinitis, polysynitis, chronic tonsillitis, adenoiditis, etc. (Gerber V.X., 1989; Komarets S.A., 1992; Grebenshchikova L.A., 1994; Lantsov A.A. et al., 1996).

Of great importance in the development of acute and chronic sinusitis is a violation of the normal function of the ciliated epithelium and mucous glands (mucociliary apparatus of the mucous membrane) caused by adverse environmental factors: cold air, air pollution by harmful industrial gases. As a result, there is inhibition or cessation of ciliary beat, which leads to a delay in the infectious onset in the nasal cavity and paranasal sinuses and its subsequent penetration through the membranes of the mucous membrane (Ostakovich V.E., 1982, Pankova VB, 1987, Piskunov G. 3 . and Piskunov S.3., 1988, Pluzhnikov M.S. and Lavrenova G.V., 1990). A significant decrease in the functional activity of the ciliated epithelium of the mucous membrane in the middle and lower nasal concha was established in acute and chronic ethmoiditis and maxillary sinusitis (Bondaruk V.V., 1996).

The development of acute and especially chronic sinusitis is promoted by chronic diseases, including diabetes.
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