pathology - jcp.bmj.com · every instance of acute mastoiditis. equally, in bone-chips obtained...

J. clin. Patn. (1956), 9, 229.

THE PATHOLOGY OF OTITIS MEDIABY

I. FRIEDMANNFrom the Department of Pathology of the Institute of Laryngology and Otology, London

(RECEIVED FOR PUBLICATION NOVEMBER 11, 1955)

Knowledge of the pathology of otitis media isconflicting in spite of the vast amount of relevantliterature.One of the objects of the present investigation

has been to re-examine this field in relation to thequestion as to whether the pathology of otitismedia and maistoiditis has changed since theadvent of the antibiotics as often suggested. Forthis purpose bone-chips removed at recent mas-toidectomy operations have been studied.

Materials and MethodsThree hundred and seventy five samples of bone

chips removed at mastoidectomy operations weredecalcified, embedded in paraffin-wax, and sec-tioned. Sections were stained with haemotoxylin andeosin, Van-Gieson, Gram, Ziehl-Neelsen, and Mas-son's trichrome. The periodic-acid-Schiff reactionwas used for the demonstration of mucus-secretingcells or glands.

25Cases of Acute MastoiditisThe number of acute infections was, as ex-

pected, fairly small. The pathological changeswere, however, intensive and characteristic.

In the early stages the mucosa of the air cellswas congested and swollen, lined with flat orcuboidal cells (Fig. 1). The lumen was filled withpus, replaced later by fibrous granulation tissue(Figs. 2 and 3). There was evidence of osteoclasticactivity and already, at an early stage about fiveto 10 days after infection, of intensive formationof new bone (Figs. 3, 4, and 5).There was great variation in a given specimen

and neighbouring mastoid air-cells presenteddifferent stages from suppuration to fibroblasticorganization and ossification.

In some cases, of streptococcal aetiology, therewas considerable haemorrhage and destruction ofbone. Equally, an occasional acute case caused byB. proteus showed evidence of widespreadsuppuration.

350 Cases of Chronic MastoiditisEvidence of inflammatory changes has been

noted in 270 cases. In 80 specimens there wasno evidence of infection and they were rejectedfor this study (these were cortical bone chips).The positive findings were (1) granulation tissue

in the bone fragments; (2) signs of bone recon-struction; (3) mucosal changes; (4) aural chole-steatoma; (5) cholesterol-granuloma.

(1) Granulations when present lay freely,covered the bone fragments, or filled the cells, theantrum, or eroded bone. They consisted of non-specific inflammatory granulation tissue infiltratedby plasmacytes, lymphocytes and enclosing gland-like structures. The granulations were on thewhole identical with the structure of the so-calledaural polyp.

(2) There was much evidence of reconstructionof bone indicated by dark-blue staining lines ofapposition of various thickness resembling the sur-face of glaciers (Fig. 6), and irregular cement linesforming an intricate mosaic pattern (Figs. 7 and 8).

(3) The mucosa of the mastoid cells whetheroedematous or fibrotic was infiltrated by roundcells and frequently lined by ciliated columnarepithelium which formed gland-like structures(Figs. 9 and 10). The " glands" contained mucusgiving a positive periodic-acid-Schiff reaction.

(4) Stratified squamous epithelium, lining chole-steatoma cavities, was often seen covering thebone chips (Fig. 11). From the inverted keratin-ized surface, multiple layers of epidermoid kerat-inized epithelium were desquamated filling thecholesteatoma cavity proper. Sometimes onlyfragments of keratinized matter surrounded bygiant cells were found (Fig. 12).

(5) Frequently no true epidermoid cholestea-toma was found but only rich deposits of choles-terol crystals surrounded by giant cells embeddedin fibrous granulation tissue (Figs. 13 and 14).

DiscussionIt has been suggested that the pathology of

otitis media may have undergone some basic

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FIG. 1(1224 54).-Mastoid cell showing congested muicosa and healthylaminated bone. Haematoxylin and eosin, 150.

FIG. 2 (837 53).-Acute mastoiditis (10 days' history). Note pus-filled mastoid cell, thickened lining. Haematoxylin and eosin,x 45.

FIG. 3.Neighbouring mastoid cell showing fibrous organizationand intensive new-bone formatin. Haematoxylin and eosin.

30. As Fig. 2.FIG. 4 (1582 53).-Acute mastoiditis (14 days' history). Newly

formed reticular bone obliteratingell. Haematoxylin and eosin,

60.FIG. 2


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FIo. 5 (120/55).-Acute mastoiditis (10 days',history), showing 'network of reticularbone replacing fibrous granulation tissue. ,*Haematoxylin and eosin, x 95. S

FiG. 5

FIG. 6 (441/53).-Glacier-like arrangement oflines of apposition. Haematoxylin andeosin, x 52.

FIG. 6


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FIG. 7 (1055 53).-Sclerotic bone fragment showing irregular cement lines. Haematoxylin and eosin, - 170.

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FIG. 8 (1998i54).-Sclerotic bone fragment showing irregular cement lines. Haematoxylin and eosin, x 325.

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FIG. 9 (181/53).-Sclerotic bone lined by pseudostratified ciliatedcolumnar epithelium. Haematoxylin and eosin, x 490.

FIG. 10 (1693,154).-Gland in granulation tissue. Haematoxylin andeosin, x 400.

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Note epidermoid squamous epithelium and lamellated keratinized material in the lumen.Haematoxylin and eosin, x 72.

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234 1. FRIEDMANN

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FIG. 12 (279 55).-Chronic inflammatory granulation tissue containing lamellated " cholesteatomatous"material surrounded by foreign-body giant cells. Haematoxylin and eosin, 150.

FIG. 13(1251 53).-Chronic otitis and mastoiditis. Chronic inflammatory granulation tissue with cholesterol granuloma.Haematoxylin and eosin, >x 72.


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THE PATHOLOGY OF OTITIS MEDIA

FIG. 14 (865!53).-Chronic otitis and mastoiditis with cholesterol granuloma. Ha

change in recent years, and that the success ofthe antibiotic treatment of the disease might havebeen due in some degree to changes of the patho-logy of otitis media.The histopathology of human otitis media and

mastoiditis has been studied in detail by, amongothers, Stewart (1928), who gave a detailed descrip-tion of the clinical, bacteriological, and histologi-cal conditions found in 50 cases of acute mastoid-itis. Stewart's material consisted of bone-chips ofdiseased tissue removed by the Schwartze opera-tion. At about the same time Lange (1928) ex-amined about 100 temporal bones showing variousstages of the disease. Both authors agree in theirdescription of the pathological changes in themastoid cell.From the present investigations it can be stated

that my observations do not differ fundamentallyfrom those of Stewart and Lange. Nevertheless,some of my principal findings merit discussion astheir significance has not been fully appreciated(Watkyn-Thomas, 1953).

tematoxylin and eosin, x 110.

Bone Formation and Bone Reconstruction

Evidence has been presented in this paper firstof all of conspicuous new bone formation in acuteand chronic mastoiditis. This was found in almostevery instance of acute mastoiditis. Equally, inbone-chips obtained from mastoidectomy opera-tions for chronic otitis new bone formation andsigns of bone reconstruction occurred regularly.An interesting feature of the bone-fragments in

chronic otitis was the bizarre irregularity of thecement Lnes which produced a mosaic-like patternresembling that found in Paget's disease. This isevidence of bone reconstruction developing in thecourse of infection and leading to osteosclerosis.

This pattern is sufficiently characteristic to assistin the differentiation of sclerotic bone from healthycompact bone; ceteris paribus in the differentia-tion of a sclerotic mastoid process rendered acellu-lar through infection from a congenital compactor ivory mastoid process with intact Haversiansystems in the latter.

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1. FRIEDMANN

In the present studies, the controversial prob-lem of pneumatization of the human mastoid pro-cess has only been touched upon. Experimentalevidence (Opheim, 1944; Friedmann, 1955a and b),and the bone changes in acute and chronicmastoiditis of man suggest that the conversion ofa pneumatized mastoid process into a sclerotic onemay well be a consequence of infection.

Mucosal ChangesTwo significant mucosal changes were noted

in chronic otitis media. The lining covering thethickened fibrous stroma infiltrated by inflamma-tory cells has often become a more highly differen-tiated columnar type, forming gland-like structureswhich produced P. A. S. positive mucus.The conception of a mucous membrane lining

the mastoid cells is not generally accepted, asnormally it lacks some of the properties of thetypical mucous membrane found in glands andsecretory epithelium.Many observers deny the presence of glands in

the mastoid lining. Ojala (1950) in his materialfound only one instance in which gland-like cavi-ties were present in the subepithelial tissue. Theywere lined by stratified high cylindrical epitheliumconsisting almost entirely of goblet cells.As shown here, under inflammatory conditions

at any rate, a true mucous membrane may developlined by a mucus-secreting epithelium forminggland-like structures.

CholesteatomaThe flattened cellular lining was frequently re-

placed by stratified squamous epithelium leadingto the formation of the so-called aural chole-steatoma. It is generally accepted that the patho-genesis of true aural cholesteatoma rests upon thepresence of a stratified squamous epithelium inthe middle ear cleft (Tumarkin, 1954). It is theorigin of this squamous epithelium that is still indoubt. Experimental evidence has been presented(Friedmann, 1955b) that migration or extension ofthe stratified squamous epithelium from the ex-ternal auditory meatus, or from the drum, can pro-duce the effects associated with true epidermoidaural cholesteatoma of man (deposition of lamel-lated, desquamated, keratinized matter). This isprobably the most frequent mechanism of thedevelopment of aural cholesteatoma in man.

Cholesterol GranulomaBesides the true epidermoid aural cholesteatoma,

in some cases clinically so diagnosed, the sectionsshowed a basically different but characteristic pie-

ture. There were cholesterol deposits surroundedby foreign-body giant-cells in the granulationtissue filling the middle ear. At operation thesestructures, here called "cholesterol-granuloma "

may often be mistaken for aural cholesteatoma.Such cholesterol deposits however, occur also atother sites of chronic inflammation and/orhaemorrhage (Stewart, 1915; Dible and Davie,1945) and it may be assumed that their presencein the infected middle ear cleft is directly con-nected with the infection. Stratified squamousepithelium, however, has no role in its formation.

SummaryThe pathology of otitis media is described.There is no evidence to support the suggestion

that the basic pathology of otitis media haschanged in the post-penicillin era, when comparedwith the findings of authors reported in the pre-penicillin era.

Infection takes place in the mucosa of the earwhich is very susceptible to infection by certainorganisms. Bone formation sets in early and, withprogression to the chronic phase, there is con-siderable reconstruction of the bone recognizableby an irregular mosaic pattern of cement lines orlines of apposition. The mucosal lining revertseither to a columnar respiratory type, when itforms gland-like structures, or may be replacedby a stratified squamous epithelium forming thepathological substrate of aural cholesteatoma.Cholesterol deposits surrounded by foreign bodygiant cells are common in chronic mastoiditis.Such structures, best called cholesterol-granu-loma, should not be mistaken for the true epider-moid cholesteatoma.

It is suggested that the hyperplastic mucosal andosteoplastic processes observed are not the cause,but the outcome, of otitis.

I wish to thank the staff of the Royal NationalThroat. Nose and Ear Hospital and to the sistersof the operating theatres for their kind co-operation.My special thanks are due to Mr. E. S. Bird andMiss V. Shepherd for the sections and to Mr. D.Connolly for the photography.

REFERENCES

Dible, J. H., and Davie, T. B. (1945). Pathology, 2nd ed., p. 2s.Churchill, London.

Friedmann, I. (1955a). J. Larvng., 69, 27.--(1955b). Ibid., 69, 5S8.Lange, W. (1928). Z. Hals-. Nasen-u. Ohrenheilk., 20, 3.Ojala, L. (1950). AcIa oto-la-rng. (Stockh.), Suppl. 86.Opheim, 0. (1944). Ibid., Suppl. 54.Stewart, J. P. (1928). J. Laryng., 43, 689.Stewart, M. J. (1915). J. Psth. Bart. 19, 305.Tumarkin, A. (1954). In Modern Trends in Diseases of the Ear, Nose

and Throat, ed. M. Ellis. p. 153. Butterworth. London.Watkyn-Thomas, F. W. (1953). Diseases of the Throat, Nose and

Ear, pp. 688,716,717. Lewis, London.

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