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Acute sinusitis - Causes and pathogenesis
Last reviewed: 06.07.2025
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Causes of Acute Sinusitis
The development of inflammation of the mucous membrane of the paranasal sinuses is facilitated by conditions of both general and local nature. General conditions include states of individual reactivity, constitutional prerequisites, immune forces of the body, as well as various unfavorable factors of the external environment. Among local factors, inflammation in the sinuses is most often facilitated by those in which the drainage function of the outlet openings, ventilation of the sinuses and the work of the mucociliary transport system are disrupted.
The causes of dysfunction of the paranasal sinus outlets can be systemic (e.g., allergy) and local (e.g., hypertrophy of the nasal turbinates). Local causes are divided into anatomical and pathophysiological. The former include curvature, spines and ridges of the nasal septum, hypertrophy of the nasal turbinates, hyperplasia of the mucous membrane or polyps, and various tumors. It has been established that the listed factors not only disrupt the drainage and ventilation functions of natural anastomoses, but also, if they exist for a long time, especially in childhood, contribute to the abnormal development of the paranasal sinuses themselves (shape, size, diameter of the anastomoses and their course).
In the etiology of both acute and chronic sinusitis, the main factor is the infection that penetrates the sinuses from the nasal cavity, teeth due to a nasal injury or with the blood flow from a distant source. In this case, coccal flora (streptococcus, staphylococcus, pneumococcus) is most often found in the sinuses, less often gram-negative and gram-positive bacilli, influenza viruses, parainfluenza, adenoviruses, fungal flora. Anaerobic bacteria are often sown. Acute sinusitis is often characterized by the presence of only one pathogen, while chronic sinusitis is characterized by polymicrobial flora.
Pathogenesis of acute sinusitis
Pathophysiological factors that contribute to the progression of the inflammatory process in the paranasal sinuses include: dysfunction of the glands of the nasal mucosa, leading to excessive accumulation or lack of secretion, a change in the direction of the flow of inhaled and exhaled air in the nasal cavity, leading to a disruption of gas exchange in the paranasal sinuses, and suppression of the functions of the ciliated epithelium of the mucous membrane.
Difficult or, conversely, freer than normal passage of air through the nasal cavity leads to changes in ventilation in the sinuses. In turn, disruption of ventilation of the paranasal sinuses and air pressure in them leads to edematous inflammatory changes in the mucous membrane, which further disrupts air exchange and drainage of the sinuses. Such changes, naturally, can become a favorable background for the development of various forms of sinusitis.
In the paranasal sinuses, due to the closure of natural anastomoses, there is stagnation of the secretion of the mucous glands, a change in pH, a disruption of metabolism in the mucous membrane, a disorder of the functions of the ciliated epithelium, and the activation of opportunistic microflora is possible.
No less important in the development of pathological conditions of the nasal cavity and paranasal sinuses is the function of the ciliated epithelium. Due to the strict rhythm of the movements of the cilia of the ciliated cells, the secretion of the mucous membrane and various foreign particles are transported from the nasal cavity and paranasal sinuses towards the nasopharynx. The impact of various factors, such as mechanical, physical, chemical, biological, disrupts the function of the ciliated epithelium, and the cilia themselves are destroyed.
In acute inflammation, exudative processes predominate. In the early stages, the exudate is serous, then mucous-serous, and when a bacterial infection is added, it becomes purulent, with a large number of leukocytes and detritus. Blood vessels are dilated, capillary permeability increases, and mucous membrane edema develops.
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