Acta Oto-Laryngologica, 2006; 126: 1036
1039

ORIGINAL ARTICLE

Acute otitis media and mastoid growth

JACOB SADÉ1, EYAL RUSSO2, CAMIL FUCHS3, & AMOS AR4

1
Hearing Research Laboratory, Department of Bio-Medical Engineering, Faculty of Engineering, and Sackler Faculty of
Medicine, Tel Aviv University, 2ENT Department, Wolfson Medical Center, Holon, 3Department of Statistics and
4
Department of Zoology, Tel Aviv University, Tel Aviv, Israel
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Abstract
Conclusions. This study implies that the hypothesis that acute otitis media (AOM) in infancy inhibits the growth of the
mastoid system cannot be accepted. Objective: To establish a relationship between AOM in children and their mastoid
pneumatization development. Patients and methods. Lateral Schüller mastoid radiographs (LMRs) were measured in two
groups of children at ages 2
11 years. Group A (n /116) had a history of recurrent AOM; group B (n /108) had no such
history. Patients were treated in a private clinic. Data were analysed at Tel Aviv University. The patients had their LMR
taken and measured planimetrically. LMR areas on left and right sides were compared in each group and age and were
tested for possible differences using the paired Student’s t test. When no left/right difference was detected, the values were
For personal use only.

averaged. Groups A and B were compared at different ages using two-tailed two-sample unequal variance and correlation
coefficients. Results. The analyses show that the LMR area became gradually and significantly larger with age in group A
(R2 /0.858; p B/0.05). It did not develop significantly in group B.

Keywords: Eustachian tube, middle ear pressure, AOM, secretory otitis media, otitis media with effusion, atelectasis,
cholesteatoma, chronic ear

Introduction group that had experienced obvious recurrent AOM,

Mastoid pneumatization and size develops in hu-
mans only after birth, reaching maximal size around
puberty [1]. However, its final size varies greatly,
and while some ears develop a large mastoid (up to
30 cm2 when measured planimetrically), in others
the mastoid does not develop at all [1,2]. The size of
the mastoid is of clinical interest since ears with the
various forms of ‘otitis media syndrome’, i.e. chronic
secretory otitis media (SOM; also termed otitis
media with effusion, OME), atelectatic ears, chronic
otitis media and cholesteatomas, mostly develop in
ears with little or no pneumatization [1
8]. The
more severe the ‘otitis’, the smaller is mastoid
pneumatization.
On the basis of this association, a controversy as to
whether the underdeveloped mastoid is a genetic
trait or follows an AOM in childhood has continued
for many years [1,2]. The aim of the present study
was to elucidate this question by comparing the
mastoid growth between two groups of children: a
and a group that had no previous AOM.
Patients and methods
Epidemiological studies indicate that SOM affects
most children at some stage. It may be preceded by
obvious AOM, or not [5]. The prognosis of SOM
was shown to be reflected by the size of its mastoid
cell development as seen and measured on lateral
mastoid radiographies (LMRs) in the Schüller pro-
jection [6
10]. This is the accepted method of
choice for studies measuring and comparing mastoid
pneumatization [1,3
10] and when SOM prognosis
is requested by the patients or their parents, such
radiographies are undertaken. This is also the
practice in our clinic, where LMR measurements
were made by two otologists independently, to
preclude any bias.
Of the 809 children (aged 2
15 years) with SOM
who came for treatment in our clinic, 116 (group A)

Correspondence: Jacob Sadé, MD, 14 Hagefen Street, Ramat Hasharon, Israel. Tel: /972 3 549 4275. Fax: /972 3 540 0924. E-mail: jsade@netvision.net.il

ISSN 0001-6489 print/ISSN 1651-2551 online # 2006 Taylor & Francis

DOI: 10.1080/00016480600617100

had a positive history of AOM at least twice in the
last 2 years
such as high temperature, otalgia and
otoscopy, as diagnosed by an otologist. Another 108
children who had positively no history of AOM were
termed group B. Both groups had their LMR taken.
All cases in which the history was not completely
clear cut or did not have LMRs were excluded from
the study.
The analysis of the data was designed to assess
possible differences of mastoid size between children
in groups A and B, at specific ages. We restricted the
analyses to five age periods of equal length between
2 and 11 years (i.e. 2
3 years, 4
5 years . . . 10

11 years), for which the sample sizes were sufficient
for meaningful statistical analyses. In general, there
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was a right and left LMR for each child, of which an
average was taken as recommended by Altman et al.
[11] and Gaihede et al. [12]. However, we tested this
assumption for each age cohort of groups A and B
separately using the paired t test. The difference in
LMR means at the various ages between the two
groups was determined using a one-tailed two-
sample equal variance t test for each specific age
group. The total number of LMRs used for our main
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statistical analyses was 224 (see above and Table I).
Results
As left and right mastoid pneumatization of the
young children (aged 2
3 years) in group A was
significantly different (p /0.029) one from the other,
they were treated as separate groups. In all other
groups no such statistical difference between right
and left was found, and the results were averaged
(Table I). The LMR regression analysis (Figure 1)
showed a significant increase in the mastoid LMR
with age in group A (R2 /0.858; p B/0.05). How-
ever, there was no such increase in the size of the
mastoids in children in group B (R2 /0.076;
NS).The regression slope shows that the increase
with age in mastoid LMR in group A is 0.52 cm2 per
year, whereas in group B it shows no growth. The
difference in size between group A and group B was
statistically significant for every age interval except
for the 10
11 years group (Table I).
Table I. A comparison of lateral mastoid area radiography (LMR: cm2) in children from group A and group B as a function of age.
Parameter 2
3 (Right ear)* 2
3 (Left ear)* 4
5
Group A9/SE (n ) 3.199/0.27 (37) 2.739/0.18 (37) 4.699/0.29 (37)
Group B9/SE (n ) 2.299/0.35 (14) 2.239/0.26 (40)
p value 0.014 NS /0.0001
*See text for explanation.
Mastoid growth 1037
Discussion
The small significant difference in group A between
left and right LMR of the 2
3-year-old children in
our present study has not been explained so far and
should be explored further.
A correlation between the arrest of the pneuma-
tization process (small mastoid) and ‘chronic ears’
has been reported and accepted for many years [1

10]. The histological association of various forms of
‘otitis media’ with a small mastoid prompted Witt-
maack [2] to deduce that mastoid pneumatization is
arrested in infancy secondarily to AOM. Concomi-
tantly AOM was considered to be related also to
‘Eustachian tube malfunction’ which, at a later
stage, was supposed to lead to a type of ‘chronic
ear’ [1,2]. Alleged support for the above theory came
later from experiments on pigs, which demonstrated
failure of mastoid development when a middle ear
inflammation was induced chemically soon after
birth [13].
The concept of infantile AOM as an inhibiting
process for mastoid pneumatization was challenged
by Diamant [1], who measured a large unselected
random cohort of mastoids and showed that mastoid
pneumatization follows a normal bell-shaped distri-
bution. He concluded that mastoid size is genetically
determined and that the small undeveloped mastoids
are part of the normal biological variation. This was
supported by five genetic studies of families and
twins [14
18]. The association of important varia-
tions of the skull base structure [19,20] or of
congenital middle ear malformations [21] with
undeveloped mastoids also supports a genetic struc-
tural variation rather than a local inflammatory
cause. The larger than average pneumatization
found in patients with cystic fibrosis [22], a geneti-
cally transmitted disorder, also indicates a genetic
factor for mastoid size. More support for the above
came from Qvarnberg [23], who showed that chil-
dren with a previous history of AOM did not have a
smaller mastoid size than a random normal cohort.
It was also shown that in children, the mastoid
increased to a normal size after acute mastoiditis [1].
Ueda and Seguchi [24] showed that mastoid size in
the general population did not change from the era
Age (years)
6
7 8
9 10
11
4.539/0.44 (26) 7.289/1.38 (13) 6.679/3.42(3)
2.719/0.36 (35) 2.559/0.32 (13) 1.839/0.18 (6)
0.001 0.003 NS
 1038 J. Sadé et al.
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Figure 1. Change in lateral mastoid radiograph (Schüller projection) with age in children in group A and group B. The data points assigned
to age groups 2
3, 4
5, 6
7, 8
9, and 10
11 years are given at 3, 5, 7, 9 and 11 years, respectively, with horizontal lines indicating the age
span of each group on the x-axis. Vertical bars indicate9/SE. Numbers in brackets are sample sizes.
prior to the advent of antibiotics to what is found
today.
Our present study supports other studies [14

18,23] which throw doubt on the assumption that
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AOM hinders the development of mastoid pneuma-
tization. It is seen that mastoid growth continues to
progress in ears with a clear history of AOM at the
rate of about 0.5 cm2 per year, but not in ears with
no such history (Figure 1). The clinical homogeneity
of each of the two groups [5], the exclusion of all
dubious cases, as well as the homogeneity and
precise histories received from the parents, in con-
junction with an examination by an otologist, all
indicate the reliability of the clinical history of these
patients.
Children in group B have smaller LMRs than
those in group A, and they also have a greater
tendency towards developing chronic SOM and
atelectasis [5]. This association may be explained
by the tendency of middle ear infections of all kinds
(as well as negative middle ear pressure) to have a
special predilection for ears with ‘small mastoids’ as
presented in group B [3
9], while ears with large
mastoid pneumatization seem to be protected from
chronic otitis media. One of the reasons for this is
probably the active [25] or passive [26,27] buffering
effect of large mastoids, which may protect a middle
ear to some degree by reducing the negative pressure
and its effects.
In conclusion, it seems that the development of
mastoid pneumatization is not inhibited by AOM,
and in the absence of any other environmental
influence, we may see our study as supporting those
studies which indicate that mastoid pneumatization
is mainly genetically determined.
Acknowledgements
Our thanks go to Ms Ann Belinsky for her help in
editing the manuscript.
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