Chronic frontal sinusitis: causes and pathogenesis

Cause of chronic frontitis

The causative agents of the disease are most likely representatives of the coccal microflora, in particular staphylococci. In recent years, there have been reports of the isolation and quality of pathogens of the association of three conditionally pathogenic microorganisms Haemophilus influenzae, Streptococcus pneumoniae and Maxarelae catharrhalis. Some clinicians do not exclude anaerobes and fungi from this list.

Pathogenesis of chronic frontitis

An important role in the formation of the inflammatory process is played by the anatomical narrowing of the frontal pocket, which creates the prerequisites for the sinus outlet port and the development of the disease. In the presence of an obstruction in the posterior parts of the nasal cavity (adenoids, hypertrophy of the posterior ends of the lower and middle nasal concha), the air stream acquires a turbulent character, traumatizing the sinus mucosa with a change in the pressure in the nasal cavity. This leads to the development of a local dystrophic process in the form of edema and mucoid swelling, especially in the nasal mouth of the frontal-nasal canal. Aerodynamics in the sinus changes, which creates the prerequisites for the emergence of acute frontitis and maintenance of chronic inflammation in the sinus.

The possibility of developing the inflammatory process in the frontal sinus is influenced by many factors, the most important of which is the condition of the mouths of the frontal-nasal canal, the normal patency of which ensures adequate drainage and aeration of its lumen. Through it, blood vessels penetrate into the sinus, and the largest number of goblet cells is concentrated in the mouth area. The mucous membrane of the mouth of the frontal sinuses experiences adverse effects more often when the aerodynamics in the nasal cavity are disturbed due to the closest position to the anterior sections of the middle nasal passage. Opposing surfaces of the mucous membrane of the ostiomeatal complex come into close contact, the movement of the cilia is completely blocked, and secretion transport stops. Inflammatory process in any of the "bottlenecks" easily spreads in the direction of nearby paranasal sinuses, which leads to the narrowing or closure of their joints. The blockade of the nasal mouth of the frontal-nasal canal by the edematous mucous membrane or local dystrophic process (polyposis) leads to the compression of the vessels and the cessation of air intake into the lumen of the sinus. This leads to hypoxia and destabilization of gas exchange in it. Reducing the partial pressure of oxygen in itself inhibits the flicker of cilia and the transfer of mucus. In connection with venous congestion, increasing edema and thickening of the mucosa increases the distance from the arterial vessels of its own layer to the epithelial cells, which leads to a violation of the delivery of oxygen to them. Under conditions of hypoxia, the mucous membrane of the frontal sinus passes to aerobic glycolysis with the accumulation of under-oxidized metabolic products. As a result of the pathological process, an acidic environment is formed in secret, which leads to a further violation of mucociliary clearance. Further, stagnation of secretion and a shift in acid-base balance develop. Metabolic acidosis also paralyzes the action of lysozyme. The inflammatory process develops in a closed cavity, in an atmosphere poor in oxygen, which provides a favorable growth of anaerobes, with the suppression of microflora adapted in the upper respiratory tract, as well as the destruction of Ig and the production of proteolytic enzymes.

[1], [2], [3]