Chronic Frontitis - Causes and Pathogenesis

Cause of chronic frontal sinusitis

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

Pathogenesis of chronic frontal sinusitis

An important role in the formation of the inflammatory process is played by the anatomical narrowing of the frontal recess, which creates the prerequisites for the block of the sinus outlet and the development of the disease. In the presence of an obstruction in the posterior sections of the nasal cavity (adenoids, hypertrophy of the posterior ends of the lower and middle nasal conchae), the air flow becomes turbulent, injuring the mucous membrane of the sinus when the pressure in the nasal cavity changes. This leads to the development of a local dystrophic process in the form of edema and mucoid swelling, especially in the nasal opening of the frontonasal canal. Aerodynamics in the sinus changes, which creates the prerequisites for the occurrence of acute frontal sinusitis and the maintenance of chronic inflammation in the sinus.

The possibility of developing an inflammatory process in the frontal sinus is influenced by many factors, the most important of which is the condition of the mouths of the frontonasal canal, the normal patency of which ensures adequate drainage and aeration of its lumen. Blood vessels penetrate into the sinus through it, and the largest number of goblet cells are concentrated in the area of the mouth. The mucous membrane of the mouths of the frontal sinuses experiences adverse effects most often when aerodynamics in the nasal cavity is disrupted due to the closest location to the anterior sections of the middle nasal passage. The opposing surfaces of the mucous membrane of the ostiomeatal complex come into close contact, the movement of the cilia is completely blocked, and the transport of secretion stops. The inflammatory process in any of the "narrow spots" easily spreads towards the nearby paranasal sinuses, which leads to a narrowing or closure of their anastomoses. Blockage of the nasal opening of the frontonasal canal by edematous mucous membrane or a local dystrophic process (polyposis) leads to compression of the vessels and cessation of air flow into the sinus lumen. This leads to hypoxia and destabilization of gas exchange in it. A decrease in the partial pressure of oxygen in itself inhibits the flickering of cilia and the transfer of mucus. Due to venous congestion, increasing edema and thickening of the mucous membrane, the distance from the arterial vessels of the proper layer to the epithelial cells increases, which leads to a violation of oxygen delivery to them. Under hypoxic conditions, the mucous membrane of the frontal sinus switches to aerobic glycolysis with the accumulation of underoxidized metabolic products. As a result of the pathological process, an acidic environment is formed in the secretion, which leads to further disruption of mucociliary clearance. Subsequently, stagnation of the secretion and a shift in the 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 ensures favorable growth of anaerobes, with the suppression of microflora adapted in the upper respiratory tract, as well as due to the destruction of Ig and the production of proteolytic enzymes.

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