Clinical Otolaryngology 1978, 3, 491-493
Middle ear and Eustachian tube lining in chronic otitis media* G . ZECHNER E N T Department, Municipial Hospital, Wien-Lainz, West Germany
Accepted for publication 17 February 1978
ZECHNER G. (1978) Clinical Otolaryngology 3, 49 I -493 Middle ear a n d Eustachian tube lining in chronic otitis media By means of histological observations we have tried to find morphological data on which to classify non-suppurative and suppurative chronic otitis media. There was also evidence of pathophysiological features which may have direct influence upon the development and behaviour of chronic inflammations of the tympanic cleft, such as disorders of ventilation and reaction of the mucoperiosteal layer. Local defence mechanisms, the species and virulence of infection also play an important role. It appears that the Eustachian tube is a very effective mechanical and immunological barrier against ascending infection which may perhaps be assisted by antibiotic treatment. Certainly non-suppurative chronic otitis media is more frequent now than in pre-antibiotic days. Keywords chronic otitis media cholesterolgranuloma Eustachian tube
Middle ear and mastoid air cells are a closed, but ventilated cleft, connected with the nasopharynx by the auditory tube. The whole system is lined by a thin mucosa, which acts as a mucociliary transportation organ and serves in local immunoglobulin and secretory enzyme production. The tube provides ventilation and clearance of the tympanic cavity and is a mechanical, immunological and biochemical barrier against ascending infection. Any kind of functional failure of the auditory tube involves the middle ear mucosa and leads to chronic otitis media, if the following conditions occur: Blockage of the tube causing adhesive otitis media. Recurrent infections and lack of local immunological defence ability leading to chronic purulent otitis media. 3 Defective healing: may give rise to persistent perforation, fibrous adhesions and patchy or diffuse calcification. I
z
Morphologically we distinguish between 2 types of chronic otitis media : non-purulent or closed and purulent or open forms;' in our material, using biopsies taken during tympanoplastic procedures and sections from our temporal bone collection, we compared the findings in middle ear and the auditory tube in both groups of chronic otitis media:
A. Non-purulent chronic otitis media (adhesive chronic otitis media) : The clinical * Read at the first international meeting of the Politzer Society, February 1978. 0307-7772/78/11oo-o~~1$02.000 1978 Blackwell Scientific Publications
491
492
G . ZECI-INER
conditions found are blockage of the tube, an intact tympanic membrane and effusion in the middle ear.’F2 Morphological criteria for the blockage of the tube: The mucosal changes are hyperplasia and metaplasia. Mucosal folds are thickened, oedematous and swollen. The goblet cell population is increased. The so-called tubal tonsil is visible as a follicle-like aggregation of immunocompetent cells within the submucosa. The salivary glands adjacent to the auditory tube are also altered.4 Some of the excretory ducts are ectatic, filled by thick mucoid secretion, others contain microliths. The glandular parenchyma is partially reduced and replaced by fat or scar tissue. One has the impression that the infection is stopped within the tube and causes the loss of tubal function. Mucosal changes in the middle ear: The mucosa is swollen, oedematous and hyperaemic. The inflammatory infiltration is limited to the surroundings of the vessels, and never reaches theunderlaying bone. Cuboidal epitheliumis transformed to secretory and ciliated elements. The basal membrane shows in silver impregnation as an interrupted and irregular fibre network, but is much thicker than normal, as demonstrated by Van Gieson and H & E staining. In biopsies of longer lasting otitis, the epithelium gives a highly positive mucopolysaccharide reaction, which means that it becomes highly secretory. These findings are very clear at the bottom of the cryptlike mucosa folds, giving rise to the term ‘grand-like structures’. The middle ear cavity is filled with an acidophilic effusion, which contains only a few cells. I n cytological smears they show up as different kinds of macrophages, such as foam cells, lipophages, and phagocytes. Histologically one cannot distinguish serous from mucoid effusion. Because of the blocked tube and the intact tympanic membrane, the effusion cannot be expelled, and produces a mucosal reaction. Finger-like folds extend into the lumen, Much enzymatic activity can be seen : acid and alkaline phosphatase, non-specific esterases and leucinaminopeptidase are demonstrable. There seems to be a digestive effort to eliminate the effusion. Organization also takes place and the formation of granulation tissue starts. A typical element is the cholesterol granuloma which consists of fibrous granulation tissue, in which large numbers of cholesterol crystals have been deposited, surrounded by foreign body giant cells. Evidence of recent haemorrhage is often seen. Untreated the disease ends in what Politzer described as ‘adhesive process’. The whole tympanic cavity may be filled with fibrous tissue and the tympanic membrane retracted or scarred. The possibility of restoration of ventilation of the tympanic cleft is restricted by connective tissue proliferation within the effusion. Other complications are tympanosclerosis, localized within the submucosa and may be patchy or diffuse.
B. Suppurativechronic otitis media or tubotympanic disease3 The clinical condition comprises permanent perforation of the tympanic membrane, recurrent otorrhcea caused by persistent mucosal disease and an irritated, but not blocked, auditory tube. MorpholoRicalJindi~zsiia the tube: The mucosa is thicker than normal, swollen by hyperaemia within Mayer’s plexus and a very dense inflammatory infiltration. The cells are not aggregated around vessels or in arranged follicles, but are distributed through the submucosa. The goblet cell population is increased. The adjacent salivary glands show evidence of in-
Lining of the nzirlrlle eur and Eustackian tube
493
creased mucus production and the acini have a strongly positive mucopolysaccharide reaction with PAS staining. At the tympanic end of the Eustachian tube the mucosa is hyperplastic and the epithelium consists of secreting and ciliated cells. The surface is often covered by cellular debris and discharge. Mucosal chrznges in the middle ear: The mucosa of the tympanic cleft is swollen and congested. There may be a profuse mucoid or mucopurulent discharge containing a considerable number of leucocytes. The inflammatory cellular infiltration is diffuse and reaches the underlying bone. Epithelial lesions are frequent and give rise to granulation buds. These are often the first sign of the organization of an effusion which is not expelled from the tympanic cleft. Aural polyps typical of suppurative otitis media consist of oedematous connective tissue and their stroma is infiltrated by a large number of inflammatory cells, often plasma cells and lymphocytes. They may include glandlike structures or cysts and their surface is covered with pseudostratified columnar epithelium, showing areas of keratosis. Polypi and swollen mucosal folds hinder the clearance of the aural discharge, giving rise to organization of the effusion and cholesterol granuloma. There is a great difference in the progression of the inflammatory process towards the underlaying bone and the ossicles, although destructive lacunar absorption may start within the bone. Surrounding the mastoid cells very soon a regenerative process begins. New bone formation creates a pagetoid pattern, characterized by irregular mosaic cement lines. I n areas of post-inflammatory reconstruction marrow spaces are filled with granulation tissue and inflammatory cells especially around the vessels. T h e disease may terminate like the non-purulent type in an adhesive process if the mucosal infection stops, and the bone reaction may lead to severe complication because of erosion, and necrosis. Persistent perforation of the eardrum membrane allows secondary infection by saprophytic or pyogenic organisms, which may be responsible for acute exacerbations of mucosal disease or infiltration by keratinizing stratified squamous epithelium-the start of cholesteatoma formation.
Acknowledgement This research was supported by Fonds zur Forderung der wissenschaftlichen Forschung in Osterreich.
References Z ~ L L N EF. R (1974) HNO-Heilkzmde. G. Thieme, Stuttgart. 2 POLITZER A. (1873) Seltener Fall eines chronischen Mittelohrkatarrhs. Archiv f i r Ohrenheilkunde 7, 48. I.B. (1968) Chronic suppurative otitis media. Proceedings of the Royal Society of Medicine 61, 3 THORBURN 395. 4 ZECHNER G. (1978) Der Formwandel yon Mittelohr-und Tubenschleimhaut in der Zeit der antibiotischen Therapie. H N O 26, 9. I
Middle ear and Eustachian tube lining in chronic otitis media* G . ZECHNER E N T Department, Municipial Hospital, Wien-Lainz, West Germany
Accepted for publication 17 February 1978
ZECHNER G. (1978) Clinical Otolaryngology 3, 49 I -493 Middle ear a n d Eustachian tube lining in chronic otitis media By means of histological observations we have tried to find morphological data on which to classify non-suppurative and suppurative chronic otitis media. There was also evidence of pathophysiological features which may have direct influence upon the development and behaviour of chronic inflammations of the tympanic cleft, such as disorders of ventilation and reaction of the mucoperiosteal layer. Local defence mechanisms, the species and virulence of infection also play an important role. It appears that the Eustachian tube is a very effective mechanical and immunological barrier against ascending infection which may perhaps be assisted by antibiotic treatment. Certainly non-suppurative chronic otitis media is more frequent now than in pre-antibiotic days. Keywords chronic otitis media cholesterolgranuloma Eustachian tube
Middle ear and mastoid air cells are a closed, but ventilated cleft, connected with the nasopharynx by the auditory tube. The whole system is lined by a thin mucosa, which acts as a mucociliary transportation organ and serves in local immunoglobulin and secretory enzyme production. The tube provides ventilation and clearance of the tympanic cavity and is a mechanical, immunological and biochemical barrier against ascending infection. Any kind of functional failure of the auditory tube involves the middle ear mucosa and leads to chronic otitis media, if the following conditions occur: Blockage of the tube causing adhesive otitis media. Recurrent infections and lack of local immunological defence ability leading to chronic purulent otitis media. 3 Defective healing: may give rise to persistent perforation, fibrous adhesions and patchy or diffuse calcification. I
z
Morphologically we distinguish between 2 types of chronic otitis media : non-purulent or closed and purulent or open forms;' in our material, using biopsies taken during tympanoplastic procedures and sections from our temporal bone collection, we compared the findings in middle ear and the auditory tube in both groups of chronic otitis media:
A. Non-purulent chronic otitis media (adhesive chronic otitis media) : The clinical * Read at the first international meeting of the Politzer Society, February 1978. 0307-7772/78/11oo-o~~1$02.000 1978 Blackwell Scientific Publications
491
492
G . ZECI-INER
conditions found are blockage of the tube, an intact tympanic membrane and effusion in the middle ear.’F2 Morphological criteria for the blockage of the tube: The mucosal changes are hyperplasia and metaplasia. Mucosal folds are thickened, oedematous and swollen. The goblet cell population is increased. The so-called tubal tonsil is visible as a follicle-like aggregation of immunocompetent cells within the submucosa. The salivary glands adjacent to the auditory tube are also altered.4 Some of the excretory ducts are ectatic, filled by thick mucoid secretion, others contain microliths. The glandular parenchyma is partially reduced and replaced by fat or scar tissue. One has the impression that the infection is stopped within the tube and causes the loss of tubal function. Mucosal changes in the middle ear: The mucosa is swollen, oedematous and hyperaemic. The inflammatory infiltration is limited to the surroundings of the vessels, and never reaches theunderlaying bone. Cuboidal epitheliumis transformed to secretory and ciliated elements. The basal membrane shows in silver impregnation as an interrupted and irregular fibre network, but is much thicker than normal, as demonstrated by Van Gieson and H & E staining. In biopsies of longer lasting otitis, the epithelium gives a highly positive mucopolysaccharide reaction, which means that it becomes highly secretory. These findings are very clear at the bottom of the cryptlike mucosa folds, giving rise to the term ‘grand-like structures’. The middle ear cavity is filled with an acidophilic effusion, which contains only a few cells. I n cytological smears they show up as different kinds of macrophages, such as foam cells, lipophages, and phagocytes. Histologically one cannot distinguish serous from mucoid effusion. Because of the blocked tube and the intact tympanic membrane, the effusion cannot be expelled, and produces a mucosal reaction. Finger-like folds extend into the lumen, Much enzymatic activity can be seen : acid and alkaline phosphatase, non-specific esterases and leucinaminopeptidase are demonstrable. There seems to be a digestive effort to eliminate the effusion. Organization also takes place and the formation of granulation tissue starts. A typical element is the cholesterol granuloma which consists of fibrous granulation tissue, in which large numbers of cholesterol crystals have been deposited, surrounded by foreign body giant cells. Evidence of recent haemorrhage is often seen. Untreated the disease ends in what Politzer described as ‘adhesive process’. The whole tympanic cavity may be filled with fibrous tissue and the tympanic membrane retracted or scarred. The possibility of restoration of ventilation of the tympanic cleft is restricted by connective tissue proliferation within the effusion. Other complications are tympanosclerosis, localized within the submucosa and may be patchy or diffuse.
B. Suppurativechronic otitis media or tubotympanic disease3 The clinical condition comprises permanent perforation of the tympanic membrane, recurrent otorrhcea caused by persistent mucosal disease and an irritated, but not blocked, auditory tube. MorpholoRicalJindi~zsiia the tube: The mucosa is thicker than normal, swollen by hyperaemia within Mayer’s plexus and a very dense inflammatory infiltration. The cells are not aggregated around vessels or in arranged follicles, but are distributed through the submucosa. The goblet cell population is increased. The adjacent salivary glands show evidence of in-
Lining of the nzirlrlle eur and Eustackian tube
493
creased mucus production and the acini have a strongly positive mucopolysaccharide reaction with PAS staining. At the tympanic end of the Eustachian tube the mucosa is hyperplastic and the epithelium consists of secreting and ciliated cells. The surface is often covered by cellular debris and discharge. Mucosal chrznges in the middle ear: The mucosa of the tympanic cleft is swollen and congested. There may be a profuse mucoid or mucopurulent discharge containing a considerable number of leucocytes. The inflammatory cellular infiltration is diffuse and reaches the underlying bone. Epithelial lesions are frequent and give rise to granulation buds. These are often the first sign of the organization of an effusion which is not expelled from the tympanic cleft. Aural polyps typical of suppurative otitis media consist of oedematous connective tissue and their stroma is infiltrated by a large number of inflammatory cells, often plasma cells and lymphocytes. They may include glandlike structures or cysts and their surface is covered with pseudostratified columnar epithelium, showing areas of keratosis. Polypi and swollen mucosal folds hinder the clearance of the aural discharge, giving rise to organization of the effusion and cholesterol granuloma. There is a great difference in the progression of the inflammatory process towards the underlaying bone and the ossicles, although destructive lacunar absorption may start within the bone. Surrounding the mastoid cells very soon a regenerative process begins. New bone formation creates a pagetoid pattern, characterized by irregular mosaic cement lines. I n areas of post-inflammatory reconstruction marrow spaces are filled with granulation tissue and inflammatory cells especially around the vessels. T h e disease may terminate like the non-purulent type in an adhesive process if the mucosal infection stops, and the bone reaction may lead to severe complication because of erosion, and necrosis. Persistent perforation of the eardrum membrane allows secondary infection by saprophytic or pyogenic organisms, which may be responsible for acute exacerbations of mucosal disease or infiltration by keratinizing stratified squamous epithelium-the start of cholesteatoma formation.
Acknowledgement This research was supported by Fonds zur Forderung der wissenschaftlichen Forschung in Osterreich.
References Z ~ L L N EF. R (1974) HNO-Heilkzmde. G. Thieme, Stuttgart. 2 POLITZER A. (1873) Seltener Fall eines chronischen Mittelohrkatarrhs. Archiv f i r Ohrenheilkunde 7, 48. I.B. (1968) Chronic suppurative otitis media. Proceedings of the Royal Society of Medicine 61, 3 THORBURN 395. 4 ZECHNER G. (1978) Der Formwandel yon Mittelohr-und Tubenschleimhaut in der Zeit der antibiotischen Therapie. H N O 26, 9. I
