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The Obstetrician & Gynaecologist 10.1576/toag.9.1.021.27292 www.rcog.org.uk/togonline 2007;9:21–26 Review

Review Dental manifestations

of pregnancy
Authors Martina Pirie / Inez Cooke / Gerard Linden / Chris Irwin

Key content:
• Pregnancy has significant effects on the periodontal tissues and pregnancy
gingivitis is a common manifestation of this.
• The host response and oral flora are affected and tooth surface loss and mobility
may develop.
• Further research is required to establish the association between periodontal
health and adverse pregnancy outcome.

Learning objectives:
• To identify the main dental manifestations of pregnancy.
• To be able to advise pregnant women on how to maintain good dental health.
• To be aware of the need for effective communication between the dental and
medical disciplines to ensure that pregnant women receive the best care possible
for oral, obstetric and general health.

Ethical issues:
• The treatment of gingivitis and periodontitis during pregnancy is safe and effective
in treating gum disease.
Keywords periodontal health / pregnancy epulis / pregnancy gingivitis /
pregnancy outcome
Please cite this article as: Pirie M, Cooke I, Linden G, Irwin C. Dental manifestations of pregnancy. The Obstetrician & Gynaecologist 2007;9:21–26.

Author details
Martina Pirie BMSc BDS MFDSRCS Inez Cooke MA MRCOG Gerard Linden BSc, BDS, PhD, FDSRCS, FFDRCSI Chris Irwin BSc, BDS, PhD, FDSRCPS
Clinical Research Fellow Senior Lecturer and Consultant Chair and Consultant Reader and Consultant
Division of Restorative Dentistry, School of Department of Obstetrics and Gynaecology, Division of Restorative Dentistry, School of Division of Restorative Dentistry, School of
Dentistry, Queen’s University Belfast, Queen’s University Belfast, UK Dentistry, Queen’s University Belfast, UK Dentistry, Queen’s University Belfast, UK
Grosvenor Road, Belfast BT12 6BP, UK
Email: m.pirie@qub.ac.uk
(corresponding author)

© 2007 Royal College of Obstetricians and Gynaecologists 21

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Introduction
The numerous physical and physiological changes
that occur during pregnancy1 affect every major
body system and result in localised physical
alterations in many parts of the body, including the
oral cavity.2 The aim of this paper is to increase
awareness of the main potential dental
manifestations which can occur in pregnancy.
The effects of pregnancy on
periodontal tissues
Pregnancy gingivitis
Gingivitis is a plaque induced inflammation of the
gingiva, part of the oral mucosa which surrounds the
tooth and covers the alveolar bone (a healthy gingiva
is shown in Figure 1). During pregnancy the
inflammatory response to dental plaque is increased,
leading to swollen gingivae which tend to bleed on
brushing. Gingivitis exacerbated by the hormonal
changes of pregnancy is known as pregnancy
gingivitis,3 although this does not essentially differ
histologically from that which develops in the non
pregnant state.4 Pregnancy gingivitis is considered
the most common oral manifestation of pregnancy
and has been reported as occurring in up to 100% of
pregnant women.5 Characteristic features of healthy
and inflamed gingivae are listed in Box 1.
Pregnancy gingivitis commonly becomes apparent
later in the second month of gestation and worsens
as the pregnancy progresses before reaching a peak
in the eighth month. In the last month of gestation
gingivitis usually decreases and immediately post
partum the gingival tissues are found to be
comparable to those seen during the second month
of gestation.5 However, this does not automatically
indicate a return to health. Although the clinical
Figure 1
Healthy gingiva
Box 1
Healthy gingiva
Characteristic features of healthy
and inflamed gingivae • Pink (melanin pigmentation present in some racial groups)
• Firm with stippled surface
• Painless
• Papillary gingiva (gingival tissue in area between adjacent
teeth) fits the interdental or interproximal space exactly while
marginal gingiva (tissue at the junction of gingiva and teeth)
finishes with knife-edge margin at tooth surface
• No bleeding in response to probing during tooth cleaning or
when eating
• Probing depths 3 mm and no pocket formation
22
The Obstetrician & Gynaecologist
features of pregnancy gingivitis may be localised or
generalised, the changes affecting the anterior teeth
are the most obvious (Figure 2),5 despite increased
amounts of plaque being associated with the
posterior teeth.6 Bearing in mind that gingivitis is
considered to be plaque induced, it is interesting
that Raber-Durlacher et al.6 demonstrated that
pregnancy gingivitis is not caused by an increase in
dental plaque. It may be due to the effects of
pregnancy on the gingival tissues where both
estrogen and progesterone receptors are found,
although exactly how these hormones increase
gingival inflammation is unknown. It is possible
that the pregnancy related gingival changes may be
explained by increased vascularity and vascular
flow alongside alterations in the immune system
and/or changes in connective tissue metabolism.4
Management of pregnancy gingivitis involves
regular dental visits for professional cleaning and
monitoring with education of the woman
regarding both the aetiology and prevention of the
condition. Elimination of factors which
compromise removal of plaque, for example
overhanging restoration margins, should be carried
out so that plaque levels can be minimised.
Pregnancy epulis (pyogenic granuloma of
pregnancy)
The pregnancy epulis (Figure 3) is a localised, soft
hyperplastic lesion which develops on the gingiva
in up to 5% of pregnancies.4,7 This bright red, highly
vascularised lesion, which may have small white
flecks superficially, is usually pedunculated and can
measure up to 2 cm in diameter. Although it can
arise from any gingival site it mostly occurs on the
interdental papillary gingiva, particularly on the
labial aspect and more commonly on the upper jaw
than the lower.8 Teeth adjacent to the pregnancy
epulis may be seen to drift and become increasingly
mobile,7 although bony destruction rarely develops
around the teeth directly involved.4 It may develop
at any time but appears to be most common in early
pregnancy. It has been suggested that this lesion
arises from an already inflamed gingival papilla,
therefore plaque is considered an important
initiating factor.
In addition to dental plaque, the pregnancy related
hormonal changes that produce an exaggerated
Gingivitis
• Red/bluish red
• Soft with shiny surface
• Usually painless, painful in severe cases
• Gingiva becomes swollen and oedematous and appearance
is blunted. Knife-edge adaptation and scalloped shape of
healthy gingiva are lost
• Bleeding in response to probing during tooth cleaning, when
eating and spontaneously
• Increased probing depths and pocket formation
© 2007 Royal College of Obstetricians and Gynaecologists
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gingival response to plaque are thought to underlie
the formation of the pregnancy epulis.4,7 It is
clinically and histologically indistinguishable from
the pyogenic granuloma in men and nonpregnant
women.4 During pregnancy, non-surgical
management involves elimination, or at least the
significant reduction, of dental plaque, particularly
around the epulis. This is best achieved by the
woman regularly attending the dentist or dental
hygienist for thorough cleaning in addition to
plaque control instruction to ensure that the oral
home care regimen is of a suitably high standard.7,9
Given the unsightly appearance of the pregnancy
epulis, which is often at the front of the mouth, and
its propensity to bleed, it is, understandably,
concerning for the woman. However, surgical
removal should only be performed during
pregnancy if the epulis is traumatised by opposing
teeth or restorations resulting in pain and
bleeding,8 if it is interfering with normal speech
and/or mastication, or if it bleeds severely and/or
becomes painful.9 Correction of any associated
local contributing factors must also be carried out.
Given the high recurrence rate of this lesion,
surgery should ideally be delayed until after
delivery, when the epulis often regresses completely
or, at the very least, is smaller, more fibrous and
easier to remove.8 However, if surgery cannot be
delayed, removal should be done during the second
trimester and the woman informed of the risk of
recurrence.
The effects of pregnancy on
the host response and
oral flora
Although the damaging processes accompanying
periodontal disease (such as bone and periodontal
ligament destruction) are associated with plaque
bacteria they are, in fact, mainly a result of the host
response to this microbial assault.
For bacteria to colonise subgingival sites and
ultimately infiltrate the underlying connective
tissue, many aspects of the host response must be
evaded. It would appear that many facets of the
immune response with regard to the periodontium
are affected by pregnancy, with the overall effect
being one of decreased activity and efficiency.4,10
The key developments are a decrease in the number
of neutrophils, decreased chemotaxis and
phagocytosis, and depressed antibody responses
and cell-mediated immunity.11
Given that estrogen and progesterone receptors are
found in the periodontal tissues, the progressive
increase in levels of these hormones in pregnancy
also affects the response of the tissues. The
extracellular matrix, gingival vessels and fibroblasts
are all affected.4 Although estrogen, which may be
© 2007 Royal College of Obstetricians and Gynaecologists
2007;9:21–26 Review
Figure 2
Pregnancy gingivitis affecting the
gingival tissues, particularly
associated with the lower anterior
teeth despite minimal plaque stains
on the tooth surfaces
Figure 3
Pregnancy epulis
involved in the regulation of cellular proliferation,
differentiation and keratinisation, seems to
stimulate matrix synthesis, along with progesterone
it also enhances the localised production of
inflammatory mediators, especially prostaglandin
E 2 (PGE 2), a potent inducer of osteoclastic activity.
Progesterone also compromises tissue homeostasis
by reducing fibroblast proliferation, altering the
pattern of collagen production and reducing the
level of plasminogen activator inhibitor type 2
(PAI-2) which is an important inhibitor of tissue
proteolysis.4,9
With regards to periodontal disease, Gram-negative
anaerobic bacteria are the main culprits. They
include: Prevotella intermedia (P. intermedia),
Tannerella forsythensis, Porphyromonas gingivalis
(P. gingivalis), Treponema denticola and
Actinobacillus actinomycetemcomitans. 12 Although
the causal role of specific bacteria in pregnancy
associated gingivitis has been difficult to establish,
gingival bleeding and inflammation appears to be
associated with a rise in the numbers of Gram-
negative rods present. 4 However, an increase in the
selective growth of P. intermedia, 6,13 P. gingivalis 10
and Tannerella species (formerly Bacteroides) 14 has
been demonstrated in subgingival plaque during
the onset of pregnancy gingivitis. This is likely to be
a result of these species being able to use the
pregnancy hormones, particularly progesterone, as
a source of nutrition.4,10 This increase in selective
growth may also be favoured by the changes that
occur in the immune system during pregnancy
alongside those that develop locally in the gingival
crevice, such as blood from bleeding gingiva
providing further nutrients and increased pocket
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depths creating a more favourable environment for
anaerobes.4
Dental caries is a chronic endogenous infection
which is multifactorial in nature and caused by the
bacterial fermentation of dietary carbohydrates
resulting in the localised destruction of the tooth. It
appears that the important organisms in the
initiation and subsequent progression of dental
caries are the Mutans streptococci (a group name for
seven different Streptococcus species), Lactobacilli
and Actinomyces species.15 It is not thought that
these are in any way affected by pregnancy directly
in terms of their cariogenicity or that the structure
of the tooth is changed resulting in the teeth
becoming more susceptible to caries. Interestingly,
increased levels of Mutans streptococci and
Lactobacilli are found in late pregnancy and during
lactation.4 The dietary changes that may occur,
especially in early pregnancy, such as regular
consumption of sugary snacks and drinks to satisfy
cravings or to prevent nausea and sickness will
result in an increased risk of dental caries unless
extra attention is paid to oral hygiene.1 This can be
further complicated if the pregnant woman is
unable to tolerate tooth brushing because of nausea
and sickness to the extent that tooth brushing is
significantly compromised.
In addition, the risk of caries may be further
increased in pregnancy as a result of the estrogen
enhanced proliferation and desquamation of the
oral mucosa. It is suggested that the desquamating
cells enhance the microenvironment by providing
nutrition and a suitable environment for bacterial
growth, therefore potentially predisposing to caries.
Alterations in saliva flow, composition, pH and
buffering capacity further compound this.16
Tooth surface loss
Tooth surface loss, primarily through acid-induced
erosion, may be seen if there has been nausea and
associated repeated vomiting during pregnancy.
The palatal surfaces of the upper incisors and
canines are often the most affected (Figure 4). The
woman commonly presents complaining of
sensitivity, which is a consequence of the resulting
dentine exposure. Management is essentially
Figure 4
Tooth surface loss on the palatal
aspects of the upper anterior teeth
due to acid erosion following
repeated vomiting
24
The Obstetrician & Gynaecologist
preventative and includes the regular use of a
fluoride mouth rinse, especially in those women
who vomit frequently. In addition, these women
should be advised to avoid tooth brushing directly
after vomiting as the effect of erosion can be
exacerbated by brushing an already demineralised
tooth surface.7 Consumption of acidic fruits and
juices as well as carbonated drinks should be
restricted to avoid the potential for contact between
additional acids and the tooth tissues. The use of
drinking straws is recommended for the same
reason, as is breaking the habit of holding such
acidic drinks in the mouth for a longer time than is
necessary.
Tooth mobility
Increased tooth mobility has been detected in
pregnancy even in periodontally healthy women.
The upper incisors are most mobile during the last
month of pregnancy.17 Development of such
mobility is possibly due to mineral shifts in the
lamina dura and not to modification of the
alveolar bone. The degree of periodontal disease
present and disturbance of the supporting
attachment tissues are also thought to contribute
to this mobility, which usually resolves post
delivery.7
The impact of periodontal
health on pregnancy
Given the considerable effect of pregnancy on oral
health it is interesting that the impact of
periodontal disease on pregnancy outcome is now
under scrutiny. The idea that it may contribute to
pregnancy outcome was presented in 1931 when
Galloway18 stated that periodontal disease may
provide ‘sufficient infectious microbial challenge’ to
have ‘potentially harmful effects on the pregnant
mother and developing fetus’. Infection, especially
symptomatic infection of the genitourinary tract, is
considered an important risk factor for preterm
birth and/or low birthweight. Essentially, bacterial
infection results in the activation of cell-mediated
immunity and the subsequent production of
cytokines such as interleukins (IL-1, IL-6), tumour
necrosis factor alpha (TNF-) and prostaglandins,
especially PGE 2.
Currently, one proposed mechanism of labour
suggests that the intra-amniotic levels of these
mediators rise steadily throughout pregnancy until
a threshold is reached at which labour is induced.
Thus, it is possible that the presence of infection
which results in an abnormally elevated production
of these normal physiological mediators of
parturition may trigger preterm birth, also
resulting in low birthweight.19 More recently, it has
been suggested that subclinical infections such as
periodontitis may also pose a challenge to the
developing fetus.
© 2007 Royal College of Obstetricians and Gynaecologists
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The Obstetrician & Gynaecologist
A frequent observation potentially linking
subclinical infection and preterm birth is that there
is an increased incidence of histologic
chorioamnionitis in preterm delivery, which is
usually the result of infection. However, given that
it may not be associated with symptomatic
infections of the genitourinary tract and that
culture may produce a negative result, it is
proposed that infection remote from the
fetoplacental complex and genitourinary tract may
play a role. Essentially, it is hypothesised that
subclinical infections such as periodontal disease
contribute to premature delivery and low
birthweight as a result of pathogenic micro-
organisms, or indeed their microbial products, such
as lipopolysaccharide (LPS), reaching the uterus via
the bloodstream, inducing cytokine release in the
decidua or the membranes, resulting in increased
prostaglandin production or, indeed, uterine
muscle contraction.20 Inflammatory mediators
such as cytokines and prostaglandins, for example
when produced in the periodontal tissues or in
other systemic organs in response to LPS
stimulation, may also pose a real threat to the
fetoplacental unit and increase the risk of preterm
delivery and low birthweight (Figure 5).19
In 1996, Offenbacher et al.19 published the results of
a case control study which suggested that
periodontitis was a statistically significant risk
factor for premature delivery and low birthweight
and, indeed, that mothers with periodontal disease
were potentially seven times more likely to have a
preterm or low birthweight baby. Subsequent
research by Jeffcoat et al. 21 supported this
suggestion. They found a four-fold increase in the
odds of preterm birth before 37 weeks of gestation,
rising to a seven-fold increase before 32 weeks of
gestation in women with generalised or severe
periodontal disease in weeks 21–24 of pregnancy.
The work of Madianos et al.22 added weight to this
argument, reporting that preterm delivery and low
birthweight were 11 times more likely to occur in
women whose periodontal disease worsened
during pregnancy compared with those who had
good periodontal health. Recently, Offenbacher
et al.23 reported that periodontal disease
progression in pregnancy may be predictive of birth
occurring at less than 32 weeks of gestation.
Not all studies have found an association between
periodontal disease and preterm delivery and low
birthweight. Davenport et al.24 found that the risk
actually decreased with increasing pocket depth.
Moore et al.25 found no association between
periodontal disease and preterm delivery and low
birthweight, although, interestingly, this work did
suggest a link between indicators of poor
periodontal health and late miscarriage. A recent
systematic review by Xiong et al.26 concluded that,
although periodontal disease may be adversely
© 2007 Royal College of Obstetricians and Gynaecologists
2007;9:21–26 Review
associated with pregnancy outcome, further Figure 5
Proposed biological mechanisms
‘methodologically rigorous’ research is required. linking periodontal disease to
Bearing all of this in mind, it is hoped that current preterm low birthweight delivery
research, in particular intervention studies on
pregnant women with periodontal disease, may
help to establish whether a significant cause and
effect relationship does exist and the impact
periodontal treatment may have during pregnancy.
Conclusion
The aim of this paper is to increase awareness of the
potential oral manifestations of pregnancy. Those
involved in obstetric and prenatal care may well be
the first health professionals to become aware of
developing oral conditions and it is important that
they can provide appropriate information, advice
and reassurance followed by referral for a dental
examination, treatment and monitoring as
necessary. Given that periodontal health may also
affect pregnancy, it is vital that effective
communication occurs between the dental and
medical disciplines to ensure that pregnant women
receive the best care possible for oral, obstetric and,
indeed, general health.
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TOG Referees 2006

TOG could not exist without its referees. Thank you very much indeed to all the
following people, who refereed articles for us in 2006:
Akkad, Andrea Gribbin, Claire O’Connor, Rory
Amso, Nazar N Haddad, Nabil Overton, Caroline
Ashe, Robin Hinshaw, Kim Patient, Charlotte
Ashworth, Janet Hunter, Alyson Pavord, Sue
Baldwin, Peter Hunter, David Ramsay, Ian N
Beatrice, Seddon Irwin, Paul Ramsay, Margaret M
Bigrigg, Alison M Jeyarajah, Arjun Read, Mike D
Black, Rebecca S Johnston, Tracey A Robins, James B
Bosio, Paul M Kaufmann, Sarah Rogstad, Karen
Browning, Andrew Keay, Stephen D Rooney, Guy
Bu’Lock, Frances Kettle, Christine Rutherford, Jane
Cahill, David J Kubba, Ali Rymer, Janice M
Campbell, Doris M Lombaard, Hennie Scherf, Caroline
Cooke, Inez E Loughna, Pamela V Smith, Gordon C
Cresswell, Janet Luesley, David M Soljak, Michael
Dalton, Maureen Lumsden, Mary A Stones, R W
Deeny, Miriam McAuliffe, Fionnuala Symonds, Ian
Dolan, Lucia M Mane, Sandeep Thein, Angela
Dwarakanath, Linga Mansour, Diana Tierney, John
Edozien, Leroy C Mathur, Raj Vause, Sarah H
Fay, Toby Mellows, Heather J Ward, Susan
Filshie, Marcus Mires, Gary Warren, Neil
Fraser, Ian Moodley, Jack Weston, Michael J
Garden, Anne S Muram, David Wood, Laurence
Gibbon, Karen Nicholas, Nick
Goodfellow, Peter O’Reilly, Barry

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