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162]

Original Article

Clinicopathological and
immunohistochemical analysis of
plasma cell gingivitis‑ A retrospective
study
Vandana Gupta, Harpreet Kaur,1 Vikender Singh Yadav, Sunny Kala,1
Deepika Mishra1

Centre for Dental Abstract:

Education and
Background: This study aims to describe the demographics and clinicopathological characteristics of the cases
Research, Division of of plasma cell gingivitis (PCG) reported in our institute, supported by a review of pertinent literature. Further,
Periodontics, All India we investigated the role of the cluster of differentiation CD138, Ki67, CD56, and CD117 immunoexpression in
Institute of Medical the differential diagnosis of PCG from plasma cell dyscrasias. Materials and Methods: All histopathologically
Sciences, 1Department confirmed cases of PCG, whose relevant details could be obtained, were included in this study. They were
of Oral Pathology and subjected to panel of immunohistochemical markers to exclude plasma cell malignancies. Further, published
Microbiology, Centre English literature for PCG since 1970–2020 was reviewed. Results: Nine histopathologically confirmed cases
for Dental Education of PCG, were retrieved from the archives of our department. The cases comprised 3 males and 6 females with
their ages ranging between 14 and 82 years. The plasma cells exhibited equivocal reactivity for kappa and
and Research, All India
lambda; and immunonegativity for CD56, CD117 with low Ki67 proliferation index. Published literature in English
Institute of Medical showed 43 cases of PCG were predominantly female; the diffuse involvement of maxilla and mandible was a
Sciences, New Delhi, common finding. Conclusion: In addition to kappa lambda reactivity, an immunoprofile of CD138, Ki67, CD56,
India and CD117 may be used as a diagnostic adjunct to exclude malignant plasma cell lesions in confusing cases.
Key words:
Benign lesion, gingival overgrowth, immunohistochemistry, plasma cells
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INTRODUCTION immune‑mediated mucous lesions and sometimes
DOI: plasma cell dyscrasias (PCDs). Thus, in complex
10.4103/jisp.jisp_67_21
Quick Response Code: P lasma cell gingivitis (PCG) is a rare benign
lesion of the gingiva with various appellations
such as plasma cell gingivostomatitis, idiopathic
cases, a multidisciplinary diagnostic approach
involving clinical and microscopic features along
with diagnostic adjuncts such as hematology
gingivostomatitis, etc.[1,2] The latest 2017 World and immunohistochemistry (wherever required)
Workshop classification has included this is often necessary. However, the role of
entity under nonplaque induced gingival immunohistochemistry is not extensively studied
lesions though the previous editions have in the diagnosis of PCG so far.
expanded its classification under conditioned
gingival enlargement.[3] The predisposing factors CD138 (syndecan) is a marker of plasma cells
responsible are allergic reactions to some known irrespective of reactive or neoplastic nature.
allergens though in the majority of the cases Kappa and lambda light chain reactivity is
Address for the cause remains unidentified.[4] Thus, PCG is commonly used to study the clonality of
correspondence: classified into 3 categories; caused by allergens,
Dr. Deepika Mishra, This is an open access journal, and articles are
neoplasms, or unknown cause.[5,6]
Department of Oral distributed under the terms of the Creative Commons
Pathology and Attribution‑NonCommercial‑ShareAlike 4.0 License, which
Microbiology, Centre for There is no particular age or sex distribution allows others to remix, tweak, and build upon the work
non‑commercially, as long as appropriate credit is given and
Dental Education and for PCG except female predominance in the new creations are licensed under the identical terms.
Research, All India Institute few.[7] Clinically it usually presents as diffuse, red,
of Medical Sciences, edematous enlargement of the marginal gingiva For reprints contact: WKHLRPMedknow_reprints@
New Delhi ‑ 110 029 India. wolterskluwer.com
extending into attached gingiva with sharp
E‑mail: deepika1904@ demarcation along the mucogingival border.[8]
gmail.com How to cite this article: Gupta V, Kaur H,
Many a times, PCGs are associated with other
mucosal lesions such as cheilitis and glossitis.[9] Yadav VS, Kala S, Mishra D. Clinicopathological
Submitted: 08‑Jun‑2021 and immunohistochemical analysis of plasma
Revised: 25‑Jul‑2021 Microscopy shows diffuse intense infiltration of
cell gingivitis‑ A retrospective study. J Indian Soc
Accepted: 31‑Oct‑2021 mature plasma cells in the stroma with marked Periodontol 2022;26:434-9.
Published: 01-Sep-2022 epithelial changes. [4,10,11] PCG mimics other

434 © 2022 Indian Society of Periodontology | Published by Wolters Kluwer - Medknow

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Gupta, et al.: Plasma cell gingivitis and its biomarkers

plasma cells.[9] CD56 is neural cell adhesion molecule which
is expressed in 70%–80% of malignant plasma cells.[12] CD117
is hematopoietic growth factor which is observed in 33%
of plasma cell myeloma (PCM) patients. However, the lack
of expression of these markers in malignant plasma cell
neoplasms indicates more aggressive behavior. Nevertheless,
normal plasma cells are typically negative for both CD56 and
CD117.[13] Ki67 is well‑known cell proliferation marker related
to aggressive biological behavior.[14] Mukherjee et al. studied
the expression of CD44, CD34, CD43, Ki67, and CD117 in
addition to kappa lambda profile in discrimination of PCG
from malignancies.[15] However CD56 expression is not yet
studied in PCG.
For the literature review, we conducted an extensive search of
published English literature from 1971 to 2020 using PubMed
and Google Scholar as the primary databases. The MeSH terms
used were PCG, gingiva, idiopathic enlargement, maxilla, and
mandible. The cases previously reported were compared with
our series of PCG.
RESULTS
The study included 9 histopathological confirmed cases of
PCG comprising 6 females and 3 males (M:F ratio‑1:2). The age
range was 14–82 years with a mean age of presentation being
45.3 years  [Table 1; Figure 1].

Thus, the aim of the present study was to retrospectively
analyze clinico‑pathological characteristics of PCG reported at
a tertiary care dental hospital. We emphasize the conventional
multidisciplinary approach integrating microscopic features
with history, clinical and imaging details for reaching
the accurate diagnosis. Further, the role of hematological
investigations and immunohistochemical evaluation of CD138,
CD56, CD117, Ki67, and kappa lambda in differentiating PCG
from malignant neoplasms is also highlighted and the relevant
literature is examined.
MATERIALS AND METHODS
After receiving institutional ethical approval and following
Helsinki Declaration and their guidelines, we retrospectively
reviewed 2044 biopsies received in the department of oral
pathology and microbiology, from January 2018 to July 2020.
The paraffin‑embedded blocks of confirmed PCG cases were
retrieved from the archives. All hematoxylin‑ and eosin‑stained
sections of PCG cases were analyzed. The pertinent details were
retrieved from case files of patients. Periodic acid Schiff (PAS)
stain was used to exclude candidiasis. To rule out overt
malignancies and to confirm the polyclonal nature of plasma
cells, immunohistochemistry with Ki67, CD56, CD117, CD138,
Kappa, and lambda were performed for each case. These cases
were re‑evaluated by the pathologists and the final diagnosis
of PCG was confirmed.
Predisposing factors remain unidentified in all except one
case where there was associated implant‑supported prosthesis
adjacent to the lesion. Clinical differential diagnosis included
idiopathic gingival enlargement, PCG, granulomatous
diseases, mucocutaneous lesions, pyogenic granuloma,
and rarely malignancies, namely leukemia, extramedullary
plasmacytoma (EMP), and PCM. Normal hematological profile
ruled out leukemia and lupus erythematosus.
Microscopy of the cases characteristically exhibited intense
plasma cell infiltrates (>50%–70%) within vascular stroma with
no cellular atypia and variable epithelial changes [Figure 2].
Epithelial characteristics
All cases were circumscribed showing epithelial covering
focally with predominant areas of ulceration. All cases
displayed hyperplasia, acanthosis, spongiosis while some
cases showed arcading pattern (Case 2, 5, and 9) and plasma
pooling (Case 6). All cases showed parakeratinization, while
4 (Case 4, 5,7, and 8) cases showed loss of keratinization in
few areas. Only 4 cases showed leukocyte exocytosis (Case
1, 2, 5, 7).
Connective tissue characteristics
There was an intense infiltration of plasma cells predominantly
arranged in sheets and lobules while few cases (1, 2, and
8) showed diffuse arrangement. All the cases showed
mild‑to‑moderate vascularity with engorged blood vessels.

Table 1: Clinical features of plasma cell gingivitis in our study

Clinical Case 1 Case 2 Case 3 Case 4 Case 5 Case 6 Case 7 Case 8 Case 9
details
Gender, Female, 26 Male, 34 Female, 82 Female, 14 Female, 26 Female, 63 Female, 24 Male, 67 Male, 46
age (years)
Location Maxilla and Maxilla and Mandible Maxilla and Maxilla and Maxilla Maxilla Mandible Maxilla and
mandible mandible mandible mandible mandible
Clinical Generalized Swollen Erythematous Generalized Generalized Localized Diffuse Localized Generalized
presentation gingival erythematous proliferative gingival gingival gingival gingival buccal gingival
enlargement mass lesion enlargement enlargement erythematous ulceration erythematous enlargement
swelling swelling
Radiographic ‑ ‑ ‑ ‑ Generalized ‑ ‑ ‑ ‑
findings horizontal
bone loss
Etiological UI UI Implant UI UI UI UI UI UI
factor supported
prosthesis
Treatment Gingivectomy Gingivectomy Surgical Gingivectomy Gingivectomy Surgical Surgical Surgical Gingivectomy
excision excision excision excision
UI – Unidentified

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Gupta, et al.: Plasma cell gingivitis and its biomarkers
In addition, Case 8 showed histiocytes and multinucleated
giant cells.
Histopathological differentials considered were PCG, IgG4
related disease (RD), and PCDs such as plasmacytoma and its
multicentric form‑PCM [Table 2]. Immunohistochemically,
plasma cells in all the cases showed mixed reactivity for both
Kappa and lambda (kappa lambda ratio of 1:01) confirming a
polyclonal nature. These cells were negative for CD117, CD56,
PAS; immunopositive for CD138 and exhibited low to negative
Ki67 proliferation index (1%–4%) [Figure 3]. The published
literature showed 43 reported cases of PCG from 1971 to
2020 [Supplementary Table 1].[1, 4-7, 9,11,15-25,27,33-48]
DISCUSSION
In the present study, 9 cases of PCG were diagnosed in the last
3 years as compared to only 43 cases reported in the literature
in the last 50 years. It can be explained by two reasons. First, it
can be suggested that the low number of PCG cases is a result
of under‑reporting since the entity is not novel, also since
only literature in English were searched and included in the
manuscript, case reports in other languages were most likely
a b
c d
e Figure 2: Histopathological presentation of plasma cell gingivitis. (a) Spongiotic
Figure 1: Clinical presentation of plasma cell gingivitis. (a) Extra-oral picture
showing facial asymmetry. (b) Preoperative generalized gingival enlargement
(frontal view). (c) Preoperative gingival enlargement (occlusal view). (d)
Postoperative view after 6 months of surgical excision of enlarged gingiva (e)
Orthopantomogram showing generalized bone loss
436 Journal of Indian Society of Periodontology - Volume 26, Issue 5, September-October 2022
overlooked. Another reason for increased frequency of PCG in
our institute can be attributed to the fact that our center is an
apex referral center. PCG does not always respond well to the
treatment prescribed due to unidentifiable etiological factors
in most situations. Hence, the patients are generally referred
to higher centers for the relief of symptoms.
The analysis of the published literature revealed female
predominance with male‑to‑female ratio of 1:1.42. The age
ranged from 12 to 70 years (mean 31.6) and presentation in the
pediatric age group was rare. The maxillary lesions were more
common, involving the anterior gingiva in the majority of cases.
The herbal toothpaste and their ingredients were recognized as
risk factors in most of the cases. Clinical appearance varied from
gingival enlargement (18 cases), followed by the erythematous
lesion (13 cases), ulcerated swollen mass (6 cases), and gingival
inflammation (6 cases).
Upon comparing the characteristic features of PCG in the
published literature with our cases, similarities were observed
in sex predilection where a female predominance was
demonstrable, with involvement of maxillary and mandibular
arch more frequently than tongue, lip, and palate. [4,17,18]
The predisposing risk factors remained unidentified in the
majority of the cases in literature which is concurrent with
our observations. Some reports have found herbal agents in
dentifrices,[19,20] Khat leaves,[21] colocasia (arbi) leaves,[1] mint,[22]
fixed prosthesis, and dietary components as contributing factors.
The lesions get eventually resolved by identifying the risk factor
and eliminating it from the patient diet.[3] Unfortunately, in our
a b
c d
e f
hyperplastic epithelium overlying inflamed stroma (inset showing psoriasiform
hyperplasia). (b) Epithelium showing marked acanthosis and leucocytic exocytosis
(red arrow). (c) Epithelium exhibiting hyperplasia with entrapped fibrovascular cores
and spongiosis. (d) Acanthosis and plasma pooling within epithelium. (e) Stroma
exhibiting intense inflammatory infiltrate with interspersed engorged blood vessels.
(f) High power showing predominantly plasma cells exhibiting eccentric nuclei
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Gupta, et al.: Plasma cell gingivitis and its biomarkers

Table 2: Differential diagnosis of Plasma cell gingivitis

Clinical differentials Histological differentials
Cicatricial Pyogenic Oral lichen planus Plasma cell dyscrasias IgG4^ related
pemphigoid (CP) granuloma Extramedullary Plasma cell Myeloma disease
discoid lupus plasmacytoma with extramedullary
erythematosus involvement
Clinical entity Mucocutaneous Pedunculated Bilaterally Head and Neck Local growth of soft Heterogeneous clinical
presenting lesions, vesicles, lesion involving symmetrical lesion most common, tissue in vicinity and radiological
granulomatous Nikolsky’s sign gingiva most involving skin, Soft tissue mass to skeleton or presentation which
overgrowth frequently buccal mucosa hematogenous spread to mimics malignancy.
most frequently any other organ or tissue
Histology Subepithelial Abundant Saw toothed rete monoclonal Similar to Storiform fibrosis,
split with variable engorged ridges, liquefactive plasmacytoid cells plasmacytoma, acquire obliterative phlebitis
inflammation in blood degeneration of with light chain blastoid morphology in and more than10/
CP* vessels in the basal layer with restriction plasmablastic plasma high power field IgG4
Hyperkeratosis, background intense lymphocytic cell myeloma positive plasma cells
follicular plugging, of mixed infiltrate (more specifically ratio
degeneration of inflammatory subepithelially of IgG4 to IgG positive
basal cells infiltrate plasma cells as >0.4)
Treatment Systemic Conservative Symptomatic Radiation therapy Chemotherapy Corticosteroids
corticosteroid, surgical cases require
immunomodulator excision variable treatment
therapy ranging from topic
corticosteroids
to antifungal
or systemic
steroids or
immunomodulators
Prognosis Generally good, Excellent, Malignant potential Better prognosis Usually incurable Irreversible injury
spontaneous occasional controversial than solitary progressive disease, to some organs if
remission in 2-5 recurrence plasmacytoma, median survival rate 5.5 therapy is not initiated
years 30% patient years in time, once fibrosis is
progress to PCM# established treatment
options are limited
CP – Cicatricial pemphigoid, PCM – Plasma cell myeloma, IgG – Immunoglobulin G

series, the predisposing factor remains unidentified except for
one case where the prosthetic component proved to be risk
factor for PCG. This was consistent with the case reported by
Prasanna et al.[23]
PCG clinically mimics other reactive lesions such as pyogenic
granuloma, peripheral giant cell granuloma, immune‑mediated
mucous lesions such as cicatricial pemphigoid and discoid lupus
erythematosus and histologically mimic PCDs and IgG4 RD.
Clinically the current cases showed generalized gingival
enlargement involving marginal and attached gingiva with
altered contour and rolled out margins that is identical to the
case reported by Vishnu et al.[7] Diffuse swollen erythematous
mass and gingival ulceration were observed which are
consistent with previous reports.[24,25] Radiographic finding
of generalized horizontal bone loss was seen in a single case
as mentioned in the literature.[15] Silverman has described
syndromic association with the triad of PCG, glossitis, and
cheilitis but no case in our series showed this association.[26]
Three cases in the literature were associated with supraglottic
lesions but none of our present cases showed laryngeal
lesions.[27] Similarly, Tandon et  al. reported a case of oral
tuberculosis that mimicked PCG on incisional biopsy, however,
chest radiograph and excisional biopsy confirmed it to be
tubercular gingivitis.[28]
Few isolated case reports have mentioned plasma cell granuloma
as a manifestation of underlying IgG4‑ RD (IgG4‑RD).[29]
IgG4‑RD is a rare fibro‑inflammatory systemic disease with
comprehensive diagnostic criteria which is a combination
of clinical, imaging, laboratory, and histopathological
findings.[30,31] None of our present cases could fulfill the
diagnostic criteria for IgG4‑RD and thus this differential was
excluded.
Barbe et al. have reported a case of sickle cell anemia mimicking
PCG the diagnosis of which was confirmed by altered
hematological profile and electrophoresis.[16] Histopathological
examination showed diffuse intense infiltrate of plasma
cells in the subepithelial connective tissue with no evidence
of cytological atypia. Vishnu et  al. reported a case of PCG
mimicking granulomatous disease.[7] Polyclonal nature of
plasma cells was confirmed by kappa lambda light chain
co‑expression is most of the cases.
Further PCDs should be excluded before labeling a lesion
as reactive PCG. [3] PCDs, are malignant neoplasms of
monoclonal plasma cells exhibiting metastatic potential.
Solitary plasmacytoma of bone is unicentric malignancy
with origin within bone whereas EMP is predominantly seen
in the head–and‑neck region. PCM is systemic malignancy
with multicentric origin within the bone with the same
histopathology as plasmacytoma but poorer prognosis.[3,32,33]
As both reactive and neoplastic plasma cells exhibit CD138
immunopositivity, the restriction in production of one of
the two (kappa and lambda) light chains is a promising way
to confirm monoclonality.[3] Immunonegativity to CD117,

Journal of Indian Society of Periodontology - Volume 26, Issue 5, September-October 2022 437
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Gupta, et al.: Plasma cell gingivitis and its biomarkers
a 3. Holmstrup P, Plemons J, Meyle J. Non-plaque-induced gingival
b
c d e Plasma cell gingivitis mimicking granulomatous disease: A
g plasma-cell gingivitis, plasmacytosis of gingiva. Oral Surg Oral
f
Figure 3: Special staining and immunoprofile of plasma cell gingivitis. (a) Periodic
acid–Schiff staining showing no fungal organisms. (b) Plasma cells exhibiting
membranous and cytoplasmic cluster of differentiation 138 immunopositivity.
(c) Ki67 proliferation index less approximately 1%. (d and e) Plasma cells displaying
immunonegativity for CD117, CD56. (f and g) plasma cells displaying equivocal
immunoreactivity for kappa and lambda light chains
CD56, low to negative Ki67proliferation index, and equivocal
reactivity for kappa and lambda in all the present cases of
PCG was in accordance with Mukherjee et  al.[15] However,
CD56 was evaluated for the first time in PCG. The results were
in agreement with the published data which showed CD56
immunonegativity in normal plasma cells.[14]
The treatment in all cases of our study constituted gingivectomy
followed by Phase I therapy and surgical excision of the
lesion. Recurrence was observed in only 1 case till 2 years
of follow‑up (Case no. 4). However, in literature, different
treatment modalities of PCG exist including nonsurgical and
surgical approaches [Supplementary Table 1]. Nonsurgical
treatments comprise oral and topical steroids, topical 2% fusidic
acid, topical chlorpheniramine maleate, and strict elimination
of recognized risk factors; surgical approach advocates
gingivectomy and surgical excision.
CONCLUSION
Our study explained in detail the clinicopathological features
of PCG in comparison with literature findings. Further, it can
be concluded that histopathology remains the gold standard to
diagnose PCG. Immunonegativity for CD56, CD117, and low
Ki67 proliferation index may be used as adjunctive diagnostic
characteristic (in addition to already established kappa and
lambda reactivity) for differentiating it from malignant PCDs.
However, instead of the small number of cases of PCG in our
study, these markers should be performed on a large sample
size to confirm our findings.
438 Journal of Indian Society of Periodontology - Volume 26, Issue 5, September-October 2022
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Supplementary Table 1: Literature review of histopathologically confirmed cases of plasma cell gingivitis from 1971
to 2020
Author, year Gender, Location Predisposing Clinical Clinical and Special stains and Treatment Follow up
age factor presentation laboratory immunohistochemistry
investigations
Kerr DA ‑ ‑ ‑ ‑ ‑ ‑ ‑ ‑
et al., 1977##
Palmer RM Female, Maxilla UI Swollen upper NHP^^ Cytology negative for Topical 2 years,
et al., 1981 29 anterior gingiva candidal hyphae triamcinolone in NR
orabase
Palmer RM Male, Maxilla UI Swollen upper NHP Special stains negative Topical 2 years,
et al., 1981 52 anterior gingiva for fungal hyphae triamcinolone in NR
orabase
Serio FG Female, Maxilla Red pepper Severe gingival NHP, negative Nonsurgical 1 month
et al., 1981 36 and inflammation Nikolsky’s sign periodontal
mandible therapy
Newcomb Female, Maxilla UI Erythema, ‑ ‑ Gingivectomy 2 year
GM et al., 12 and gingival
1982* mandible enlargement
D’Angelo M ‑ ‑ ‑ ‑ ‑ ‑ ‑ ‑
et al., 1983##
Maioli S ‑ ‑ ‑ ‑ ‑ ‑ ‑ ‑
et al., 1984##
Lubow RM M,36 Maxilla Dynamints Ulcerated History of NA Gingivectomy 8 months,
et al., 1984 marginal gingiva psoriasis, NR
NHP except
increased
eosinophils
Macleod RI ‑ ‑ Herbal ‑ ‑ ‑ ‑ ‑
et al., 1989** toothpaste
Timms MS Female, Maxilla UI Gingival Supraglottic Positive reactivity for Systemic steroids Long term
et al., 1991 70 and erythema and laryngeal kappa and lambda light
mandible laryngeal lesions involvement chains and various
heavy chains
Timms MS Female, Maxilla UI Gingival Supraglottic Positive reactivity for Systemic steroids Long term
et al., 1991 32 and erythema and laryngeal kappa and lambda light
mandible laryngeal lesions involvement chains and various
heavy chains
Timms MS Female, Maxilla UI Gingival Supraglottic Positive reactivity for Systemic steroids Long term
et al., 1991 57 and erythema and laryngeal kappa and lambda light
mandible laryngeal lesions involvement chains and various
heavy chains
Nitta H et al., ‑ ‑ UI Gingival ‑ ‑ Conventional ‑
1991* enlargement periodontal
therapy
Sollecito TP Female, Maxilla UI Erythematous NHP, negative Non‑specific Topical steroids 3 weeks,
et al., 1992 61 gingiva lupus band immunofluorescence, remission
test and ANA cell marker analysis
antibodies suggestive of reactive
infiltrate
Sollecito TP Female, Maxilla UI Erythematous NHP NA Topical steroids 3 weeks,
et al., 1992 62 gingiva remission
Reed BE Female, Maxilla UI Generalized NHP Direct and indirect Conventional ‑
et al., 1993 37 and swelling immunofluorescence periodontal
mandible revealed reactive treatment
plasma cells
Gargiulo AV ‑ ‑ ‑ ‑ ‑ ‑ ‑ ‑
et al., 1995*
Mahler V Female, Maxilla UI Erythematous NA 90% IgG producing Topical 2% 10 weeks,
et al., 1996 53 maxillary gingiva plasma cells, Special fusidic acid resolution
stains negative for
fungal hyphae, positive
reactivity for kappa and
lambda
Marker P Male, Mandible Khat Erythematous Marked bone PAS negative for fungal Nonsurgical 2 weeks,
et al., 2002 30 gingiva destruction on hyphae periodontal remission
imaging therapy

Contd...
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Supplementary Table 1: Contd...

Author, year Gender, Location Predisposing Clinical Clinical and Special stains and Treatment Follow up
age factor presentation laboratory immunohistochemistry
investigations
Roman CC F,13 Maxilla UI# Erythematous Low serum PAS negative, positive electrocoagulation 2 years,
et al., 2002 gingiva and secretory reactivity for kappa and NR
IgA, other lambda
hematological
and
biochemical
tests normal
Velez et al., ‑ ‑ Kitchen Erythema, ‑ ‑ ‑ ‑
2005* cleaning enlargement
solution
Anil S et al., Male, ‑ ‑ Inflamed gingiva NHP ‑ Nonsurgical 1 to
2007* 26 periodontal 2 weeks,
treatment remission
Anil S et al., Male, ‑‑ ‑ Inflamed gingiva NHP ‑ Nonsurgical 1 to
2007* 27 periodontal 2 weeks,
treatment remission
Anil S et al., Male, ‑ ‑ Inflamed gingiva NHP ‑ Nonsurgical 1 to
2007* 36 periodontal 2 weeks,
treatment remission
Bhatavadekar Female, Maxilla UI Erythematous Periapical ‑ Surgical excision ‑
N et al., 2008 17 gingiva imaging
normal
JadwatY Female, ‑ ‑ ‑ ‑ ‑ ‑ ‑
et al., 2008* 19
Bali D et al., Female, Maxilla Colocasia Generalized NHP NA Surgical excision 2 weeks,
2012 48 leaves diffuse gingivitis NR
Lamdari N Female, ‑ Herbal Erythematous ‑ ‑ Nonsurgical 1 month,
et al., 2012* 29 dentifrice gingiva periodontal remission
therapy and
discontinuation
of herbal
dentifrice
Wood NH Female, Maxilla UI Generalized ‑ Gingivectomy ‑
et al., 2012§ 70 and gingival
mandible enlargement
Janam P Female, Maxilla UI Generalized NHP, NBP NA Gingivectomy 8 months,
et al., 2012 15 and gingival Mild
mandible enlargement recurrence
Makkar A Female, Maxilla Acacia Arabia Gingival NHP, NA Gingivectomy Recurrence
et al., 2013 17 and (herbal enlargement progressive after 1 year
mandible extract) with bone loss bone loss on
imaging
Abhishek K Male, Maxilla UI Gingival NHP, NBP NA Gingivectomy 1 year, NR
et al., 2013 16 and enlargement
mandible
Kumar V Male, Maxilla UI Localized NHP and Positive reactivity for Surgical excision 6 months,
et al., 2014 42 swelling in the
severe kappa and lambda NR
upper anterior
alveolar
jaw bone loss in
radiographs
Joshi C Male, Mandible Herbal Bleeding swollen Negative NA Gingivectomy 3 months,
et al., 2014 27 toothpowder mass Nikolsky’s NR
sign, NHP
Ranganathan Male, Maxilla UI Enlarged Nikolsky’s sign NA Topical 10 months,
AT et al., 20 maxillary negative, NHP chlorpheniramine NR
2015 anterior gingiva maleate
Mishra MB Female, ‑ Herbal agents ‑ ‑ ‑ ‑ ‑
et al., 2015* 15 in dentifrices
Mukherjee M M,26 Maxilla Possibly Gingival NHP, negative CD34, CD117, Ki67, Gingivectomy 2 years,
et al., 2015 and herbal enlargement Nikolsky’s sign CD43 negative, CD44 NR
mandible toothpaste positive, positive
reactivity for kappa and
lambda (10:1)

Contd...
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Supplementary Table 1: Contd...

Author, year Gender, Location Predisposing Clinical Clinical and Special stains and Treatment Follow up
age factor presentation laboratory immunohistochemistry
investigations
Prasanna JS Female, Maxilla Fixed partial Gingival NHP NA Gingivectomy 6 months,
et al., 2016 19 and denture enlargement NR
mandible
Prasanna JS Male, Maxilla UI Gingival NHP NA Gingivectomy 6 months,
et al., 2016 15 and enlargement NR
mandible
Negi BS Male, Maxilla UI Gingival NHP Positive reactivity for Laser assisted 3 years
et al., 2019 12 and enlargement and kappa and lambda gingivectomy
mandible erythema
Chauhan Y Male, Maxilla UI Gingival Negative Positive reactivity for Gingivectomy 8 months,
et al., 2019 18 and enlargement Nikolsky’s kappa and lambda NR
mandible with cheilitis sign, NHP
Barbe AG Male, Maxilla UI Gingival Microcytic Positive reactivity for Gingivectomy 6 months,
et al., 2020 33 and enlargement erythrocytosis, kappa and lambda, NR
mandible no anemia, IgG4/IgG: 0.279
deficiency
of Vitamin D
and folic acid,
electrophoresis
showed sickle
cell anemia
Vishnu V Female, Maxilla Diffuse gingival NHP and NA Gingivectomy 1 year
et al., 2020 13 enlargement crestal
bone loss in
radiographs,
AFB; negative,
calcium, ACE
enzyme levels,
cANCA, chest
radiograph
normal**
*Only abstract available full article not accessible; **This case showed foreign body giant cells and granuloma formation histologically along with intense plasma
cell infiltrate. Thus, granulomatous diseases such as tuberculosis, sarcoidosis, Wegener granulomatosis were considered as differentials and were ruled out
by AFB negativity, normal ACE and calcium levels; normal chest radiograph and cANCA levels respectively; #Thought to be chewing gum associated but on
discontinuation of its usage lesion did not disappear and after surgical treatment usage of chewing did not cause recurrence of lesion; ##No abstract available;
§
This was the case of concomitant PCG with diffuse peripheral odontogenic fibroma. UI – Unidentified; NHP – Normalhematological profile; NR – No recurrence;
NA – Not accessed; AFB – Acid‑fast bacilli; ACE – Angiotensinconvertase enzyme; cANCA – Antineutrophilic cytoplasmic antibodies; NBP – Normal biochemical
profile; ANA – Antinuclear antibody; Ig – Immunoglobulin; PAS – Periodic acid–Schiff; CD – Cluster of differentiation; M – Male; F – Female