In approaching the problem of atrophic rhinitis and ozena, one is confronted with two distinct diseases that have been considered throughout the literature as one and the same disease.Until the time of Gr\l=u"\nwald,1 in 1890, the name of ozena was applied to practically all nasal conditions producing a foul odor. In this manner there were grouped under ozena, syphilitic ulcers of the nose, tuberculosis, nasal diphtheria and, in fact, every nasal condition characterized by a foul odor. When Gr\l=u"\nwaldobserved that the accessory nasal sinuses were frequently the source of the profuse purulent and foulsmelling nasal discharges, he proceeded to consider ozena, which term was used synonymously with atrophic rhinitis, as the end-result of sinusitis. He attempted to refute the case reports of Fr\l=a"\nkel,2 who described ozena as a disease characterized by a triad of symptoms, a foul odor, atrophy and crust formation without loss of tissue substance. Michel, Gr\l=u"\nwaldand Hajek 3 showed that this symptom triad occurred also in syphilis, tuberculosis, foreign bodies, rhinoscleroma and leprosy. This discussion was carried to a point where practically any diagnosis of ozena not of sinus origin was questionable.
The discovery and synthesis of vitamin C has made possible a significant advance in calcium therapy sufficient to warrant reexamination of the value of calcium therapy in otolaryngology.Vitamin C possesses the unique property of solubilizing and ionizing calcium to a degree not previously attainable by oral or intramuscular administration. In calcium cevitamate, the calcium salt of vitamin C, there is available a more effective approach to calcium therapy than that of the previously used gluconate.
The establishment of the differential diagnosis of ozena as primary atrophic rhinitis of vascular origin and secondary atrophic rhinitis of infective source and the presentation of a definite pathologic picture for each condition have made possible a scientific approach to the therapy.At the Third International Rhinolaryngological Congress, held in Madrid in 1932, I had the privilege of demonstrating a series of pathologic photomicrographs on the basis of which the heterogeneous group of conditions characterized by shrinkage of the expansile tissues of the nose, with increase in the nasal space, associated with fetid crusts, and commonly called synonymously atrophic rhinitis and ozena, could be separated pathologically into two subtypes. One of these (atrophic rhinitis, or secondary atrophic rhinitis) presented the pathologic picture of inflammatory reaction to infection that had invaded the tunica propria of the mucosa; the other, ozena, or primary atrophic rhinitis, was due to changes in the blood vessels.In the second type I demonstrated a pathologic picture of vascular disturbance relatively free from infection, with pronounced thickening of the media of the arteries, leading in some instances to true endarteritis. There is an associated loss of the expansile mechanism of the nasal mucosa with erosion of the superficial mucosa and formation of crusts. In the secondary atrophie rhinitis one sees no involvement of the blood vessels, but rather round cell infiltration of the tunica propria, with chronic inflammatory processes disturbing the distensile mechanism of the nasal mucosa.Fortunately, the pathologic picture is further supported by a sharp roentgenographic differentiation, which I described. In all the cases of secondary atrophie rhinitis rarefaction of the bone was present through¬ out, with a thin vomer and a fragile lateral nasal wall, whereas in cases of the primary atrophie type the bony structure of the septum, the lateral nasal wall and the sinus walls were definitely sclerotic. This made possible an easy differential diagnosis without resorting to tissue sections.As an example of the confusion that existed prior to my pathologic differentiation of secondary and primary atrophie rhinitis (ozena), I
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