Tympanosclerosis

Abstract

Tympanosclerosis is a disease which affects the tympanic membrane (TM) and middle ear. The locus for the essential pathology is in the connective tissue component of the drum which is the lamina propria. In the middle ear, the pathology is in the basement membrane. In the early stages there is a minimal involvement of the mesenchymal component, usually seen as a small white macula, or scar, in the drum. In advanced disease, the hyalinization of the mesenchymal component together with the attraction of the calcium ion leads to a thick, dense, calcified scar. The theory of pathogenesis for this disease entity is that the connective tissue component of these structures is stimulated by infection, inflammation, or trauma involving some degree of local immunological hypersensitivity. With severe middle ear infection, the mucosa of the inner surface of the drum becomes permeable, and the ground substance of the lamina propria becomes edematous taking up water together with components of complement from the middle ear disease. The abnormal middle ear secretions contain the immunoglobulin components capable of participating in the process. If there is any damage to the connective tissue, the adsorption and repair permits the body to react immunologically against the destroyed tissue, thereby sensitizing this area. Experiments were performed with the guinea pig in which the tympanic membrane was removed and the lamina propria isolated and prepared as an immunological antigen. When this material was injected into the rabbits, a high, satisfactory antiguinea pig tympanic membrane antibody was formed (anti-GPTM). It was then possible to remove this anti-GPTM antibody from the serum. The tissue specificity was determined by immunofluorescent staining which showed it to be adsorbed onto the TM, middle ear mucosa, as well as the basement membrane of the respiratory tract. The guinea pigs which were passively sensitized with anti-GPTM antiserum demonstrated the binding of the antibodies on the tympanic membrane when subject to trauma, infection, or cautery. The manifestation was in the anatomical area related to the injury. Complement fixation was, likewise, demonstrated. Controlled animals which were not traumatized, or were not passively sensitized, included those which were injected with IgG from rabbits not sensitized against GPTM. They showed no fixation of antibody or complement in the TM. Following injury the antibody and complement bound to the TM provide the necessary elements for the subsequent immunopathologic disease entity known at tympanosclerosis.