The surface features of atrophic rhinitis are shown and it is suggested that these explain the majority of symptoms. It seems clear that any lesion preventing the formation or maturation of large numbers of motile cilia, or the production of mucus capable of forming confluent sheets suitable for continuous propulsion, may cause atrophic rhinitis. In both familial and idiopathic forms of the disease, both abnormalities are present. It would be most interesting to know the ultrastructure of the cilia in transverse section of this condition. Transverse electron microscopic studies in Retinitis Pigmentosa, Usher's syndrome and Kartagener's syndrome now becoming known as the low cilia motility diseases show clearly the primary lesions in the micro-tubules and dynein arms of the cilia. A similar transmission electron microscopic study in atrophic rhinitis may show the fundamental cilial lesions. Surgical closure of the nasal passages has much to offer the patient with severe symptoms as the clinical features of the disease improve with the increasing normal micro-anatomical features demonstrated in this paper as a result of closure. This improvement in structure is not in all cases sufficient to fulfil the above criteria so a complete cure is improbable in the majority of cases.