Desquamative Gingivitis: Causes, Symptoms and Treatment

DESQUAMATIVE GINGIVITIS
PRESENTED BY : DR. SHRUTI PATIL
DEPARTMENT OF PERIODONTOLOGY

CONTENTS
History
Introduction
Classification
Clinical forms of desquamative gingivitis
Etiopathogenesis
Diagnosis of Desquamative Gingivitis: A Systematic Approach
Diseases That Can Manifest as Desquamative gingivitis
Treatment
Periodontal management of desquamative gingivitis
Conclusion
references

HISTORY
First described in 1894 by Tomes and Tomes.
Term chronic desquamative gingivitis was coined by Prinz in 1932.
It describes a reaction characterized by intense erythema,
desquamation, and ulceration of the free and attached gingiva
Newman MG, Takei H, Klokkevold PR, Carranza FA. Carranza's clinical periodontology. Elsevier health sciences; 2011 Feb
14.
Prinz H. Chronic diffuse desquamative gingivitis. Dent Cosm, 1932, 74:332-333

In 1960, McCarthy and colleagues suggested that
Desquamative gingivitis was not a specific disease entity
but was instead a gingival response associated with a
variety of conditions
This concept has been supported by numerous immunopathologic studies.
Nisengard RJ, Neiders M. Desquamative lesions of the gingiva. J Periodontol. 1981;52(9):500–510.
Sklavounou A, Laskaris G. Frequency of desquamative gingivitis in skin diseases. Oral Surg Oral Med Oral
Pathol.1983;56(2):141–144.
McCarthy FP, McCarthy PL. Chronic desquamative gingivitis: a reconsideration. Oral Surg. 1960;13:1300

• Approximately 75% of desquamative gingivitis cases have a
dermatologic genesis.
• Lichen planus and cicatricial pemphigoid account for 84% of the
desquamative gingivitis cases.
Neville BW, Damm DD, Allen CM, et al. Oral and maxillofacial pathology. ed 4. Elsevier: St. Louis; 2016.
Leao JC, Ingafou M, Khan A, et al. Desquamative gingivitis: retrospective analysis of disease associations of a large
cohort. Oral Dis. 2008;14(6):556–560.

• Many other mucocutaneous autoimmune conditions can manifest as
desquamative gingivitis :
 bullous pemphigoid
 pemphigus vulgaris
linear immunoglobulin A [IgA] disease
dermatitis herpetiformis
lupus erythematosus
 chronic ulcerative stomatitis
Dermatomyositis
mixed connective tissue disease.
Scully C, Porter SR. The clinical spectrum of desquamative gingivitis. Semin Cutan Med Surg. 1997;16(4):308–313

• Other conditions that must be considered in the differential diagnosis of
desquamative gingivitis :
Chronic bacterial
Fungal and viral infections
Reactions to medications mouthwashes, and chewing gums.
Rees T, Burkhart NW. Desquamative gingivitis 2016.
Scully C, Porter SR. The clinical spectrum of desquamative gingivitis. Semin Cutan Med Surg. 1997;16(4):308–313

Despite a systematic diagnostic approach, the cause of desquamative gingivitis
cannot be elucidated in up to one-third of cases.
It is important to ascertain the disease responsible for desquamative gingivitis
to establish the appropriate therapeutic approach.
To achieve this goal, a clinical examination is coupled with a thorough history
and routine histologic and immunofluorescence studies
Lo Russo L, Fedele S, Guiglia R, et al. Diagnostic pathways and clinical significance of desquamative gingivitis. J Periodontol.
2008;79(1):4–24.
Ress TD. Adjunctive therapy. Proceedings of the world workshop in clinical periodontics. American Academy of Periodontology:
Chicago; 1989

Classification of DG was based on the etiological, histological, and immunological findings :
(Modified classification by Mcarthy and others)
1. Dermatological
diseases
• Lichen planus
• Cicatricial pemphigoid
• Bullous pemphigoid
• Pemphigus vulgaris
• Psoriasis
• Linear Iga disease
Robinson NA, Wray D. Desquamative gingivitis: A sign of mucocutaneous disorders‐a review. Australian dental Robinson NA,
Wray D. Desquamative gingivitis: A sign of mucocutaneous disorders‐a review. Australian dental journal. 2003
Dec;48(4):206-11.journal. 2003 Dec;48(4):206-11.
Al-Abeedi F, Aldahish Y, Almotawa Z, Kujan O. The Differential Diagnosis of Desquamative Gingivitis: Review of the Literature
and Clinical Guide for Dental Undergraduates. J Int Oral Health. 2015;7(Suppl 1):88-92. PMID: 26225114; PMCID:
PMC4516075.

2. ENDOCRINAL
IMBALANCE
• Estrogen deficiency in females
(menopause, following
hysterectomy and oopherectomy)
• Testosterone deficiency in males

3. Chronic
infections
• Tuberculosis
• Chronic candidiasis
• Histoplasmosis

4. Idiopathic agents
Drug reactions (lichenoid reactions)
• Toxic antimetabolites
• Allergic- barbiturates,
antibiotics etc
• Conditions mimicking DG
 Crohn disease
 Chronic ulcerative stomatitis
 Plasma cell gingivitis
 Grafts versus host disease
 Factitious lesions
 Kindler syndrome
 Wegener granulomatosis
 Foreign body gingivitis
Robinson NA, Wray D. Desquamative gingivitis: A sign of mucocutaneous disorders‐a review. Australian dental Robinson NA, Wray D. Desquamative
gingivitis: A sign of mucocutaneous disorders‐a review. Australian dental journal. 2003 Dec;48(4):206-11.journal. 2003 Dec;48(4):206-11.

Nisengard RJ, Rogers III RS. The treatment of desquamative gingival lesions. Journal of periodontology. 1987 Mar;58(3):16772.

3 CLINICAL FORMS OF
(according to Glickman & Smulow)
Mild form • Diffuse erythema.
• Condition is usually
painless.
• Blanching may be seen.
• Intolerance to hot and
spicy food.
Stoopler ET, Sollecito TP, DeRossi SS. Desquamative gingivitis: early presenting symptom of mucocutaneous disease. Quintessence International. 2003;34(8):582.
Lemus Corredera I, González Díaz ME, Chinea Meneses EM, Toledo Pimentel B, Colectivo de autores. Diagnóstico, pronóstico y tratamiento de la enfermedad
periodontal inflamatoria crónica. Colectivo de autores. Compendio de Periodoncia. La Habana: Ciencias Médicas. 2006:215-9.

Moderate form
• Patchy distribution of bright red and
grey areas.
• Smooth, shiny and soft gingiva.
• Burning sensation, sensitivity to
temperature.
• Inhalation of air may be painful.
• Massaging gingiva results in
peeling of epithelium.
• Intolerance to spicy food, citrus
fruits and drinks.
• Brushing is highly
discomforting, readily bleeds.

Severe form
• Wide areas of the oral cavity
is involved.
• Surface epithelium appears
shredded.
• Surface epithelium seems to
be easily peeled away.
• Gingiva seems to be speckled.
• Blowing of air causes bubble
in gingival epithelium.
• Very painful.
• Constant dry and burning
sensation.
Stoopler ET, Sollecito TP, DeRossi SS. Desquamative gingivitis: early presenting symptom of mucocutaneous disease. Quintessence International. 2003;34(8):582.

ETIOPATHOGENESIS
• The oral mucosa consists of a stratified epithelial layer and connective tissue
underneath.
• Keratinized and non-keratinized.
• The gingiva is keratinized in order to resist the trauma caused by masticatory
forces.
TOFAN EC, PĂRLĂTESCU I, ŢOVARU Ş, NICOLAE C, PREDA AS, FUNIERU C. Desquamative Gingivitis-A Clinicopathological Review. Current health sciences journal.
2018 Oct 1;44(4):331-6.
Presland RB, Jurevic RJ. Making sense of the epithelial barrier: what molecular biology and genetics tell us about the functions of oral mucosal and epidermal
tissues. Journal of dental education. 2002 Apr;66(4):564-74.

• The oral mucosa consists of three layers:
1. Stratified squamous cell epithelium
1. Lamina propri
2. Basement membrane that separates them.
• Electron microscopy studies have shown that the basement membrane
consists of the following layers.
TOFAN EC, PĂRLĂTESCU I, ŢOVARU Ş, NICOLAE C, PREDA AS, FUNIERU C. Desquamative Gingivitis-A Clinicopathological Review. Current health sciences journal.
2018 Oct 1;44(4):331-6.
Newman MG, Takei H, Klokkevold PR, Carranza FA. Carranza's clinical periodontology. Elsevier health sciences; 2011 Feb 14.

TOFAN EC, PĂRLĂTESCU I, ŢOVARU Ş, NICOLAE C, PREDA AS, FUNIERU C. Desquamative Gingivitis-A Clinicopathological Review.
Current health sciences journal. 2018 Oct 1;44(4):331-6.
Textbook Of Periodontics Paperback – 30 April 2017 by Shalu Bathla

• Some of the epithelial proteins assure inter-cell and cell-membrane integrity.
• The autoimmune diseases target these proteins (considered to be antigens)
and auto-antibodies are formed against them.

TOFAN EC, PĂRLĂTESCU I, ŢOVARU Ş, NICOLAE C, PREDA AS, FUNIERU C. Desquamative Gingivitis-A Clinicopathological Review.
Current health sciences journal. 2018 Oct 1;44(4):331-6.

Diagnosis of Desquamative Gingivitis: A Systematic
Approach
• Desquamative gingivitis is a clinical term and not a diagnosis.
• After the condition is identified, a series of laboratory procedures should be
used to arrive at a final diagnosis.
• The success of any therapeutic approach depends on the establishment of an
accurate final diagnosis.
• The following sections describe a systematic approach to determining the
disease that is triggering desquamative gingivitis.

Clinical History
Complete data regarding symptoms associated with the condition as well as historical aspect.
When did it start (acute or chronic)?
Aggrevating & alleviating factors?
Are the lesions recurrent? If yes how often ?
Extraoral involvement?
History of fever, malaise, lymphadenopathy?
Drug/medications history
Maderal AD, Salisbury III PL, Jorizzo JL. Desquamative gingivitis: Diagnosis and treatment. Journal of the American Academy of
Dermatology. 2018 May 1;78(5):851-61.

Clinical examination
Recognition of pattern of disease: focal/multifocal
If only gingiva involved other areas also.
Nikoliskys sign
slight rubbing of the skin results in exfoliation of
the outermost layer, forming a blister within
minutes.
Dermatology. 2018 May 1;78(5):851-61.

Mignogna MD, Fortuna G, Leuci S, Ruoppo E, Marasca F, Matarasso S. Nikolsky's sign on the gingival mucosa: a clinical tool for
oral health practitioners. Journal of periodontology. 2008 Dec;79(12):2241-6.

Auspitz sign
Appearance of punctate bleeding spots when
psoriasis scales are scraped off.
Kobners
phenomenon
Appearance of lesion along the line of
trauma/injury.
Sanchez DP, Sonthalia S. Koebner Phenomenon.
Supraja R Dr; From the proceedings of Insight Ayurveda 2013,
Coimbatore. 24th and 25th May 2013. OA01.01. A case report on
psoriasis. Anc Sci Life. 2013 Jan;32(Suppl 2):S1. doi: 10.4103/0257-
7941.123812. PMCID: PMC4147477.

Biopsy
Incisional biopsy is best to begin microscopic and immunological evaluation.
A perilesional biopsy should avoid areas of ulcerations because necrosis and epithelial
denudation hamper diagnostic process
In some lesions such as lichen planus, subacute lupus erythematosus only lesion tissue can be
used.
Sylvie-Louise Avon DM, Klieb HB. Oral soft-tissue biopsy: an overview. J Can Dent Assoc. 2012;78:c75.

Microscopic examination
H&E staining and light
microscopic
Immunoflourescence
Direct Immunoflourescence Indirect Immunoflourescence

Buffered formalin (10%) should be
used to fix the tissue for
conventional hematoxylin and
eosin (H&E) evaluation.
Manual of Oral Histology and Oral Pathology (English, Paperback, Jose Maji)

incubated with a variety
of fluorescein-labeled,
antihuman serum
Unfixed frozen sections of oral or
esophageal mucosa from an
animal such as a monkey are first
incubated with the patient's serum
to enable attachment of serum
antibodies to the mucosal tissue.
The tissue is then incubated with
fluorescein-labeled antihuman
serum
Direct Immunoflourescence Indirect Immunoflourescence
Michel’s buffer (i.e.,
ammonium sulfate
buffer, pH 7.0) is
used as the
transport solution
for
immunofluorescence
assessment.

Diseases That Can Manifest as Desquamative Gingivitis
1. Pemphigus :
• Pemphigus is a group of rare autoimmune mucocutaneous disorders
presented with epithelial blistering of cutaneous and/or mucosal surfaces.
• These are serious conditions and turn out as potentially life-threatening
events.
• The term “pemphigus’ is derived from the Greek word “Pemphix”, meaning
“bubble or blister

Classification of pemphigus
Kershenovich R, Hodak E, Mimouni D. Diagnosis and classification of pemphigus and bullous pemphigoid. Autoimmunity
Reviews. 2014 Apr 1;13(4-5):477-81.

Main types of pemphigus
Pemphigus Vulgaris Paraneoplastic Pemphigus
• Most common type of
pemphigus.
• Usually associated with
lymphoproliferative disease
1. Mucosal-dominant type (limited
cutaneous involvement)
2. Mucocutaneous type (both mucosal and
cutaneous involvement)
3. Cutaneous type (cutaneous involvement
alone)
The clinical hallmark of paraneoplastic
pemphigus is painful and persistent
stomatitis which is extremely resistant to
therapy
Reviews. 2014 Apr 1;13(4-5):477-81.

IgG plays a pivotal role in pemphigus, not only as a diagnostic marker
but also as the main pathogenic agent acting against the cell surface
of keratinocytes producing Acantholysis and thus the clinical
presentation of blisters.
Reviews. 2014 Apr 1;13(4-5):477-81.

Clinical findings
Pemphigus vulgaris
Histopathology Biopsy of
Perilesional
Mucosa
Biopsy of
Uninvolved
Mucosa
Serum
Ragged erosions and
ulcerations plus Nikolsky
sign
Location: buccal and
labial mucosa, palate,
and
tongue
Other findings:
cutaneous flaccid bullae
and
erosions, other mucosal
surface involvement
Acantholysis and
intraepidermal
cleft
formation;
preservation of
basal
keratinocytes
Intercellular
deposits in
epithelium; IgG
in all cases and
C3 in most cases
Same as for
perilesional
mucosa
Intercellular
antibodies
(IgG) in
≥90% of cases
Dermatology. 2018 May 1;78(5):851-61.

Figure 1
The initial examination revealed a patchy
erythematous labial gingiva around teeth
no. 7 and 8.
Figure 2
Gentle palpation with a periodontal probe
elicited some desquamation of the gingiva
around tooth no. 27.
Ohta M, Osawa S, Endo H, Kuyama K, Yamamoto H, Ito T. Pemphigus vulgaris confined to the gingiva: a case report.
International journal of dentistry. 2011 May 11;2011.

Systemic corticosteroids remain gold standard for treatment of pemphigus
vulgaris
Gregoriou S, Efthymiou O, Stefanaki C, Rigopoulos D. Management of pemphigus vulgaris: challenges and solutions. Clin
Cosmet Investig Dermatol. 2015 Oct 21;8:521-7. doi: 10.2147/CCID.S75908. PMID: 26543381; PMCID: PMC4622091.
Optimal oral hygiene is essential as, as to prevent plaque associated gingivitis
and periodontitis which can exacerbate the condition.
To minimize the risk of morbidity of longterm use of steroids, alternate day
steroid therapy, steroid sparing drugs and topical steroids can be combined

Pemphigus associated with lymphoproliferative diseases.
Paraneoplastic pemphigus

Paraneoplastic pemphigus
Clinical findings Histopathology Biopsy of
Perilesional
Mucosa
Biopsy of
Uninvolved
Mucosa
Serum
Diffuse mucosal
erosions and
stomatitis
Location: vermilion
lip
Other findings:
widespread mucosal
involvement and
polymorphic
cutaneous
lesions
Acantholysis and
intraepidermal
blister,
subepidermal
blister, and dense,
band-like
infiltrate at the
dermoepidermal
junction
IgG and C3
deposition
intercellularly within
epidermis and along
the
dermoepidermal
junction
Same as for
perilesional
mucosa
Intercellular
antibodies (IgG) in
≥90% of cases
Dermatology. 2018 May 1;78(5):851-61.

Rosas MP, Villalba MN, Rubí JM, Mora AG, Nuño JS. Pénfigo paraneoplásico. Reporte de un caso. Revista Mexicana de
Periodontología. 2019 Jan 3;9(3):50-4.

Treatment :
• After the diagnosis is established, the dentist must choose the optimal
management strategy.
• The choice depends on following:
1. Practitioner's experience
2. Systemic impact of the disease
3. Systemic complications of the medications.

1. Dental practitioner takes direct and exclusive
responsibility for the treatment of the patient. This
occurs with conditions such as erosive lichen planus,
which is responsive to topical steroids
2. Dentist collaborates with another health care provider to
evaluate and treat a patient concurrently. The classic example
is seen with cicatricial pemphigoid, in which dentists and
ophthalmologists work together to provide treatment.
Although the dentist addresses the oral lesions, the
ophthalmologist monitors the integrity of the ocular
conjunctiva.
3. Patient is immediately referred to a dermatologist for
further evaluation and treatment. This occurs with
conditions for which the systemic impact of the disease
transcends the boundaries of the oral cavity and results
in significant morbidity or mortality.
Newman MG, Takei H, Klokkevold PR,
Carranza FA. Carranza's clinical
periodontology. Elsevier health
sciences; 2011 Feb 14.

Pemphigus vulgaris is an example of a condition that, after diagnosis by the
dentist, requires immediate referral to a dermatologist.
The complications (e.g., diabetes mellitus, osteoporosis,
methemoglobinemia) of chronically administered systemic
medications that are indicated for the management of
diseases such as pemphigus vulgaris or nonresponsive mucous
membrane pemphigoid (MMP) warrant referral to a
dermatologist or a specialist in internal medicine.

Cicatricial pemphigoid
Perilesional
Mucosa
Biopsy of
Uninvolved
Mucosa
Serum
Erythematous
patches, bullae, and
erosions
Location: gingiva,
buccal mucosa, and
palate
Other findings:
ocular, genital,
nasopharyngeal,
esophageal, and
laryngeal
involvement may
occur
Subepithelial
clefting with
epithelial
separation from
the underlying
lamina propria,
leaving an intact
basal layer.
Linear deposits
of C3 with or
without IgG at
the basement
membrane zone
in most cases
Same as for
perilesional
mucosa
Basement
membrane zone
antibodies (IgG) in
10% of
cases
Dermatology. 2018 May 1;78(5):851-61.

Newman MG, Takei H, Klokkevold PR, Carranza
FA. Carranza's clinical periodontology. Elsevier
health sciences; 2011 Feb 14.
Vijayan V, Paul A, Babu K,
Madhan B. Desquamative
gingivitis as only
presenting sign of mucous
membrane pemphigoid.
Journal of Indian Society
of Periodontology. 2016
May;20(3):340.
2. Bulla formation in
relation to marginal
gingival and interdental
papilla of 21 and 22
3. Desquamation evident
in relation to 21 and 22

Disease Therapy
Mild Cases Recalcitrant
Cases
Severe or Refractory Cases
Cicatricial
pemphigoid
Rx: Lidex (0.05% fluocinonide) gel
Disp: One tube (15 g)
Sig: Apply to affected area pc
and hs
Rx: Temovate (0.05%
clobetasol propionate)
Sig: Apply to affected area
qid
Refer to dermatologist for
management with
prednisone (20–30 mg/day);
concomitant use of
azathioprine may be needed;
dapsone, sulfonamide, and
tetracycline are other
alternatives

Connective tissue grafting to alleviate root surface sensitivity and to
improve aesthetics has been used with success to manage gingival
recession in a patient with cicatricial pemphigoid.
Lorenzana ER, Rees TD, Hallmon WW. Esthetic management of multiple recession defects in a patient with cicatricial
pemphigoid. Journal of periodontology. 2001 Feb;72(2):230-7.

Bullous pemphigoid
Perilesional
Mucosa
Biopsy of
Uninvolved
Mucosa
Serum
Tense cutaneous
bullae that rupture
and become flaccid.
Skin lesions of
bullous Pemphigoid
clinically resemble
those of Pemphigus,
the microscopic
picture is quite
distinct
Subepithelial
clefting with
epithelial
separation from
the underlying
lamina propria,
leaving an intact
basal layer
Linear deposits
of C3 with or
without IgG at
the basement
membrane zone
in most cases
Same as for
perilesional
mucosa
Basement
membrane zone in
40%–70% of cases

Lawson WM. Bullous oral erosions: clues to identifying-and managing-the cause. Consultant. 1998 Nov 1;38(11):2657-66.

In many cases, the clinical findings are probably the best way to discriminate
between them.
Accordingly, the term bullous pemphigoid is preferred when the disease is
nonscarring and mainly affects the skin.
The term cicatricial pemphigoid is favored when scarring occurs, and the
disease is mainly confined to mucous membranes, although scarring may be
absent with some subtypes of MMP.

Treatment :
• Designed to control its signs and symptoms.
• The primary treatment is a moderate dose of systemic prednisone.
• Steroid-sparing strategies (i.e., prednisone plus other immunomodulatory
drugs) are used when high doses of steroids are needed or when the steroid
alone fails to control the disease.
• For localized lesions of bullous pemphigoid, high-potency topical steroids or
tetracycline with or without nicotinamide can be effective.
Dermatology. 2018 May 1;78(5):851-61.

Lichen planus
• Several clinical forms of oral lichen planus :
 reticular
Patch
Atrophic
Erosive
 bullous
The most common are the reticular and erosive subtypes

• The typical reticular lesions are asymptomatic and bilateral, and they consist
of interlacing white lines on the posterior region of the buccal mucosa.
• The lateral border and dorsum of the tongue, the hard palate, the alveolar
ridge, and the gingiva may also be affected.
• The reticular lesions can have an erythematous background, which is a
feature associated with coexisting candidiasis.
Kalmar JR. Diagnosis and management of oral lichen planus. J Calif Dent Assoc. 2007 Jun;35(6):405-11.
Reticular oral lichen
planus of the
posterior right buccal
mucosa with well-
defined lace-like
pattern
Erosive oral lichen
planus presenting as
desquamative
gingivitis in the
canine-molar region
of the right maxilla.

• The erosive subtype of lichen planus is often associated with pain.
• It manifests as atrophic, erythematous, and often ulcerated areas.
• Fine, white radiating striations are observed bordering the atrophic and
ulcerated zones.
• These areas may be sensitive to heat, acid, and spicy foods

Michele Giuliani et al. concluded that, OLP may be considered potentially
malignant disorders.
He suggested that erosive type, female gender and tongue site should be
considered as risk factors for OLP malignant transformation.
Major efforts should be done to establish strict clinical and histological criteria to
diagnose OLP and to perform sounder methodological observational studies.
Giuliani M, Troiano G, Cordaro M, Corsalini M, Gioco G, Lo Muzio L, Pignatelli P, Lajolo C. Rate of malignant transformation of
oral lichen planus: A systematic review. Oral diseases. 2019 Apr;25(3):693-709.

Perilesional
Mucosa
Biopsy of
Uninvolved
Mucosa
Serum
Wickham striae,
erosions, and
koebnerization
Location: buccal,
gingival, and labial
mucosa
Hyperkeratosis,
hydropic
degeneration of
the basal layer,
and sawtooth rete
pegs; lamina propria
exhibits
dense, bandlike
infiltrate,
primarily of T
lymphocytes;
colloid bodies
Fibrillar deposits
of fibrin at the
dermal–
epidermal
junction
Negative Negative

The keratotic lesions of oral lichen planus are asymptomatic and
do not require treatment after the microscopic diagnosis has
been established.
However, evaluation of the patient every 6 to 12 months is
warranted to monitor suspicious clinical changes and to look for
the emergence of an erosive component.

Disease Therapy
Cases
Erosive
lichen
planus
Delivery of therapeutic agent is enhanced
with use of vacuum-formed custom trays
Disp: One tube (15 g), Sig: Apply to
affected area pc and hs. Monitoring of
patient's oral cavity warranted because
candidiasis may develop after a few weeks
of topical steroid use; concomitant use of
antifungal may be necessary
Rx: Clotrimazole 10-mg troches
Disp: 90, Sig: Dissolve in mouth tid, then
expectorate for 30 consecutive days
Rx:
Protopic
(0.1%
tacrolimus)
ointment
Disp: One
tube (15 g)
Sig: Apply
to affected area bid.
Refer to dermatologist for
management with systemic
corticosteroids

• Lidex can also be mixed 1 : 1 with carboxymethylcellulose (Orabase) paste or
another adhesive ointment.
• A gingival tray can be used to deliver 0.05% fluocinonide ointment or gel or
0.05% clobetasol propionate with 100,000 IU/ml of nystatin in Orabase.

Chronic ulcerative stomatitis
• First reported in 1990.
• Manifest with chronic oral ulcerations.
• Predilection for women during fourth decade of life

Chronic Ulcerative Stomatitis
Perilesional
Mucosa
Biopsy of
Uninvolved
Mucosa
Serum
Chronic oral ulcerations, painful
solitary small blisters and erosions
with surrounding
erythema occur mainly on the
gingiva and the lateral border of
the tongue. Because of the
magnitude and clinical features of
the gingival lesions, a diagnosis of
desquamative gingivitis is
considered
Similar to erosive
lichen planus.
IgG deposits in
the nuclei of the
basal layer of
epithelial cells
Same as for
perilesional
mucosa
ANA specific
for basal cells
of
stratified
squamous
epithelium

Initial
presentation. Note
diffuse erythema
present on the
maxillary and
mandibular
attached gingiva.
Lorenzana ER, Rees TD, Glass M, Detweiler JG. Chronic ulcerative stomatitis: A case report. Journal of Periodontology. 2000
Jan;71(1):104-11.

Disease Therapy
Cases
Chronic
Ulcerative
Stomatitis
Topical steroids (e.g., fluocinonide,
clobetasol propionate) and topical
tetracycline
Sig: Apply to affected area qid
Rx: Temovate (0.05% clobetasol
propionate)
Sig: Apply to affected area qid
High dose of a systemic
corticosteroid is needed to
achieve remission.
Unfortunately, reduction of the
corticosteroid dose results in
relapse of the lesions.
Hydroxychloroquine sulfate at a
dosage of 200 to 400 mg per day
seems to be the treatment of
choice to produce complete,
long-lasting remission

Drug-Related Eruptions
• Eruptions in the oral cavity that result from sensitivity to drugs that have been
taken orally or parenterally are called stomatitis medicamentosa.
• The local reaction from the use of a medicament in the oral cavity (e.g.,
stomatitis resulting from topical penicillin use) is referred to as stomatitis
venenata or contact stomatitis.

Clinical features:
• Most drug eruptions in the oral cavity are multiform.
• Vesicular and bullous lesions occur most often, but pigmented or
nonpigmented macular lesions are also frequently observed.
• Erosions, which are often followed by deep ulceration with purpuric lesions,
can occur.
• The lesions are seen in different areas of the oral cavity, with the gingiva often
being affected

Common drugs/agents causing reactions:
Mercurial compounds in dental amalgam
 Tartar control toothpaste (Pyrophosphates and flavoring agents)
Cinnamon compounds (i.e., cinnamon oil, cinnamic acid, or cinnamic
aldehyde) that are used to mask the taste of pyrophosphates in tartar control
toothpaste

Areas showing desquamative gingival lesions in relation
to teeth numbers 45 and 46
Yajamanya SR, Jayaram P, Chatterjee A. Desquamative gingivitis mimicking mild gingivitis. Journal of Indian Society of
Periodontology. 2016 Sep;20(5):565.

Treatment
• Elimination of the offending agent .
• If removal of the offending medication is not possible, topical corticosteroids
and topical tacrolimus can be used to treat the lesions.

Dermatitis Herpetiformis
• Dermatitis herpetiformis is a chronic condition that usually develops in young
adults between the ages of 20 and 30 years.
• Dermatitis herpetiformis is cutaneous manifestation of celiac disease.
• Slight predilection for men.
• Clinical manifestations :
 bilateral and symmetric pruritic papules or vesicles that are primarily
restricted to the extensor surfaces of the extremities

• Clusters of vesicles or papules arise on the skin.
• These vesicles or papules eventually resolve and are followed by
hyperpigmentation of the skin, which ultimately wanes.
• The oral lesions of dermatitis herpetiformis range from painful
ulcerations preceded by the collapse of ephemeral vesicles or bullae to
erythematous lesions.

Treatment
• Gluten enteropathy can be severe in about two-thirds of patients.
• A gluten-free diet is essential for the treatment of celiac disease and
dermatitis herpetiformis.
• Oral dapsone is usually needed for patients with newly detected dermatitis
herpetiformis to alleviate symptoms promptly.

Lupus Erythematosus
Lupus erythematosus is an autoimmune disease with three different clinical
presentations:
1. Systemic
2. Chronic cutaneous
3. Subacute cutaneous

Systemic Lupus Erythematosus :
• Can affect kidneys, heart, skin, and mucosa.
• The classic cutaneous lesions characterized
by a rash on the malar area with a butterfly distribution.
• oral lesions of SLE are usually ulcerative or similar to those of lichen
planus.

Chronic Cutaneous Lupus Erythematosus
No systemic signs or symptoms; lesions are
limited to the skin or the mucosal surfaces.
The skin lesions are referred to as discoid
lupus erythematosus (DLE).
Oral lesions: Lichen-planus–like plaques on
the palate and the buccal mucosa

Treatment
Depends on the severity and extent of the disease.
• Range from topical steroids to NSAIDS
• For chronic cutaneous lupus erythematosus:
Topical steroids for cutaneous and oral lesions.
• For severe systemic organ involvement:
Moderate to high doses of prednisone.
Immunosuppressive drugs .

Erythema Multiforme
• Erythema multiforme is an acute bullous and macular inflammatory
mucocutaneous disease.
• Ages of 20 and 40 years.
• Target (i.e., iris) lesions with central clearing are the hallmark of erythema
multiforme.
• It can be a mild condition (i.e., erythema multiforme minor) or a severe and
possibly life-threatening condition (i.e., erythema multiforme major or
Stevens–Johnson syndrome).

• Erythema multiforme minor lasts approximately 4 weeks and exhibits
moderate cutaneous and mucosal involvement.
• Stevens–Johnson syndrome can last a month or longer.
• It involves the skin, conjunctiva, oral mucosa, and genitalia, and it requires
more aggressive therapy than erythema multiforme minor.
• Toxic epidermal necrolysis to be the most severe form of erythema
multiforme,

Most common etiologic factors
Herpes simplex infection Drug reactions
•Sulfonamides
•Penicillins
•Quinolones
•Chlormezanone
•Barbiturates
•Oxicam
•NSAIS’s
•Anticonvulsant drugs

Oral lesions :
• Multiple,large, shallow, painful ulcers with an erythematous border.
• They affect the entire oral mucosa in approximately 20% of patients with
erythema multiforme.
• The lesions are so painful that chewing and swallowing are impaired.
• The buccal mucosa and the tongue are the most frequently affected sites,
followed by the labial mucosa.

Shah SN, Chauhan GR, Manjunatha BS, Dagrus K. Drug induced erythema multiforme: two case series with review of
literature. J Clin Diagn Res. 2014 Sep;8(9):ZH01-4. doi: 10.7860/JCDR/2014/10173.4761. Epub 2014 Sep 20. PMID: 25386550;
PMCID: PMC4226002.
Target lesion

• Areas that are less often affected include the floor of the mouth, the hard
and soft palates, and the gingiva.
• Erythema multiforme is rarely confined exclusively to the gingival tissues,
prompting a clinical diagnosis of desquamative gingivitis.
• Hemorrhagic crusting of the vermilion border of the lips may occur, which is
helpful for arriving at a clinical diagnosis of erythema multiforme.

TREATMENT
• There is no specific treatment for erythema multiforme.
• For mild symptoms, systemic and local antihistamines, topical anesthetics, and
debridement of lesions with an oxygenating agent are adequate.
• In patients with bullous or ulcerative lesions and severe symptoms,
corticosteroids are considered the drug of choice, although their use is
controversial and not completely accepted.

Periodontal Management of DG
• Control of dental plaque and local irritants.
• Oral hygiene maintainance using soft brush with gentle brushing,
use of floss or waterpik, & antiseptic mouth rinses.
• While active erosions are present, using a modified Bass technique
Dermatology. 2018 May 1;78(5):851-61.

•Caustic mouthwashes avoided.
•Dietary changes with avoidance of spicy food.
•Emphasis on oral hygiene, along with frequent SRP
•Multidisciplinary consultation
Dermatology. 2018 May 1;78(5):851-61.

Decolonization:
• Institution of an antiseptic protocol with regular antifungal prophylaxis.
• This can be performed with the twice-daily use of an antiseptic mouth rinse
containing hydrogen peroxide and daily use of antifungal troches.
• We also perform empiric treatment with a short course of an oral antifungal
at the time of diagnosis, then as needed for evidence of candidal disease.
Dermatology. 2018 May 1;78(5):851-61.

Medical therapies
Topical therapies:
• Topical therapies alone can be sufficient to control disease when mild to
moderate.
• For immunobullous diseases, systemic therapies are generally required, but topical
modalities represent an important adjunctive treatment.
• The most commonly used first-line topical therapy is a topical corticosteroid.
• We prefer either a class 1 or class 2, as a gel, which can sting, or an ointment,
which may be seen to wash away but is effective.
Dermatology. 2018 May 1;78(5):851-61.

• For more refractory lesions, intralesional administration can be used.
• Adverse effects of topical corticosteroids include mucosal atrophy, oral
dryness, and secondary candidiasis.
• Topical calcineurin inhibitors (TCIs) represent an additional topical treatment
for DG.
• TCIs can be delivered via gel, cream, or as a suspension to swish and spit,
created by dissolving a 1-mg capsule into a liter of water
Dermatology. 2018 May 1;78(5):851-61.

Systemic therapies
When patients continue to have erosions and pain despite compliance with
topical therapy, treatment with systemic therapy is indicated.
Dermatology. 2018 May 1;78(5):851-61.

Effect of desquamative gingivitis on periodontal status
• From a theoretic point of view, disorders causing DG may have potential
harmful outcomes on the development and progression of plaque related
periodontal disease.
These potential injuries may be related to both direct and indirect relationships.
Lo Russo LU, Guiglia R, Pizzo G, Fierro G, Ciavarella DO, Lo Muzio LO, Campisi G. Effect of desquamative gingivitis on
periodontal status: a pilot study. Oral Diseases. 2010 Jan;16(1):102-7.

Indirect effect:
Symptoms associated with DG
Prevent proper oral hygiene
Plaque
periodontal disease
Indirect effect:
May also be plausible based
on the possible shared
pathogenetic mechanisms ⁄
mediators.
Lo Russo LU, Guiglia R, Pizzo G, Fierro G, Ciavarella DO, Lo Muzio LO, Campisi G. Effect of desquamative gingivitis on
periodontal status: a pilot study. Oral Diseases. 2010 Jan;16(1):102-7.

STUDIES
Ramon-Fluixa et al, 1999 : Increased plaque and calculus deposits are associated
to a significantly higher incidence of atrophic-erosive gingival lesions in patients
with Oral lichen planus.
Akman et al, 2008: PV might contribute to the development and / or progression
of periodontitis. PV patients should be encouraged for long‐term periodontal
follow up.
Ramon‐Fluixa C, Bagán‐Sebastián JV, Milián‐Masanet MA, Scully C. Periodontal status in patients with oral lichen planus: a
study of 90 cases. Oral diseases. 1999 Jul;5(4):303-6.
Akman A, Kacaroglu H, Yilmaz E, Alpsoy E. Periodontal status in patients with pemphigus vulgaris. Oral Diseases. 2008
Oct;14(7):640-3.

• Recalcitrant gingival erythematous lichen planus lesions comprise a
considerable therapeutic problem.
• This case of chronic desquamative gingivitis in a 25-year-old woman with
erosive oral lichen planus was treated with topical and systemic corti-
costeroid administration, followed by placement of a free gingival graft on
right upper quadrant.
Vatankhah M, Taghi Chitsazi M, Mehdipour M, Taghavi Zenouz A, Estakhri R. Treatment of desquamative gingivitis with free
gingival graft: a case report. J Dent Res Dent Clin Dent Prospects. 2010 Winter;4(1):33-6. doi: 10.5681/joddd.2010.009.
Epub 2010 Mar 14. PMID: 22991593; PMCID: PMC3429958.

• Recurrence of the lesions was observed following both treatment modalities.
• Free gingival graft despite being an aggressive therapy, proved more effective
and with fewer side effects compared with topical or systemic steroid therapy.
• It seems to be a promising treatment modality with the benefit of more stable
results, among others.
Vatankhah M, Taghi Chitsazi M, Mehdipour M, Taghavi Zenouz A, Estakhri R. Treatment of desquamative gingivitis with free
gingival graft: a case report. J Dent Res Dent Clin Dent Prospects. 2010 Winter;4(1):33-6. doi: 10.5681/joddd.2010.009.
Epub 2010 Mar 14. PMID: 22991593; PMCID: PMC3429958.

• Treatment of chronic desquamative gingivitis using tissue-engineered human
cultured gingival epithelial sheets.
• Study concluded that, human cultured gingival epithelial sheets fabricated
using tissue engineering technology showed significant promise for gingival
augmentation in periodontal therapy.
Okuda K, Momose M, Murata M, Saito Y, Inoie M, Shinohara C, Wolff LF, Yoshie H. Treatment of chronic desquamative
gingivitis using tissue-engineered human cultured gingival epithelial sheets: a case report. International Journal of
Periodontics & Restorative Dentistry. 2004 Apr 1;24(2).

• Conducted a study on low-level laser therapy in the treatment of mucous
membrane pemphigoid.
• Concluded that, healing of mucous membrane pemphigoid was achieved when
LLLT was used as an adjunct to the application of a local corticosteroid.
Yilmaz HG, Kusakci‐Seker B, Bayindir H, Tözüm TF. Low‐Level Laser Therapy in the Treatment of Mucous Membrane
Pemphigoid: A Promising Procedure. Journal of periodontology. 2010 Aug;81(8):1226-30.

M Mhaske et al. treated a desquamative gingivitis case successfully using
systemic antioxidant therapy along with oral hygiene maintenance.
Clinical anecdotal evidence supporting the beneficial use of antioxidants for
desquamative gingivitis lesion was found.
Therefore antioxidants can be added to the traditional treatment modalities of
such lesions & can be use as a first treatment option as a substitute to the
corticosteroids.
Mhaske M, Thakur N, Bansode S, Kedar P. “Desquamative Gingivitis Treated By An Antioxidant Therapy-A.

A diagnostic biopsy was obtained from the gingiva of patients with DG using the
stab‐and‐roll technique.
The gingival epithelium was well maintained, and the relationship with the
underlying connective tissue was diagnostic.
In the future, this stab‐and‐roll biopsy technique may facilitate early diagnosis
and treatment of diseases causing DG.
Rees TD, Allen EP, Kuyama K, Aoki S, Yamamoto H. A Stab-and-Roll Biopsy Technique to Maintain Gingival Epithelium for
Desquamative Gingivitis: Hiroyasu Endo,*, , , Shinichiro Aoki,* Hirotsugu Yamamoto, and Takanori Ito. Journal of
periodontology. 2014(6):802-9.

Rees TD, Allen EP, Kuyama K, Aoki S, Yamamoto H. A Stab-and-Roll Biopsy Technique to Maintain Gingival Epithelium for
Desquamative Gingivitis: Hiroyasu Endo,*, , , Shinichiro Aoki,* Hirotsugu Yamamoto, and Takanori Ito. Journal of
periodontology. 2014(6):802-9.

Concluded that, the efficacy of maintaining personal and professional oral
hygiene in patients with GD, reducing the clinical signs of the disease,
regardless of its pathogenesis.
Garcia-Pola MJ, Rodriguez-López S, Fernánz-Vigil A, Bagán L, Garcia-Martín JM. Oral hygiene instructions and professional
control as part of the treatment of desquamative gingivitis. Systematic review. Med Oral Patol Oral Cir Bucal. 2019 Mar
1;24(2):e136-e144. doi: 10.4317/medoral.22782. PMID: 30818305; PMCID: PMC6441599.

CONCLUSION
• In patients with suspicious desquamative lesions of the gingiva, it is imperative
to establish a definitive diagnosis via histopathologic and immunologic
findings.
• The goal of treatment should focus on eradication of the lesions prior to any
periodontal therapy, following a conservative approach.
• These diseases may not be limited to the oral cavity, and it is crucial that
appropriate consultations are made to ensure optimal patient care.
• The Periodontist has a unique opportunity to make the diagnosis and then
refer the patient to a medical specialist for treatment.

REFERENCES
• Newman MG, Takei H, Klokkevold PR, Carranza FA. Carranza's clinical
periodontology. Elsevier health sciences; 2011 Feb 14.
• Garcia-Pola MJ, Rodriguez-López S, Fernánz-Vigil A, Bagán L, Garcia-Martín JM.
Oral hygiene instructions and professional control as part of the treatment of
desquamative gingivitis. Systematic review. Med Oral Patol Oral Cir Bucal.
2019 Mar 1;24(2):e136-e144. doi: 10.4317/medoral.22782. PMID: 30818305;
PMCID: PMC6441599.
• Yilmaz HG, Kusakci‐Seker B, Bayindir H, Tözüm TF. Low‐Level Laser Therapy in
the Treatment of Mucous Membrane Pemphigoid: A Promising Procedure.
Journal of periodontology. 2010 Aug;81(8):1226-30.

• Mhaske M, Thakur N, Bansode S, Kedar P. “Desquamative GingivitisTreated By
An Antioxidant Therapy-A.
• Okuda K, Momose M, Murata M, Saito Y, Inoie M, Shinohara C, Wolff LF,
Yoshie H. Treatment of chronic desquamative gingivitis using tissue-
engineered human cultured gingival epithelial sheets: a case report.
International Journal of Periodontics & Restorative Dentistry.

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