Paranasal sinus anatomy and pathophysiology.
Mucociliary function keeps the normal sinuses free of drainage despite the fact that several of the sinus otia are not favorably located for gravitational drainage. This function of drainage is lost if the ostium becomes occluded or mucociliary function is impaired. The precise mechanisms of ostial occlusion remain to be elucidated. The normal healthy sinus is free of bacteria, despite the presence of normal bacterial flora in the nasopharynx. In sinusitis bacteria probably gain access to the sinus via the ostium, although in some cases (eg, dental abscess) bacteria penetrate from contiguous structures. Bacteria in an occluded sinus rapidly convert the gas environment to favor their rapid growth. The increased growth and purulence as well as the low PO2 may impair local immune defense mechanisms by degradation of immunoglobulins as well as impaired granulocyte killing. The natural course of sinusitis continues until the ostial occlusion resolves, allowing mucociliary function to drain the affected sinus. In this way spontaneous resolution of sinusitis is possible. Spontaneous drainage cannot occur if the mucociliary function is congenitally deficient, damaged by scarring from previous severe infection, or surgically removed. In addition, chronic sinusitis may occur if there is persistent ostial obstruction from nasal polyps or tumors. The drainage may be diminished by an anatomically small ostium or tortuous drainage duct. Drainage of the sinus may be increased by the effects of erect posture on ostial resistance. Besides adequate drainage, the importance of the local immune defense mechanisms must be emphasized. The occurrence of chronic sinusitis in patients with various immunoglobulin deficiencies reinforces this point.(ABSTRACT TRUNCATED AT 250 WORDS)
D002923:Cilia / Q000502:physiology; D006801:Humans; D009092:Mucous Membrane / Q000502:physiology; D010256:Paranasal Sinuses / Q000033:anatomy & histology* / Q000276:immunology / Q000503:physiopathology; D012852:Sinusitis / Q000503:physiopathology / Q000628:therapy