Australian Dental Journal 2010; 55:(1 Suppl): 5560

doi: 10.1111/j.1834-7819.2010.01199.x
Gingival enlargements and localized gingival overgrowths
NW Savage,* CG Daly
*School of Dentistry, The University of Queensland and Maxillofacial Unit, The Royal Brisbane and Womens Hospital.
Discipline of Periodontics, Faculty of Dentistry, The University of Sydney.
ABSTRACT
Gingival enlargements are a common clinical nding and most represent a reactive hyperplasia as a direct result of plaque
related inammatory gingival disease. These generally respond to conservative tissue management and attention to plaque
control. However, a small group are distinct from these and whilst they also represent a reactive tissue response, this occurs
at the level of the supercial bres of the periodontal ligament. These epulides grow from under the free gingival margin and
not as a result of a primary inammatory gingival enlargement. This distinct aetiopathogenesis separates this group of
lesions both in terms of their specic clinical presentation and behaviour and their propensity for recurrence if managed
inadequately.
Keywords: Gingival enlargement, epulis.
Abbreviations and acronyms: AG = angiogranuloma; GCL = giant cell lesion; GVHD = graft-versus-host disease; PF = peripheral fibroma;
PGCG = peripheral giant cell granuloma.
INTRODUCTION
Gingival enlargement is a common nding in clinical
practice and the appropriate treatment depends on
correctly diagnosing the cause of the enlargement. The
most common form of enlargement is due to plaque-
induced inammation of the adjacent gingival tissues
(inammatory hyperplasia) and this tends to be asso-
ciated most commonly with the interdental papillae and
may be localized or generalized. Such gingival enlarge-
ment can be exaggerated by hormonal effects, as found
in puberty and pregnancy, and may also be complicated
by certain systemic medications.
1
Plaque-induced
inammatory hyperplasia should resolve with debride-
ment of plaque and calculus and improved oral hygiene,
especially when the gingival tissue is oedematous.
Where the gingival tissue is brotic, resolution of
enlargement may not occur, resulting in the persistence
of periodontal pocketing such that effective oral
hygiene is impeded. This scenario requires a more
detailed assessment and a longer term management
plan designed to map the level of gingival and possibly
periodontal involvement. Surgical management to
remove enlarged tissue and provide improved access
for the patients oral hygiene may be required.
In addition to plaque-induced gingival enlargement,
there are a number of other types ranging from the
bland gingival brous nodule
2
and retrocuspid papilla
3
to malignant disease. Historically, localized gingival
enlargements have been termed epulides,
4
a term
describing pedunculated or sessile swellings of the
gingiva. However, epulides is a topographic term which
gives no histologic description of a specic lesion and so
the term reactive lesion of the gingiva has often been
used instead.
5
This paper describes a subset of reactive lesions of the
gingiva
6
presenting as localized gingival enlargements.
For completeness, examples of localized and general-
ized gingival enlargements are detailed in Table 1.
Localized reactive gingival enlargements
5,6
constitute
a group of epulides with a number of distinguishing
features that clinically separate them from plaque-
induced inammatory enlargements. This distinction
allows a clinical diagnosis and denes a treatment
protocol designed to minimize recurrence.
7
The two dening features of this small cluster of
epulides are rstly, their derivation from the supra-
bony bres of the periodontal ligament and secondly,
their primary reactive and non-inammatory nature.
These allow a reasoned explanation for their clinical
appearance and behaviour. Specically, these epulides
do not originate from the gingival surface and so do
not simply represent an enlargement of the commonly
inamed interdental papilla. They can occur at any
2010 Australian Dental Association 55
Australian Dental Journal
The ofcial journal of the Australian Dental Association
site along the free gingival margin and characteristi-
cally grow out from the gingival sulcus with a cervical
displacement of the gingival margin. In many lesions,
the original free gingival margin can be seen running
across the lesion and this denes the site of origin, the
dominant direction of growth (supra or subgingival)
and the likely disruption to the attached gingiva and
mucogingival junction during any subsequent surgical
procedure (Fig 1). The dening features of this group
are shown in Table 2. The members of the group
identied for discussion are the brous epulis periph-
eral broma (PF), angiogranuloma pyogenic granu-
loma (AG) and the peripheral giant cell lesion gran-
uloma (PGCG). A number of large case studies
5,6
have
been published and these are consistent in the general
demographic features with PF being the most fre-
quently encountered, followed by AG, PF with calci-
cation and PGCG. There is some variation in
male female distribution but most favour a M:F ratio
ranging from 1:1.31 for PF to 1:1.99 for AG and 1:1.5
for PGCG.
6
The site and size also vary but with a
dominant presentation in the maxilla and size within
the 0.5 to 1.5 cm range.
Fibrous epulis peripheral broma
This lesion represents the archetype and most common
of the epulides with a female bias and predominantly
adult distribution. It is also the endpoint for some
epulides that may progressively mature and undergo
brosis, e.g., some angiogranulomas.
The PF is essentially a reactive brous hyperplasia.
The lesion typically presents in adults as a rm, pink
and uninamed mass growing from under the free
gingival margin or interdental papilla (Fig 2). The
Table 1. Examples of localized and generalized gingi-
val enlargements
Developmental
Retrocuspid papilla
Fibrous nodule
Gingival cyst
Fibrous nodule
Reactive bromatosis gingivae
Focal mucinosis
Focal epithelial hyperplasia (viral)
Fibrous nodule
Hamartomatous
Gingival epithelial hamartoma
Cowdens syndrome
Idiopathic
Neoplastic
Benign malignant
Fig 1. Epulis growing from beneath the free gingival margin and
showing the derivation from the deeper tissues of the periodontium.
Table 2. Common features of epulides
Derivation from periodontal ligament
Develop from under free gingival margin
Reactive aetiology
Not primarily plaque related
High growth rate
High recurrence rate
Specic management requirements
Fig 2. Peripheral broma emanating from under the free gingival
margin and displacing this apically. There is a trauma related
inammation on the anterolateral aspect with central focal ulceration.
The lesion has extended into the previously existing diastema but has
not displaced the teeth.
Table 3. Differential diagnosis of angiogranuloma
Peripheral giant cell granuloma
Peripheral broma
Haemangioma
Pregnancy tumour
Periodontal granulation tissue
Kaposis sarcoma, bacillary angiomatosis
Non-Hodgkins lymphoma
Metastatic tumour
56 2010 Australian Dental Association
NW Savage and CG Daly
surface texture and presentation reects the previous
history of the lesion, e.g., hyperkeratosis or occasional
ulceration. The lesion is generally painless unless
traumatized during toothbrushing, ossing or eating.
There is no erosion of underlying bone and no
interdental spread unless there is a pre-existing dia-
stema or pre-existing interdental bone loss due to
chronic periodontitis. They may slowly increase in size
and some can reach impressive proportions and com-
promise the outcome of surgical removal, but this is an
uncommon nding.
The PF differs from a gingival hyperplasia in not
having dental plaque as a primary aetiological agent
and hence being non-inammatory unless secondarily
involved by plaque and calculus accumulation. Its
growth from under the gingival margin rather than
representing an inammatory enlargement of the sur-
face gingiva itself clearly distinguishes this lesion as a
separate entity.
The histological features of the PF readily separate
this lesion from gingival brous hyperplasia. The
lesion typically and diagnostically has a broblastic
reaction pattern although the peripheral sectors may
be mature and brocytic. The mass is discrete and
polypoid but non-encapsulated. The surrounding epi-
thelium is uninvolved and its histological appearance
reects the previous history of the surface with respect
to trauma and so varies from an atrophic, but
otherwise unremarkable epithelium, to areas of ulcer-
ation, although uncommon, and signicant hyperpla-
sia. This lesion frequently has a focus of calcication
which is variable and is seen as irregular dystrophic
calcication (peripheral broma with calcication) to
cementicles (PF with cementication) and trabeculae
of bone (PF with ossication). This latter feature is
responsible for the alternative term of calcifying
broblastic granuloma.
8
There is some evidence that
the calcication, generally regarded as dystrophic
calcication, may actually arise from pericyte differ-
entiation to osteogenic cells.
The treatment of the PF focuses specically on an
understanding of the derivation from the periodontal
tissues and so a supercial gingivectomy type proce-
dure will frequently result in recurrence. Mucoperio-
steal aps are best raised so that the lesion can be
excised entirely, suprabony connective tissue curetted
and the adjacent tooth and root surfaces debrided of
plaque and calculus or plaque-retaining factors in an
effort to minimize recurrence. The cosmetic result
will depend on the site of the lesion, the periodontal
bone support present and the amount of attached
gingiva (Figs 3a and 3b). Post-operative use of
antiseptic mouthrinses such as 0.2% chlorhexideine
gluconate should be utilized to assist healing
until mechanical oral hygiene procedures can be
restarted.
Angiogranuloma pyogenic granuloma
The angiogranuloma also presents mainly in adults and
although having some similarities to the PF, is clearly
distinguishable from it by recalling its very descriptive
title, angiogranuloma. The lesion is a smooth surfaced
mass, characteristically ulcerated (Fig 4), which grows
(a)
(b)
Fig 3. (a) A small peripheral broma on the labial aspect of 41 with
gingival margin displacement and showing the typical pink uninamed
appearance of this lesion. (b) The lesion has been removed with
attention to its deep attachment and a return of the gingival to its
premorbid status with no loss of contour or height.
Fig 4. Typically ulcerated angiogranuloma which is highly vascular
and has a characteristic red pink colour.
2010 Australian Dental Association 57
Gingival enlargements and overgrowths
from beneath the gingival margin and so displaces this
apically. Compared with the PF it is highly vascular,
variably compressible, typically bleeds readily and has a
characteristic red pink colour.
The angiogranuloma also shows the proliferative and
regenerative potential of the periodontium. This lesion
typically grows rapidly within the rst few weeks and
then slows to a gradual ongoing enlargement. Bone
erosion is uncommon but the mass can penetrate
interdentally and present as a bi-lobular mass con-
nected through the col area. Understandably, it has a
greater recurrence rate than the PF.
Histologically, the angiogranuloma accurately re-
ects its clinical presentation. It is an ulcerated and
inamed angiomatous lesion with numerous small
vascular channels and angioblastic foci consisting on
non-canalized clusters of endothelial cells. Many of
these brovascular lesions mature with the older basal
and lateral areas appearing brocytic and not dissimilar
to reactive gingival brous hyperplasias. Inammation
is inevitably present and its absence should raise the
possibility of a vascular malformation as opposed to an
angiogranuloma. The option of calling this lesion a
capillary haemangioma, granuloma type, has been
raised on a number of occasions but, given our current
understanding of the aetiopathogenesis of this lesion,
the term angiogranuloma seems most appropriate. A
current discussion on this issue has been presented by
Epivatianos et al.
9
Although micro-organisms may be
present on the surface, they are contaminants only and
the term pyogenic granuloma is a misnomer, but one
which persists even in the absence of any pyogenic
component.
The treatment is identical to the surgical excision of
the PF and recurrence, whilst signicant, seems depen-
dent on thorough surgical technique and primary
closure to minimize further proliferation of granulation
tissue.
9
The exception to this may be lesions that are
haemorrhagic and sclerotherapy
10
with injection of
sodium tetradecyl sulphate may be a consideration but
caution is required in consideration of the potential
toxicity and destructiveness of this agent. It has proven
useful in the authors practice in the treatment of lip
lesions as a preliminary procedure prior to denitive
surgical removal in a less hypervascular state. A recent
report also identies a possible role for corticosteroids
in treatment.
11
An interesting aspect of the angiogranuloma is its
appearance during pregnancy and hence the terms of
pregnancy epulis tumour and granuloma gravidarum
are used. The distinction between angiogranulo-
ma pyogenic granuloma and the pregnancy epulis is
clinical only, but the lesion is reported to occur in up to
5% or more of pregnancies.
12,13
These typically present
during the second trimester and, provided it does not
cause signicant functional restrictions or cosmetic
concerns, can be left until after delivery. Most preg-
nancy epulides will resolve fully approximately six
weeks post-partum or will reduce considerably in size
and be much less haemorrhagic, thus permitting easier
surgical excision. Failure to remove a residual mass
following pregnancy can lead to larger lesions at
subsequent pregnancies causing signicant functional
and cosmetic problems (Figs 5a and 5b).
The angiogranuloma can also occur in intraoral or
perioral sites unconnected with the gingiva, commonly
(a)
(b)
Fig 5. (a) Large multilobular angiogranuloma pregnancy epulis that
remained untreated following delivery with extensive involvement and
was removed after two years. (b) The excised lesion showing both
typical angiogranuloma and areas that have matured to a pink brous
tissue.
58 2010 Australian Dental Association
NW Savage and CG Daly
the lateral margin of the tongue and buccal mucosa
following trauma and the vermilion of the lip, partic-
ularly during pregnancy. In these sites management is
simple excision with a very low recurrence rate. There
have also been occasional associations with graft-vesus-
host disease (GVHD)
14
and following bone marrow
transplantation.
15
Peripheral giant cell granuloma
This lesion has also attracted a number of names, but
consideration of the histopathology and clinical behav-
iour
16
favours the above title. The peripheral giant cell
granuloma (PGCG) typically occurs in younger patients
and is common either as an isolated epulis in the
anterior mouth (Fig 6) or in the mixed dentition phase
in the posterior segments where teeth are erupting.
They are the most aggressive of the epulides and their
purplish-red almost cyanotic colour and propensity for
haemorrhage attests to a highly vascular lesion (Fig 7).
They will penetrate interdentally and bi-lobular lesions
are a common occurrence with associated erosion of the
adjacent cortical bone and separation of adjacent teeth
(Figs 8a and 8b) with their very signicant growth
potential.
17
The lesion is not restricted to periodontal
tissue and has been reported recently to occur with peri-
implant tissues.
18
A detailed analysis of their demo-
graphics and comparison with central giant cell lesions
has been reported by Motamedi et al.
19
The histology of this group is deceptively bland given
their clinical behaviour. The PGCG contains a single or
multi-nodular foci of mononuclear cells with proven
immunohistochemical derivation from the blood mono-
cyte lineage. They lie in a highly vascular brous stroma
interspersed with variable numbers of multi-nucleate
giant cells which are often closely related to the thin-
walled vascular channels. The lesion is not primarily
inamed although this is often a secondary focal
phenomenon due to local trauma or plaque related
inammation. The mass is partially surrounded by large
thin-walled vascular channels and this contributes to
the clinical cyanotic appearance and its haemorrhagic
tendency.
Fig 6. Typical highly vascular deeply coloured giant cell lesion with
lateral extension and displacement of the gingival margin.
Fig 7. Giant cell lesion with a multilobular contour and showing the
propensity for local extension often seen with this lesion.
(a)
(b)
Fig 8. (a) Giant cell lesion in a young patient with active displacement
of the coincident incisors and interdental spread. (b) Radiograph
showing interdental bone destruction caused by the PGCG.
2010 Australian Dental Association 59
Gingival enlargements and overgrowths
The histological appearance of the PGCG is impor-
tant as it explains the nature of this group of lesions and
their aggressive and often destructive clinical course.
They can be markedly haemorrhagic during surgery
and clinicians should be prepared to manage this,
particularly in the posterior areas of the mouth where
haemostasis can be difcult to obtain. The anterior
lesions are usually readily managed by a similar surgical
approach to the other epulides, but with the awareness
of likely bone erosion and requirement for very
thorough curettage of the supercial cortex and crestal
tissues. Suturing of a periodontal dressing material over
the excision site as a compression pack can assist with
haemostasis.
The PGCG is usually readily identied clinically due
to its colour and whilst it has the highest recurrence rate
of this group, it can generally be managed conserva-
tively. There are very occasional lesions that may recur
on multiple occasions and require extensive removal of
adjacent hard and soft tissues and, rarely, the involved
teeth. It is also worth noting that the peripheral PGCGis
unrelated to the central giant cell lesion (GCL) and they
should not be regarded as an extension of one other.
SUMMARY
Localized gingival enlargements represent a specic
group of lesions with a constant group of common
features but with distinctive clinical presentations and,
at least for the PGCG, an often aggressive clinical
course. They are reactive lesions emanating from the
supercial bres of the periodontal ligament and their
rapid growth is consistent with the high turnover rate of
the periodontal tissues. Removal must be thorough and
based on an understanding of the lesion type. Every
effort should be made to obtain primary closure of the
surgical site to facilitate healing and so discourage
proliferative granulation tissue formation which her-
alds early recurrence. Follow-up is required to ensure
that any recurrence is detected early and dealt with and
that the post-surgical gingival contour is maintained as
close as possible to its preoperative state.
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Address for correspondence:
Dr Neil W Savage
School of Dentistry
The University of Queensland
200 Turbot Street
Brisbane QLD 4000
Email: n.savage@uq.edu.au
60 2010 Australian Dental Association
NW Savage and CG Daly