CONTENTS Introduction History Definition Etiology Prevalence Classification Clinical Presentation Differential Diagnosis Oral Lichen Planus Pemphigus Vulgaris Mucous Membrane Pemphigoid Paraneoplastic Pemphigoid Erythema Multiforme Complex Aphthosis Graft Versus Host Disease Plasma Cell Gingivitis Foreign Body Gingivitis Diagnosis Treatment Prognosis Conclusion References

1. Presented By:-
Dr. Faheem Ahmed
MDS 2nd Year

2. CONTENTS
 Introduction
 History
 Definition
 Etiology
 Prevalence
 Classification
 Clinical Presentation
 Differential Diagnosis
 Oral Lichen Planus
 Pemphigus Vulgaris
 Mucous Membrane
Pemphigoid
 Paraneoplastic Pemphigoid
 Erythema Multiforme
 Complex Aphthosis
 Graft Versus Host Disease
 Plasma Cell Gingivitis
 Foreign Body Gingivitis
 Diagnosis
 Treatment
 Prognosis
 Conclusion
 References
2

3. INTRODUCTION
 The term “desquamation” is derived from the Latin
word ‘Desquamare’, which means scraping fish flakes.
 As a word, desquamation means ‘loss of epithelial
elements in small and large amounts, peeling of skin,
and exfoliation’.
 Chronic desquamation of the gingiva is referred to as
desquamative gingivitis (DG) (Scully C, Porter SR
1997).
3

4.  In actual use, the term ‘Desquamative gingivitis’ is
used for a specific clinical symptom and it is not a
diagnosis alone (Scully C, Porter SR 1997, Guiglia R
et al 2007, Endo H et al 2008, Lo Russo Let al 2009,
Rees TD. 2011 ).
 DG is a clinical finding, which progresses with
vesicular formation, atrophy, erosion and
desquamation, characterized with diffuse erythema of
the marginal and keratinized gingiva (Lo Russo Let al
2009, Endo H, Rees TD 2011, Rogers RS et al 1982,
Stoopler ET et al 2003).
4

5.  Lesions start with diffuse erythema and minimal
desquamation. The affected gingiva epithelium is very
fragile and tends to exfoliate easily, even with the
slightest trauma (Guiglia R et al 2007).
 Large ulceration areas can be observed in some cases
(Corrocher G et al 2006).
5

6.  Desquamation of epithelial tissue is generally seen in free
and keratinized gingiva. Generally, the lesions that affect
the buccal/labial surfaces of the gingiva, although not
formed due to bacterial plaque, are exacerbated with
plaque accumulation (Leao JC et al 2008).
 Although they are generally observed in the anterior
region, they can be seen in any gingival area (Lo Russo L
et al 2009).
 Similar lesions can be seen in the edentulous alveolar ridge.
 While only desquamations can be observed in the patients,
there can also be associated vesicular-bullous lesions, in
addition to ulcerative and lichenoid lesions.
6

7.  In severe cases, it can be seen generalized at the oral
mucosa, and the alveolar mucosa can be affected
together with the gingiva (Leao JC et al 2008).
 The patient can either have no complaints or there can
be a burning sensation or severe pain.
 In general, there is chronic pain, which especially
increases with the intake of acidic foods.
 Limitation of oral function and speech difficulties due
to pain can also be observed (Scully C, Porter SR
1997, Lo Russo L et al 2009).
7

8.  Nisengard and Levine (1995) have mentioned some
characteristics in order to diagnose the clinical
findings as DG, since gingival erythema is not
associated with plaque and presence of gingival
desquamation.
 They also emphasized that the Nikolsky phenomenon
is generally positive in DG patients.
8

9. HISTORY
 TOMES & TOMES, 1894 : Described for the first time.
 Goodby, 1923 : mentioned in his book
 Prinz, 1932 : coined the term “chronic diffuse desquamative
gingivitis”
 Meritt, 1933 : a disease of unknown etiology
 Stoloff, 1933 : “Periodic transitory meno-gingivitis“
 Ziskin and Zegarelli, 1942 : discussed the clinical and
microscopic features of chronic desquamative gingivitis.
9

10.  Schour & Massler, 1947 : gave the term gingivosis in anemic
hospitalized children of postwar Italy.
 McCarthy et al, 1960 : Not a specific disease entity but a
gingival response associated with a variety of conditions.
 Hosiosky, et al, 1961: suggested treatment of DG by
improving cervical oral hygiene.
 Glickman and Smulow, 1962 : studied the histopathology
and histochemistry. Two basic microscopic types
recognized: a bullous type, and a lichenoid type.
 Glickman and Smulow, 1964 : advocated a treatment
regimen of systemic corticosteroid therapy and removal of
local irritants.
10

11. DEFINITIONs
 Desquamative gingivitis is an erythematous (red),
desquamatous (shedding) and ulcerated appearance of the
gums. (Carranza's clinical periodontology, 11th ed.)
 “A peculiar condition characterized by intense erythema,
desquamation, and ulceration of the free and attached
gingiva.” - Prinz (1894)
 McCarthy and colleagues (1960) suggested that
“desquamative gingivitis was not a specific disease entity
but rather a gingival response associated with a variety of
conditions.”
11

12. Etiology
 Initially, it was suggested that gingival desquamations were
related to hormonal changes due to menopause on the
basis that gingival desquamations were more common in
the middle-aged and in women (Leao JC et al 2008).
 In 1964, Glikman and Smulow stated that DG could be
the symptom of severe conditions, especially
mucocutaneous diseases.
 Recently, it has been generally accepted that DG can be the
initial symptom of vesicular bullous diseases and can
emerge as a result of reactions against some chemicals and
allergens, and that it is not related to hormones (Scully C,
Porter SR 1997, Guiglia R et al 2007, Lo Russo L et al
2009, Stoopler ET et al 2003, Robinson NA, Wray D
2003, Leao JC et al 2008).
12

13.  Several different disease processes can lead to DG. The
most common are oral lichen planus (OLP), cicatricial
pemphigoid (CP), and pemphigus vulgaris (PV),
representing 75%, 9%, and 4% of patients with DG,
respectively. (Lo Russo L et 2009)
 Other etiologies include erythema multiforme (EM),
graft-versus-host disease (GVHD), paraneoplastic
pemphigus (PNP), and epidermolysis bullosa acquisita
(EBA), among others. (Lo Russo L et 2009)
 Irritant and allergic contact dermatitis can also be
potential initiating or exacerbating factors. The most
common contactants are mouthwashes, toothpastes,
dental materials, and medications. (Al-Abeedi F et al
2015)
13

14. Prevalence
 The desquamative gingivitis is seen after puberty, especially
in individuals over 30 years of age (Guiglia R et al 2007).
 It is more common in women than in men.
 It has been reported that it can rarely be observed in
children (Scully C, Porter SR 1997, Guiglia R et al 2007,
Endo H, Rees TD 2011, Robinson NA, Wray D. 2003).
 Although the intraoral presence of desquamative gingival
lesions differ, various durations from 2 months to 25 years
have been reported (Leao JC et al 2008).
14

15. CLASSIFICATION
15
Based on etiological considerations, desquamative gingival
lesions are classified as (MODIFIED CLASSIFICATION OF
MCCARTHY AND OTHERS)
Dermatoses
Lichen planus
Cicatrical
pemphigoid
Bullous
pemphigoid
Pemphigus vulgaris
Psoriasis
Linear IgA
disease

16. Endocrinal
imbalance
16
Estrogen deficiency in females
(menopause, following
hysterectomy and
oopherectomy)
Testosterone deficiency in
males
Chronic
infections
Tuberculosis
Chronic candidiasis
Histoplasmosis

17. Idiopathic
Drug reactions (lichenoid
reactions)
• Toxic antimetabolites
• Allergic-
barbiturates,
antibiotics etc
17
Conditions mimicking DG
• Crohn disease
• Chronic ulcerative
stomatitis
• Plasma cell gingivitis
• Grafts versus host
disease
• Factitious lesions
• Kindler syndrome
• Wegener granulomatosis
• Foreign body gingivitis

18. GLICKMAN & SMULOW:
3 forms of desquamative gingivitis
18
Mild Moderate
Severe

19. 19

20. Disease-specific findings
 It is usually difficult on clinical features alone to
distinguish various diseases associated with DG.
 Histopathologic and immunopathologic and enzyme-
linked immunosorbent assay should be assessed to
assign a diagnosis before the institution of systemic
therapy.
 Wickham striae are lacy, net-like, whitish-gray plaques
that are usually found on the buccal mucosa, tongue,
and gingiva.
20

21.  Though Wickham striae
are the most recognized
sign of OLP, they are not
always present. (Eisen D
et al 2005)
 The erosive form of OLP
can present
predominantly with
extensive erosions and
erythema, but Wickham
striae can usually be seen
at the periphery of the
lesion and may provide a
clue to the diagnosis.
(Ismail SB et al 2007)
Oral lichen planus. Wickham striae.
21

22.  Other diseases can mimic this
finding, including graft-versus-
host disease (GVHD) and oral
lichenoid reactions, and
therefore Wickham striae are
suggestive but not
pathognomonic of OLP.
(Alrashdan MS et al 2016)
 Well-healed scars not on
gingiva from MMP can also
produce similar findings.
(Mutasim DF et al 1993)
 Leukoedema of the bite line
often causes confusion, but is a
common oral examination
finding. Leukoedema of the bite line.
22

23.  The Nikolsky sign is the
production of a blister (or
epidermal separation)
when lateral pressure is
applied adjacent to an
active erosion or blister.
 It is considered suggestive
of pemphigus vulgaris (PV)
and Stevense Johnson
syndrome (SJS) or toxic
epidermal necrolysis
(TEN), but can on occasion
also be seen in patients
with mucous membrane
pemphigoid (MMP).
(Scully C et al 1999)
Positive Nikolsky sign associated with PV
MMP
23

24.  Other features that can aid in distinguishing between
PV and MMP are the appearance of the ulcers; in
patients with PV, they tend to present as more ragged
ulcers, while in patients with MMP, they are often
smooth and blisters are more commonly observable.
 The Nikolsky sign can aide in distinguishing different
forms of pemphigus, because it is often negative in
patients with paraneoplastic pemphigus (PNP).
(Czernik A et al 2011)
 Finally, the presence or absence of certain skin
findings can aid in narrowing the differential
diagnosis.
24

25. Long-term consequences
 There are several long-term consequences to
periodontal health that occur because of chronic DG
and resultant reduced oral hygiene.
 Because of pain with brushing and flossing and
reduced oral hygiene practices, patients with DG have
statistically poorer plaque scores. (Thorat MS et al
2010)
 This plaque worsens periodontitis, which can lead to
alveolar bone loss and ultimately tooth loss.
25

26. Cycle of oral hygiene in desquamative gingivitis.
26

27.  Patients with DG from PV were found to have significantly
poorer plaque scores, probing depth, and clinical
attachment levels compared to controls. (Thorat MS et al
2010)
 These parameters were associated with increased clinical
disease severity.
 These findings have also been demonstrated in patients
with DG from other causes, including OLP and MMP. (Lo
Russo L et al 2014, Ramon-Fluixa C et al 1999, Arduino
PG et al 2011, Schellinck AE et al 2009)
 Patients with DG have also been found to have higher
numbers of carious teeth than healthy controls, (Akman
A, et al 2008) increased bone loss, (Thorat MS et al 2010)
and increased tooth loss, (Arduino PG, et al 2011) with an
average of 8.5 missing teeth. (Lo Russo L et al 2010)
27

28.  Therefore, a proper examination of every patient with
DG should include a dental evaluation for dental
plaque, gingival recession (evidence of dental root
exposure), and tooth loss.
 Other long-term consequences from chronic DG
include decreased oral food intake as a result of pain
with mastication and bacterial and fungal overgrowth.
28

29. 29

30.  The differential diagnosis of
desquamative gingivitis (DG)
includes a wide spectrum,
such as chemical and
electrical burns, allergic
reactions, hormonal disorders
and mucocutaneous diseases.
 Furthermore, a similar clinical
pattern can be observed in
reactions developing against
mouthwashes, toothpastes,
chewing gums, cosmetic
products, drugs, cinnamon
and dental materials
(Richards A 2005).
Mucosal and gingival
desquamation developing
as a result of an allergic
reaction against toothpaste.
30

31.  It is suggested that the disease may be observed when
there is lack of estrogen or progesterone (Yih WY et al
2000).
 Additionally, there are idiopathic gingival
desquamative lesions without any etiologic factors
(Guiglia R, et al 2007).
31

32.  There are conflicting arguments on whether it is a
symptom of oral lichen planus, mucous membrane
pemphigoid, or a clinical manifestation of these
diseases (Robinson NA, Wray D 2003, Scully C,
Laskaris G 1998).
 The definitive diagnosis of desquamative gingivitis is
very difficult and complicated.
 Determination of the etiologic factors that cause the
lesions or making the diagnosis of the underlying
systemic disease can take a long time.
32

33.  Detailed history of the patient, systemic symptoms,
presence of similar lesions at other sites of the body,
medications used, contact with chemical materials
and the family history should be questioned (Guiglia
R et al 2007).
 If there is suspicion of allergy, a patch test against
dental materials can be performed on the patient
(Richards A. 2005).
 Several mucocutaneous diseases in which clinical
desquamative gingivitis is observed have been
reported in the literature.
33

34. 34

35. 35

36. ORAL LICHEN PLANUS (OLP)
 OLP is a chronic inflammatory disease of the mucosa
and the most common cause of DG.
 The overall prevalence is 0.5% to 2%, with an onset
typically between 30 and 60 years of age and a slight
female predominance. (Eisen D et al 2005, Scully C
et al 1998, Al-Hashimi I et al 2007)
 The pathogenesis is unknown, but increasing evidence
shows that it is likely a T cell-mediated disease that
causes tissue destruction by inducing apoptosis of
basal keratinocytes through Fas expression.
(Sugerman PB et al 2000)
36

37.  This aberrant response may be the result of a traumatic,
infectious, or medication trigger. (Alrashdan MS et al
2016)
 There are 6 clinical variants of OLP, including
1. Reticular (wickham striae),
2. Plaque-like,
3. Atrophic,
4. Erosive/ulcerative,
5. Papular, and
6. Bullous, although papular and bullous are rarely seen.
 OLP typically progresses through series of relapses and
remissions, but the erosive/ulcerative form is often
chronic and persistent.
37

38.  The most commonly affected sites
are the buccal mucosa, tongue,
gingiva, and labial mucosa;
involvement of the palate, floor of
the mouth, and upper lip are
uncommon. (Alrashdan MS et al
2016)
 Involvement of the gingiva alone
(presenting as DG) is seen in 10%
of patients. (Mignogna MD et al
2005, Scully C, Carrozzo M.
2008)
38

39.  Like cutaneous LP, OLP demonstrates the Koebner
phenomenon.
 Evaluation for a traumatic component to disease, such
as ill-fitting dental prostheses or sharp tooth cusps
that rub, should be performed.
 Exclusion of other causes of oral lichenoid lesions,
such as lichenoid contact dermatitis with amalgam or
dental metals, lichenoid drug reactions, or GVHD
should be performed in all patients.
 Finally, there is a 0.4% to 9% risk of malignant
transformation, most commonly seen in the erosive/
ulcerative form, that should be monitored for at each
visit, with a biopsy specimen obtained from any
unusual or changing erosive lesions. (Ismail SB et al
2007, Al-Hashimi I et al 2007)
39

40. Pemphigus Vulgaris
 PV is a chronic autoimmune
blistering disease characterized
clinically by the formation of
blisters and erosions on the
mucosa and skin, and
histologically by acantholysis.
 PV is associated with antibodies
directed against desmosomal
cadherins, impairing cellular
adhesion, and leading to
acantholysis, skin fragility,
blistering, and erosion.
40

41.  In mucosal dominant PV, the antibodies target desmoglein
3, which is integral to mucosal integrity, and in
mucocutaneous PV, patients also have antibodies targeting
desmoglein 1, expressed in high quantities in the skin of
the face, scalp, and upper trunk. (Ioannides D et al 1992)
 These antibodies are pathogenic and are markers of disease
activity. (Bystryn JC, Rudolph JL. 2005)
 The mean age of onset is 50 to 60 years of age, and it is
more common in those of Mediterranean or Jewish
ancestry. (Bystryn JC, Rudolph JL. 2005, Ioannides D
2008)
 Oral involvement is usually the presenting manifestation of
PV and often precedes skin manifestations by several
months.
41

42.  Typically, ragged erosions and
painful ulcerations are noted
along the buccal and labial
mucosa, followed by the palate
and tongue.
 These erosions arise from
otherwise healthy-appearing
mucosa, without surrounding
erythema or edema. Bullae are
infrequently seen, as they are
prone to rupture, but the
Nikolsky sign can be elicited
adjacent to an active lesion.
42

43.  The ulcerations are persistent and do not
spontaneously heal.
 Nasal and laryngeal mucosal
involvement can also occur, presenting
as nasal congestion, epistaxis,
odynophagia, and hoarseness.
 ≤49% of patients had symptoms of
laryngeal or nasal involvement. (Hale
EK, Bystryn JC et al 2001)
 Other mucosal sites that can be involved
include the conjunctiva, vulva, cervix,
urethra, and rectal mucosa, but these
sites are rarer. (Ioannides D et al 2008)
43

44.  Skin involvement typically
occurs on the scalp, face, and
upper trunk, and is rare on the
legs (Ioannides D et al 1992).
 It presents with flaccid bullae
and erosions on normal or
slightly erythematous skin
that heal without scarring but
leave residual
hyperpigmentation.
44

45.  Left untreated, PV has a high mortality rate because of
skin loss, oropharyngeal ulcerations, nutritional
deficiency, inanition, and secondary infection.
 With the institution of effective therapy, the mortality
rate has decreased to much less than 5% to 10%.
(Bystryn JC et al 2005)
45

46. Mucous Membrane Pemphigoid
(MMP)
 It is also referred to as cicatricial pemphigoid, oral
pemphigoid, and ocular pemphigoid, is a disease
phenotype encompassing several autoimmune bullous
diseases characterized by subepithelial blisters and
erosions with scarring of mucous membranes, skin or
both, and linear deposition of immunoglobulin G,
immunoglobulin A, or complement component 3
along the epithelial basement membrane zone on
direct immunofluorescence.
46

47.  Various subgroups have been described, including
antiepiligrin MMP, which is associated with
malignancy; a purely ocular variant, associated with
antibodies to alfa-6, beta-4 integrin; mucosal and
skin variant with antibodies targeting bullous
pemphigoid antigen 2 (Chan LS et al 1993); a purely
oral variant, which tends to follow a more benign
course (Mobini N et al 1998); and finally, a
heterogeneous group with involvement of several
mucosal surfaces without skin involvement.
47

48.  The overall incidence is low, between 1 in 12,000 and 1
in 20,000 individuals, and it typically presents in older
patients between 60 and 80 years of age. (Mondino
BJ, Brown SI. 1981, Jolliffe DS, Sim-Davis D. 1977,
Rosenbaum MM et al 1984)
 The oral mucosa is the most commonly involved site in
mucous membrane pemphigoid, affecting 85% of
patients, followed by conjunctiva (64%) and the skin
(24%). (Ahmed AR, Hombal SM. 1986)
 The most commonly affected site of the oral mucosa is
the gingiva, followed by the buccal mucosa and palate,
and the most frequent presentation is of DG.
(Laskaris G et al 1982, Nguyen QD, Foster CS. 1996)
48

49.  Oral involvement typically presents as erythematous
patches that progress to bullae, erosions, and
pseudomembranous lesions.
 Healing occurs slowly and often overt scarring in the
oral mucosa is not obvious, though it can heal with
reticulated white plaques resembling Wickham striae.
(Chan LS et al 2002)
49

50.  Involvement of the oral mucosa alone, or with skin
involvement only, which is typically confined to the
head and upper trunk, is associated with a better
prognosis and a better response to treatment.
 In contrast, involvement of other mucosal sites, such
as ocular, genital, nasopharyngeal, esophageal, and
laryngeal sites, are associated with a poorer prognosis,
because scarring leads to greater loss of function.
50

51. Paraneoplastic Pemphigoid (PNP)
 PNP, also referred to as paraneoplastic autoimmune
multiorgan syndrome, is a condition characterized by
severe stomatitis alone or in conjunction with
erosions and bullae of the skin in the setting of a
known or occult tumor or malignancy.
 The neoplasms most commonly associated are non-
Hodgkin’s lymphoma (42%), chronic lymphocytic
leukemia (29%), and Castleman disease (10%). (Porro
AM et al 2014)
51

52.  It is associated with several autoantibodies targeting
both epidermal and dermoepidermal junction
proteins, including desmoplakin I, desmoplakin II,
envoplakin, periplakin, alfa-2-macroglobulin-like-1
protein, desmoglein 1, desmoglein 3, plectin, and
bullous pemphigoid antigen 1. (Schepens I et al 2010)
 Therefore, it presents with features of both pemphigus
(flaccid bullae and erosions) and pemphigoid (tense
bullae).
 It is also associated with a robust inflammatory tissue
response, producing analogous inflammatory lesions.
52

53.  PNP is a rare form of pemphigus,
seen most commonly in men 45 to
70 years of age. (Kimyai-Asadi A, Jih
MH. 2001)
 PNP most often presents with severe,
painful mucosal erosions, with
preferential involvement of the
tongue and intractable stomatitis
(Kaplan I et al 2004)
 In contrast to PV, where unaffected
mucosa appears healthy, in PNP the
entire oral mucosa is involved with
erythema, edema, vesicles, erosions,
and ulcerations. (Czernik A et al
2011)
53

54.  Widespread mucosal involvement is common in PNP,
including involvement of the esophagus, stomach,
duodenum, and colon. (Wakahara M et al 2005)
 Desquamation of bronchial mucosa leads to
bronchiolitis obliterans and subsequent respiratory
failure, a cause of death in patients with PNP.
(Nousari HC et al 1999)
 Cutaneous lesions are polymorphic, presenting as
vesicles, bullae, and targetoid patches and plaques,
often on acral sites. In the past, patients may have
been misdiagnosed with SJS.
54

55.  The diagnostic criteria include the presence of severe
stomatitis, with preferential involvement of the
tongue, suggestive histopathologic features and
immunofluorescence pattern, and association with an
underlying lymphoproliferative disorder. (Anhalt GJ.
2004)
 Overall, treatment is poor with a mortality rate of 68%
in 1 study. (Leger S et al 2012)
55

56. ERYTHEMA MULTIFORME (EM)
 It is a mucocutaneous hypersensitivity reaction that
presents with skin or mucosal lesions.
 It is divided into EM minor and major, depending on
the absence or presence of mucosal involvement,
respectively, and mucosal involvement can occur alone.
EM Major EM Minor 56

57.  The episodes can be self-limited, typically lasting 2 to
6 weeks, or recurrent, classified as recurrent EM.
(Sokumbi O, Wetter DA. 2012)
 Patients with recurrent EM often have an average of 6
episodes per year, with a mean disease duration of 6 to
10 years. (Wetter DA, Davis MD. 2010, Schofield JK
et al 1993)
 The incidence of EM is <1%, and EM occurs more
commonly in young adults. (Huff JC et al 1983,
Weston WL 2005)
 EM is no longer considered on the spectrum of
SJS/TEN because the former has classic target lesions
and involvement of fewer mucosal sites with fewer
systemic signs and symptoms.
57

58.  Stevense Johnson syndrome (SJS) / Toxic epidermal
necrolysis (TEN) is characterized by atypical targetoid
lesions and areas that range in extent with Nikolsky
sign positive cutaneous erosions.
 Target lesions of EM and targetoid lesions of SJS both
feature identical findings of apoptosis at the
dermoepidermal junction histopathologically.
 In contradistinction to SJS/TEN, which is
predominantly caused by medications, EM is
medication-induced in <10% of patients, and is often
caused by infectious etiologies, the most common
being herpes simplex virus, especially in recurrent EM.
(Huff JC et al 1983)
58

59.  Mucosal manifestations are common, and have been reported
in 25% to 70% of patients with EM. (Wetter DA, Davis MD.
2010, Schofield JK et al 1993, Huff JC et al 1983)
 The oral mucosa is most commonly involved. Lesions begin as
areas of erythema with edema that progress to erythematous
plaques and bullous and erosive lesions with pseudomembrane
formation.
 The labial mucosa, buccal mucosa, nonattached gingivae, and
vermilion lip are most commonly affected. (Wetter DA, Davis
MD. 2010, Schofield JK et al 1993)
59

60.  Other mucosal surfaces can be
involved, including ocular, nasal,
pharyngeal, laryngeal, and
anogenital. (Ayangco L, Rogers
RS 2003)
 These lesions can progress to
scarring from secondary trauma or
infection, producing significant
morbidity.
Erythema multiforme major.
Targetoid lesions on
the palms.
60

61.  Mucosal involvement often occurs in conjunction with
skin involvement, which may provide a clue to the
diagnosis when typical and atypical targetoid lesions
are found, often in an acral distribution.
 Mucosal involvement in isolation can make the
diagnosis more challenging. (Wetter DA, Davis MD.
2010)
 Prodromal symptoms can aid in the diagnosis, because
these are often seen with EM major and always with
SJS/TEN.
61

62. Complex aphthosis/Behcet
disease.
 Oral aphthosis is a common condition that occurs on
nonkeratinized mucosa. The individual ulcers are
categorized as minor, major, or herpetiform. (Letsinger JA
et al 2005)
 Minor aphthae are the most common (Approx. 80%), are
small (<10 mm), are commonly on the buccal and labial
mucosa, nonattached gingivae, and heal without scarring.
62

63.  Major aphthae are larger (>10
mm), deeper, are located on
additional mucosal sites, such as
the soft palate, tonsils, and
pharynx, and heal with scarring.
 Herpetiform aphthae are
grouped and smaller (1-3 mm) and
may occur on keratinized surfaces.
 Aphthae often recur, termed
recurrent aphthous stomatitis,
which is the most common oral
inflammatory disorder. (Rogers
RS 1997)
63

64.  The disease often develops during adolescence or young
adulthood, and improves with time, with development of
fewer and milder outbreaks. (Hutton KP, Rogers RS 1987)
 Recurrent aphthous stomatitis can further be divided
into simple or complex, where complex is defined by the
almost constant presence of multiple (≥3) oral ulcers or
recurrent oral and genital aphthae and the exclusion of
Behcet disease. (Letsinger JA et al 2005)
 Complex aphthosis may be primary or caused by an
underlying disease, including inflammatory bowel disease,
HIV, vitamin deficiencies, or cyclic neutropenia, and these
must be excluded. (McCarty MA et al 2003)
 The aphthae often precede the confirmation of other
systemic features in those with secondary aphthosis.
64

65.  Behcet disease is another important diagnosis to exclude
because it is a chronic, multisystem disease that not only
manifests with recurrent oral and genital aphthae, but
patients may have ocular, vascular, articular,
gastrointestinal, neurologic, and cardiopulmonary
involvement, with significant morbidity and mortality.
(Gurler A et al 1997)
 Behcet disease presents most commonly in young adults, in
the third to fourth decades of life, and oral aphthae are
often the only manifestation for 6 to 7 years before another
symptom presents. (Gurler A et al 1997)
 Systemic manifestations and disease confirmation using
international criteria usually follow a significant increase in
aphthosis in 1 to 2 years.
65

66.  Clinically, aphthae present as sharply
demarcated round or oval ulcers,
often with a pseudomembranous
base, on the buccal and labial
mucosa, sulci, lateral and ventral
surfaces of the tongue, soft palate,
and oropharynx. (Hutton KP,
Rogers RS 1987)
 The aphthae in primary and
secondary aphthosis, as well as in
patients with Behcet disease, are
indistinguishable, and minor
aphthae are the most common
presentation in patients with Behcet
disease.
66

67.  Exclusion of underlying causes is recommended for all
patients with complex aphthosis with herpes simplex
virus culture or polymerase chain reaction studies, a
complete blood cell count, vitamin B12, iron, folate,
urinalysis, human leukocyte antigen-B27, and
considerations of referral to ophthalmology,
gastroenterology, neurology, and rheumatology when
indicated. (Ghate JV, Jorizzo JL. 1999)
67

68. Graft-versus-host Disease
 GVHD is a multiorgan disease occurring most commonly
in patients who have undergone allogeneic stem cell
transplantation.
 Oral involvement is a frequent manifestation of GVHD,
occurring in 33% to 75% of patients with acute GVHD, and
≤ 80% of patients with chronic GVHD. (Imanguli MM et
al 2008)
 Acute GVHD is characterized by cutaneous,
gastrointestinal, and hepatic dysfunction, and typically
occurs within the first 100 days of transplantation
(Alrashdan MS et al 2016). In acute GVHD, the oral
involvement typically occurs in patients with more severe,
erosive cutaneous disease as an extension from adjacent
skin. (Ziemer M. 2013)
68

69.  Chronic GVHD, on the other hand, can affect
multiple organ systems and has overlapping features
with autoimmune disease. It typically occurs after 100
days of transplantation, but can occur any time after
transplant. In chronic GVHD, the oral lesions typically
present similar to oral lichen planus, with white,
reticulated, sometimes eroded plaques involving the
buccal mucosa, gingiva, and lips.
 Other mucosal involvement is common, including
genital and ocular involvement, and should be
screened for in these patients.
69

70. Plasma Cell Gingivitis
 Plasma cell gingivitis is a rare condition characterized by
diffuse and massive infiltration of plasma cells into the sub-
epithelial gingival tissue. (Macleod RI, Ellis JE. 1989)
 Clinically, the illness presents as a diffuse reddening
together with edematous swelling of the gingiva, with
sharp demarcation along the mucogingival border.
 The etiology of PCG is not clear, but due to the obvious
presence of plasma cells many authors suggest that it is an
immunological reaction to allergens; these latter may occur
in toothpaste, chewing gum, mint pastels and certain food.
(Poswillo D. 1968)
70

71.  It has been suggested that strong spices and some
herbs such as chilli, pepper, clove and cardamom may
be important factors. (Poswillo D. 1968)
 Kerr et al. reported a case of PCG in 1971 resulting from
an allergic reaction to one of the flavoring agents
cinnamon in chewing gums. Flavoring agents such as
cinnamonaldehyde and cinnamon in chewing gums
and dentifrices were also shown as etiologic factors in
the development of PCG. (Lamey PJ et al 1990)
71

72.  Flavoring agents added to chewing gum and
dentifrices can produce an inflammatory reaction of
both attached and free gingiva. The inflammatory
reaction is characterized by intense hyperemic and
erythematous changes. It is common for the patient to
complain of “bleeding from mouth.” (Marker P,
Krogdahl A. 2002)
 Some authors sub-divide PCG into three types: (1)
Caused by an allergen, (2) neoplastic, (3) unknown
cause.
72

73. Presented By:-
Dr. Faheem Ahmed
MDS 2nd Year

74. CONTENTS
 Introduction
 History
 Definition
 Etiology
 Prevalence
 Classification
 Clinical Presentation
 Differential Diagnosis
 Oral Lichen Planus
 Pemphigus Vulgaris
 Mucous Membrane
Pemphigoid
 Paraneoplastic Pemphigoid
 Erythema Multiforme
 Complex Aphthosis
 Graft Versus Host Disease
 Plasma Cell Gingivitis
 Foreign Body Gingivitis
 Diagnosis
 Treatment
 Prognosis
 Conclusion
 References
74

75. Foreign body gingivitis (FBG)
 It is a rare, chronic inflammatory
disease characterized by an immune
mediated reaction against embedded
foreign organic or inorganic dental
restorative materials.
 Clinically, FBG is characterized by
gingival erythema or erosions within
the interdental papillae and free
gingival margin that develop months
to years after abrasive microtrauma
from dental restoration or dental
prophylaxis. (Gordon S. 2000)
75

76.  FBG is an unusual, likely underreported condition in
the literature with approximately 150 cases to date.
 In 1990, Daley and Wysocki first coined the term
FBG to describe a cohort of patients with refractory
gingival disease and histopathologic features of
granulomatous gingivitis coupled with deposition of
foreign particles in the lamina propria. The authors
later documented FBG in 0.3% of 19,534 oral biopsies
at a Canadian university-based tertiary referral center
in a 6-year interval.
76

77.  At the time, they acknowledged that FBG was
unrecognized, so an incidence of 0.3% may
alternatively be interpreted as the minimum incidence
of FBG. According to prior studies, women (68%-84%)
are more frequently affected than men (16%-32%),
with a mean age of 48 years, which is similar to the
demographics of patients with desquamative
gingivitis, particularly lichen planus. (Eisen D. 2002,
Rogers RS et al 1982, Sklavounou A, Laskaris G.
1983)
77

78.  The etiopathogenesis of FBG is not well understood.
The leading hypothesis is an association with
compromised gingival epithelium, which permits
introduction of foreign bodies as a nidus for chronic
inflammation in and around the gingival sulcus.
(Gordon S. 2000)
 Risk is perhaps highest in patients who have
predisposition for mucosal ulceration and chronic
inflammation at the gingival sulcus, such as those with
oral lichen planus (OLP), mucous membrane
pemphigoid, or chronic periodontal disease.
78

79.  Granulomatous inflammation is seen in only 50% of
FBG cases. (Gordon SC, Daley TD. 1997)
Consequently, FBG may be misdiagnosed as one of
several heterogeneous mucocutaneous conditions. In
particular, FBG most closely mimics the clinical and
histopathologic features of OLP.
 FBG and OLP have many similarities with subtle
differences that enable separation. The clinical
distribution of OLP is symmetrical, and lesions may
migrate with disease progression, whereas FBG is
typified by fixed lesions within the marginal or
interdental gingiva.
79

80. DIAGNOSIS
 Diagnosis of DG-associated disease begins with a
detailed history of the presenting complaint, review of
past and current medical history, followed by clinical
examination.
 Differentiation of the cause is essential as many will
share a similar clinical presentation, but often have
different management and prognosis.
80

81. Algorithm for the approach to the patient with desquamative gingivitis.
81

82. Medical history and history of
complaint
 An appropriate medical history should consider the
patient’s systemic disease history and current
therapies.
 This will be of importance in identifying potential
conditions which may associate with DG.
 A history of any extra-oral skin lesions or eye problems
is also important to note. This may include any
investigation/therapy the patient is undergoing with
other relevant specialties, including dermatologists,
ophthalmologists, gynaecologists: and ear, nose and
throat specialists.
82

83.  Lesions associated with OLP may be asymptomatic at
initial presentation and the patient may not even be
aware of their existence.
 Those presenting as full desquamative lesions can have
symptoms that range from mild discomfort on
toothbrushing or eating certain foods (spicy or acidic
foods in particular), to more significant pain which
impacts on the patient’s quality of life.
 A history of blistering or ulceration is important to
note as this may be suggestive of vesiculobullous
conditions.
 The onset and progression of lesions should be
carefully investigated. Some conditions can present
acutely where others can be more progressive.
83

84.  The history of day or weeks preceding the outbreak of
lesions may help identify potential triggering factors
such as drugs or infections.
 A history of what products patients utilize as part of
their self performed oral hygiene regimen is also
important to note. Sodium lauryl sulphate is a widely-
used detergent added to many dental hygiene
products. For some patients, its use has been
associated with mucosal irritation. (Herlofson BB,
Barkvoll P. 1996)
84

85. Clinical examination
 The purpose of the clinical examination is to look for oral
lesions with a specific appearance that can assist in
diagnosing different DG-associated Disorders.
 OLP lesions tend to present with very characteristic
features. They generally involve multiple oral sites and have
a keratotic papular or reticular form.
Characteristic appearance of
oral lichen planus.
Desquamative gingivitis as a manifestation
of oral lichen planus. Characteristic white
striae of lichen planus at the periphery, and
sparing of the interdental papillae. 85

86.  When a desquamative type lesion associated with OLP is
present in the attached gingivae, it may be difficult to
differentiate from other forms of DG, but often there is a
keratotic lesion at the margin or interspersed within the
desquamative area which can support a provisional
diagnosis.
 A careful note should also be made of the position of
dental restorative materials and their approximation to
lesions.
86

87.  Some restorative materials (amalgam, composites,
nickel and cobalt) have been reported to induce
lichenoid type reactions.
 Lesions are similar to OLP lesions in presentation, but
may resolve when the dental material is replaced with
an alternative. Patch testing may be of use in some of
these patients to identify hypersensitivity reaction.
(Gawkrodger DJ. 2005)
 MMP and PV lesions may present with widespread
erythema and blister formation, with subsequent
breakdown leading to areas of ulceration.
87

88. Definitive diagnosis
 It include indirect immunofluorescence on a blood
sample, and examination of a tissue sample using H&E
staining and direct immunofluorescence.
 Histological changes of diseases associated with DG
generally involve both the epithelium and underlying
connective tissue.
 Changes observed in OLP are usually in the form of
epithelial thickness, including reduction (erosive
forms of OLP) and increases (hyperkeratosis of OLP).
88

89.  Antibody mediated diseases such as MMP and PV are
characterized by blister formation:
subepithelial for MMP and Intraepithelial for PV
89

90.  In addition to histopathological assessment,
pathologic immunoreactants present in DG-associated
diseases can be investigated with immunofluorescence
studies.
Direct immunofluorescence of mucous
membrane pemphigoid lesion shows
characteristic linear deposition of IgG in
the basement membrane zone.
Direct immunofluorescence of pemphigus
vulgaris lesion shows characteristic
intercellular deposition of IgG (‘chicken-wire’
pattern). (Prof. PJ Lamey).
90

91.  The types of immunoreactants include various
immunoglobulin classes (IgG, IgM and IgA),
complement cascade factors, fibrinogen and fibrin,
and immune complexes. (Lo Russo L 2008)
 Immunofluorescence studies are of particular use in
helping to diagnose DG-associated disease accurately,
especially when typical features are not present in
histopathological analysis.
91

92. 92

93.  Management generally involve a thorough history and
examination.
 The low incidence rates of some of the diseases associated
with the development of DG mean that their presentation
in general practice may be quite rare.
 Nonetheless, as an oral complaint, patients will likely seek
dental advice as their first point of contact. Therefore, an
understanding of potential conditions that are causing
their symptoms, as well as some general measures which
may help improve their condition, are important.
93

94. General measures
 Triggering factors such as drugs, local irritants such as
spicy foods and overly aggressive toothbrushing habits
should be discontinued.
 Topical analgesics, such as benzydamine
hydrochloride 0.15% (rinse or spray), are useful to
relieve pain and discomfort, particularly prior to eating
or toothbrushing.
94

95.  An outline of practical steps and advice that can be
offered to patients is displayed in Table 1.
95

96.  Dental plaque is an important aggravating factor to
whatever is the underlying cause, so initial management in
these cases should be centred on optimizing plaque control
while reducing any associated inflammation through non-
surgical periodontal therapy.
 A recent study aimed to examine the effect of a structured
plaque control intervention on clinical and patient-centred
outcomes for patients with gingival manifestations of oral
lichen planus. (Stone SJ et al 2015)
 Eighty-two patients with a diagnosis of OLP with gingival
involvement (confirmed by biopsy and histopathological
analysis) were divided into two groups: intervention and
control.
96

97.  The intervention was structured plaque control
comprising powered toothbrushing and inter-dental
cleaning advice.
 Control subjects continued with their normal dental
plaque control regimen.
 The mean plaque index scores reduced for the intervention
group by 39.5% at the 20-week follow-up, compared to a
marginal improvement of 4.1% in the control group
(p<0.001).
 Corresponding improvements were observed using
mucosal disease indices at both 4- and 20-week follow-up
(p<0.001).
 The authors concluded that a structured plaque control
intervention was effective in improving the oral health-
related quality of life and clinically observed gingival
lesions.
 This study highlights that intensive plaque control should
be an important initial phase of treatment.
97

98. Specific therapies
 Specialist management will be specific to the diagnosis
established and may involve a multidisciplinary
approach, especially when there is extra-oral
involvement.
 Depending on the definitive diagnosis, treatment of
the disease associated with DG is aimed at controlling
lesions along with symptoms, and preventing further
disease progression.
98

99. Oral lichen planus (OLP)
 In symptomatic lesions, topical corticosteroids are the drug
of choice.
 Topical corticosteroids are available in different strengths
and preparations and provide an anti-inflammatory and
immunosuppressant effect.
 Ointments such as fluticasone mixed with Orabase® are
suitable for the management of small isolated accessible
lesions such as the buccal mucosa, tongue, gingiva or
palate. Application is normally 3−4 times daily.
99

100.  Where multiple lesions exist, corticosteroid
mouthrinses, utilizing betamethasone 500 mcg
soluble tablets or fluticasone 400 mcg nasules can be
very effective.
 The use of vacuum-formed steroid carrier trays have
also been advocated as a way of extending drug
permanence onto oral lesions. (Gonzalez-Moles MA
et al 2003)
 It is important that the use of such custom trays do not
themselves cause trauma or irritation to the gingivae.
 Patients should be informed about possible adverse
side-effects of using topical corticosteroid
preparations; the most common being secondary
candidiasis.
100

101.  Antifungals such as miconazole gel and/or
chlorhexidine mouthwash may be useful in
preventing secondary candidiasis.
 Other drug treatments which further ‘dampen down’
the immune system can be added so that the dose of
corticosteroid can be reduced as soon as possible.
These include azathioprine and mycophenolate
mofetil.
 In those individuals who are steroid unresponsive,
topical calcineurin inhibitors, such as tacrolimus or
pimecrolimus, are important treatment options for
patients. (Shichinohe R et al 2006)
 Side-effects, including transient burning or stinging
at the site of application, have been reported.
101

102. Mucous membrane pemphigoid
(MMP)
 Therapy for oral MMP may similarly involve high
potency topical corticosteroids.
 However, systemic corticosteroids are generally the
first line treatment for patients with severe progressive
mucosal lesions associated with immune-mediated
diseases.
 Systemic corticosteroids may be useful for short term
(2−3 week) treatment to achieve improvement in DG
lesions, with treatments being further supplemented
with, or followed by, topical agents.
102

103.  Potential side effects of systemic steroid treatment
need to be considered which includes adrenal
suppression, hypertension, blurred vision, elevated
blood glucose, and GI haemorrhage.
 Secondary systemic immunosuppressants, such as
azathioprine and mycophenolate mofetil, may
again be required depending on the severity and
duration of lesions.
 Dapsone has been successfully used in MMP patients
with both oral and ocular lesions. (Sacher C,
Hunzelmann N 2005)
 Side-effects to consider include anaemia, shortness of
breath and tiredness.
103

104. Pemphigus vulgaris (PV)
 With the risk of mortality in PV, moderate to high
doses of systemic corticosteroids are the mainstay of
treatment.
 Other immunosuppressant drugs may again be
additionally required.
 Intravenous immunoglobulins have previously been
successfully used in cases of steroid resistant PV. (Yeh
SW et al 2005)
104

105. Conclusion
 Desquamative gingivitis can be the clinical symptom
of some dermatitis and mucocutaneous diseases and
the underlying primary cause should be evaluated
meticulously.
 Taking detailed patient history, performing a careful
intraoral examination and determining the presence or
absence of similar lesions at other sites of the body are
the most important steps in clinical practice.
105

106.  Definitive diagnosis of DG should be made by
incisional biopsy, histopathological examination and
DIF.
 Gingival lesions are controlled by improving oral
hygiene and the use of topical corticosteroids.
 If there is an underlying systemic disease, the case
should be consulted with the physician.
106

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