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Chronic rhinitis (chronic runny nose) - Causes and pathogenesis
Last reviewed: 04.07.2025

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Causes of chronic rhinitis
As a rule, the occurrence of chronic rhinitis is associated with circulatory and trophic disorders in the mucous membrane of the nasal cavity, which can be caused by such factors as frequent acute inflammatory processes in the nasal cavity (including various infections). Irritating environmental factors also have a negative effect. Thus, dry, hot, dusty air dries out the mucous membrane of the nasal cavity and inhibits the function of the ciliated epithelium. Long-term exposure to cold leads to changes in the endocrine system (especially in the adrenal glands), which indirectly affect the development of a chronic inflammatory process in the mucous membrane of the nasal cavity. Some industrial gases and toxic volatile substances (for example, mercury vapor, nitric, sulfuric acid), as well as radiation exposure, have an irritating toxic effect on the mucous membrane of the nasal cavity.
A significant role in the development of chronic rhinitis can be played by general diseases, such as diseases of the cardiovascular system (for example, hypertension and its treatment with vasodilators), kidney disease, dysmenorrhea, frequent coprostasis, alcoholism, endocrine disorders, organic and functional changes in the nervous system, etc.
In addition, important etiologic factors of chronic rhinitis are local processes in the nasal cavity, paranasal sinuses and pharynx. Narrowing or obstruction of the choanae by adenoids contributes to the development of stasis and edema, which in turn leads to increased mucus secretion and growth of bacterial contamination. Purulent discharge during sinusitis infects the nasal cavity. Violation of normal anatomical relationships in the nasal cavity, for example, with a deviated nasal septum, leads to unilateral hypertrophy of the nasal turbinates. Hereditary predispositions, malformations and defects of the nose, injuries, both domestic and surgical (excessively radical or repeated surgical intervention in the nasal cavity) may be important. A foreign body in the nasal cavity, chronic tonsillitis and long-term use of vasoconstrictor drops contribute to the development of chronic inflammation of the nasal cavity.
An important role in the development of chronic rhinitis is played by nutritional conditions, such as monotonous food, lack of vitamins (especially group B), lack of iodine substances in water, etc.
Pathogenesis of chronic rhinitis
The combined effect of some exogenous and endogenous factors over different periods of time can cause the appearance of one or another form of chronic rhinitis. Thus, mineral and metal dust injures the mucous membrane, and flour, chalk and other types of dust cause the death of the cilia of the ciliated epithelium, thereby contributing to the occurrence of its metaplasia, disruption of the outflow from the mucous glands and goblet cells. Dust accumulations in the nasal passages can cement and form nasal stones (rhinoliths). Vapors and gases of various substances have a chemical effect on the nasal mucosa, causing first its acute and then chronic inflammation.
Various forms of chronic rhinitis are characterized by their inherent pathomorphological changes in the nasal cavity.
In chronic catarrhal rhinitis, pathomorphological changes are expressed insignificantly. The most pronounced changes occur in the epithelial and subepithelial layers. The integumentary epithelium becomes thinner, in places metaplasia of the ciliated columnar epithelium into flat epithelium is observed. In some areas, the epithelial cover may be absent. The number of goblet cells increases. In the subepithelial layer, pronounced tissue infiltration is observed, mainly by lymphocytes and neutrophils. The mucous subepithelial glands are dilated due to the secretion accumulated in them. Synchronicity in the action of the secretory glands disappears. Particularly pronounced infiltration by lymphoid elements is observed around the mucous glands. Inflammatory infiltration may not be diffuse, but focal. With a long course of rhinitis, sclerosis develops in the subepithelial layer. The surface of the mucous membrane is covered with exudate, which consists of the secretion of the mucous and goblet glands and leukocytes. The number of leukocytes in the exudate varies depending on the severity of the inflammatory phenomena.
Morphological changes in chronic hypertrophic rhinitis largely depend on the form of the disease. A proliferative process is observed in all areas of the mucous membrane. The epithelial cover is diffusely thickened, hyperplastic in places, and the basement membrane is thickened. Lymphoid, neutrophilic, and plasma cell infiltration is most pronounced in the glands and vessels. The fibroblastic process begins in the glands and subepithelial layer, subsequently reaching the vascular layer. Fibrous tissue either compresses the cavernous plexuses of the turbinates or promotes their expansion and new vessel formation. Compression of the excretory ducts of the glands leads to the formation of cysts. Sometimes bone hyperplasia of the turbinates is observed. In the polypoid form of hypertrophy, the swelling of the mucous membrane is more pronounced, in papillomatous hypertrophy, changes are observed in the epithelial layer, the hyperplastic layers of the epithelium are immersed in certain areas, while fibrosis of these areas is significantly expressed. Morphological changes in nonspecific chronic atrophic rhinitis are observed in the mucous membrane. In this case, along with the atrophic, a completely normal mucous membrane is detected. The greatest changes are noted in the epithelial layer: there is no mucus on the surface of the mucous membrane, goblet cells disappear, the cylindrical epithelium loses cilia, metaplasizes into a multilayered squamous epithelium. In later stages, inflammatory infiltrates occur in the subepithelial layer, changes in the mucous glands and blood vessels.
In vasomotor rhinitis (neurovegetative form), the decisive role in the pathogenesis is played by the disruption of the nervous mechanisms that determine the normal physiology of the nose, as a result of which ordinary irritants cause hyperergic reactions of the mucous membrane. In this form of rhinitis, no specific changes are observed in the mucous membrane of the nose. The lining epithelium is thickened, the number of goblet cells is significantly increased. Fibering and edema of the underlying layer are observed. The cellular reaction is weakly expressed and is represented by lymphoid, neutrophilic, plasma cells and foci of macrophages. Cavernous vessels are dilated. With a long course of the disease, signs characteristic of hypertrophic rhinitis (collatenosis of the interstitial tissue) appear.
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