Desquamative Gingivitis

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Chapter 1
Desquamative Gingivitis
Hiroyasu Endo, Terry D. Rees, Hideo Niwa,
Kayo Kuyama, Morio Iijima, Ryuuichi Imamura,
Takao Kato, Kenji Doi, Hirotsugu Yamamoto and
Takanori Ito
Additional information is available at the end of the chapter
http://dx.doi.org/10.5772/intechopen.69268
Provisional chapter
© 2016 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons
Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution,
and reproduction in any medium, provided the original work is properly cited.
DOI: 10.5772/intechopen.69268
Desquamative Gingivitis
Hiroyasu Endo, Terry D. Rees, Hideo Niwa,
Kayo Kuyama, Morio Iijima, Ryuuichi
Imamura, Takao Kato, Kenji Doi, Hirotsugu
Yamamoto and Takanori Ito
Additional information is available at the end of the chapter
Abstract
Desquamative gingivitis (DG) is characterized by erythematous, epithelial desquama‐
tion, erosion of the gingival epithelium, and blister formation on the gingiva. DG is a
clinical feature of a variety of diseases or disorders. Most cases of DG are associated
with mucocutaneous diseases, the most common ones being lichen planus, mucous
membrane pemphigoid, and pemphigus vulgaris. Proper diagnosis of the underlying
cause is important because the prognosis varies, depending on the disease. This chapter
presents the underlying etiology that is most commonly associated with DG. The current
literature on the diagnostic and management modalities of patients with DG is reviewed.
Keywords: gingival diseases/pemphigus/pemphigoid, benign mucous membrane/lichen
planus, oral/hypersensitivity/autoimmune diseases
1. Introduction
Manifestations of desquamative gingivitis (DG) include erythematous gingiva, epithelial des‐
quamation, and erosion of the gingival epithelium, as well as blister formation on the gingiva
[1, 2] (Figure 1). The DG lesions may be localized or generalized and may extend into the
alveolar mucosa. Similar lesions are often found on the buccal mucosa, tongue, and palate
in the oral cavity. The signs of DG are clearly dierent from those of dental plaque‐induced
gingivitis. Patients having DG may be asymptomatic or symptomatic [3]. Most symptomatic
patients complain of mild or moderate oral discomfort, gingival soreness, or a burning sensa‐
tion [4, 5]. DG occurs more often in females than males; approximately 80% of the patients
are female [4–8]. Most patients with DG are middle‐aged and older, although rare cases have
© 2017 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons
Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use,
distribution, and reproduction in any medium, provided the original work is properly cited.

been observed in children [4, 6, 8, 9]. Early investigators believed that there was a single
etiology for DG. However, it is apparent that the condition is a nonspecic manifestation of
several diseases or disorders and therefore has multiple etiologies [1, 2]. Most cases of DG are
associated with mucocutaneous diseases, the most common ones being lichen planus (LP),
mucous membrane pemphigoid (MMP), and pemphigus vulgaris (PV) [1, 2, 4–8, 10, 11]. A
variety of other potential causes, such as lupus erythematosus [12], mixed connective tissue
disease [5, 10], graft versus host disease [13], erythema multiforme [14], epidermolysis bullosa
[15, 16], epidermolysis bullosa acquisita [17], Kindler syndrome [18], chronic ulcerative sto‐
matitis [10, 19, 20], lichen planus pemphigoides [21, 22], plasmacytosis [23], plasma cell gingi‐
vitis [24], orofacial granulomatosis [25, 26], foreign body granulomas [27], candidal infection
[28], and linear IgA disease [29, 30], may cause DG lesions. Factitious injury of the gingiva
may also present with clinical features consistent with DG [31–34], which was suggestive of
mucocutaneous diseases including MMP [32, 33] or PV [34]. Contact stomatitis due to den‐
tal hygiene products, dental materials, or food avorings and preservatives may mimic DG
[1, 11, 25, 35–39], while several systemic disorders, including Crohn’s disease [40], psoriasis
[41–43], sarcoidosis [44], and adverse drug reactions [38, 45], may possess some but usually
not all of the clinical features of DG.
2. Diagnosis
It is very important to accurately diagnose diseases or disorders causing DG because the
prognosis varies widely, depending on the cause. Although PV rarely occurs, it is a poten‐
tially life‐threatening disease, so it is important to diagnose and treat it in its early stages.
Airway obstruction due to laryngeal scarring and blindness due to conjunctival scarring
Figure 1. Desquamative lesions on the aached gingiva. Gentle palpation with the periodontal probe elicited some
desquamation of the gingival surface (positive Nikolsky’s sign).
Insights into Various Aspects of Oral Health4

would certainly deteriorate the quality of life for MMP patients. Early recognition and treat‐
ment of the lesions can prevent serious complications. Histopathological examination and
direct immunouorescence (DIF) testing of biopsied tissues are often required to deter‐
mine the underlying etiology of DG [6–8, 10]. For histopathological study, the biopsy site
should be selected from an area of intact epithelium and include perilesional tissue. This
may require two separate biopsies, one lesional and one non‐lesional. The perilesional tissue
or non‐lesional biopsy site should show a nonspecic inammatory response in suspected
non‐autoimmune disorders such as LP, erythema multiforme, foreign body gingivitis, facti‐
tious disorder, and contact stomatitis [1, 7, 10]. In contrast, the DIF test should be performed
on normal‐ appearing tissue rather than perilesional sites in suspected autoimmune diseases
such as MMP, PV, and chronic ulcerative stomatitis [1, 7, 10, 46, 47]. Since immune deposits
in autoimmune bullous disease are present in all oral tissue, a positive result from DIF tests
may be obtained from biopsies taken from distant normal mucosa [46]. The DIF test is consid‐
ered to be the best diagnostic evidence for MMP, PV, chronic ulcerative stomatitis, and other
autoimmune disorders; therefore, DIF testing is often essential in obtaining a nal diagnosis
since clinical features may be so similar [6–8, 10, 47, 48]. On the other hand, DIF ndings are
supportive but not diagnostic for LP, psoriasis, lupus erythematosus, and mixed connective
tissue disease because the DIF features of these diseases can also be found in other condi‐
tions [6, 10, 48]. A negative result from DIF tests should be anticipated in biopsies of contact
stomatitis [1].
Biopsy sites appearing to have an intact epithelial surface should be selected. If lesions are
present at several mucosal sites, including the gingiva, it is usually best not to use the gingiva
for the biopsy [1, 49, 50]. However, in approximately half of DG cases, the gingiva was the
only site of involvement [50, 51]. In these cases, the gingiva should be selected for the biopsy.
Rees and Burkhart [1] described the six steps to be considered when a gingival biopsy is
required in DG patients. They highlight the importance of careful site selection for gingival
biopsies in order to obtain diagnostic tissue samples. An inadequate surgical site selection
may easily lead to the loss of the gingival epithelium, since the biopsied gingival tissue is thin
and tends to be fragile. The stab‐and‐roll biopsy technique is a procedure specially designed
to prevent the epithelium from being removed from the biopsy specimen [1, 46, 52]. This
biopsy technique prevents the occurrence of lateral shear forces. The operator applies gentle
pressure on the gingiva with the tip of a #15 blade until the bone surface is reached and then
the blade is rolled from the tip along the entire cuing edge. If a larger specimen is needed,
the tip of the blade can be repositioned and the rolling stroke extended. The gingival epithe‐
lium was well maintained, and the relationship with the underlying connective tissue was
diagnostic from the gingiva of DG patients using the stab‐and‐roll biopsy technique [1, 46, 52].
3. Oral mucosal diseases or disorders that are associated with DG
3.1. Lichen planus (LP)
LP is a relatively common, T‐cell‐mediated chronic inammatory disease of unknown etiology. LP
commonly occurs in middle‐aged and older people, and women are aected more frequently
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than men [53, 54]. The lesions are found in multiple regions including the skin, genitalia, or
oral mucosa, although they are conned to the gingiva alone in some cases [53–56] (Figures 2
and 3). In many instances, atrophic, ulcerative, and bullous forms are combined as erosive LP.
The reticular, popular, and plaque‐like forms of LP are often asymptomatic, whereas erosive
forms may be quite painful when a patient is eating spicy foods or performing oral hygiene
procedures [53–55, 57] (Figures 4–6). For these reasons, erosive LP usually requires treat‐
ment. Histopathologically, specimens may demonstrate hyperortho‐ or hyperparakeratosis,
degenerative changes to the basal cells, and band‐like subepithelial inltrate composed of
lymphocytes [11] (Figure 7). When available, DIF testing is also valuable in establishing the
diagnosis, although DIF ndings are only suggestive, rather than diagnostic, of LP [6, 10, 48,
58]. Characteristic DIF ndings in oral LP include a linear paern of anti‐brin or anti‐brino‐
gen in the basement membrane zone and, to a lesser degree, the presence of IgM or IgG depos‐
its in cytoid bodies [6, 10, 48, 58] (Figure 8).
3.2. Mucous membrane pemphigoid (MMP)
MMP is an autoimmune, subepithelial blistering disease that aects mucous membranes.
Most patients with MMP are between 60 and 80 years of age [59–61]. However, on relatively
rare occasions, MMP has been reported in children [9]. Women are aected nearly two times
more frequently than men [59–61]. MMP can involve any oral mucosal site, although the
gingiva is aected far more often than other oral tissues [52, 59–62] (Figures 9–13). In more
than half of early developing cases, the gingiva is the only site of lesions [61, 63]. Extraoral
areas including the conjunctiva, skin, pharynx, nose, larynx, genitalia, anus, and esophagus
may also be aected [52, 62, 64, 65]. Scarring of the mucous membranes is often considered
the clinical hallmark of MMP, although scarring is rarely a feature of oral MMP [52, 64, 65].
Figure 2. Desquamative gingivitis associated with oral lichen planus. Erythematous lesions on the aached gingiva.
Insights into Various Aspects of Oral Health6

Multiple target antigens of MMP were identied in cell‐to‐basement membrane adhesion
components by the presence of circulating autoantibodies in the patients’ serum. These
antigens include bullous pemphigoid antigens (BP180 and BP230), α6 β4 integrin, type VII
collagen, and laminin 332 [62, 63, 66, 67]. The loss of cell‐to‐basement membrane adhesion
Figure 3. Desquamative gingivitis associated with oral lichen planus. Patchy erythematous lesion was found on the
palatal mucosa.
Figure 4. Desquamative gingivitis associated with oral lichen planus. Reticular lesions of buccal mucosa in addition to
gingiva.
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caused by these antibodies may result in subepithelial blistering. Histopathologically, MMP
is characterized by subepithelial bulla formation [11] (Figure 14). During DIF testing, the lin‐
ear deposition of complement component C3, IgG, or other immunoglobulin is observed in a
linear paern along the basement membrane zone [48, 62] (Figure 15).
Figure 6. Oral lichen planus patient. The examination revealed diuse erythematous lesions on the gingiva (A and B).
Lesions were also found on the buccal mucosa (C) and tongue (D).
Figure 5. Extraoral lesion associated with oral lichen planus. The reticular lesion was observed on the lip.
Insights into Various Aspects of Oral Health8

3.3. Pemphigus vulgaris (PV)
PV is an autoimmune blistering disease characterized by acantholysis in the epithelium.
Most patients with PV are middle‐aged and elderly [68–71]. The disease is equally common
in men and women [71], and it is a potentially life‐threatening disease [72]. Characteristics
Figure 8. Direct immunouorescence of oral lichen planus. A linear deposition of brinogen at the basement membrane
zone was found.
Figure 7. Hematoxylin‐eosin‐stained section of oral lichen planus. The basal layer liquefaction and shortened rete ridges
were found. A band‐like inltration of lymphocytes in the lamina propria was also observed.
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of the PV lesions are accid bulla formation, erosion, and ulceration in the skin or mucosa [1,
68] (Figures 16–19). PV frequently begins with oral lesions and later progresses to involve the
skin [73, 74] (Figure 20). Oral lesions are the most common evidence and develop in almost
all patients having PV [68, 71]. Lesions may aect the gingiva, and occasionally, the gingiva
is the only site of involvement in early lesions [69, 73–75]. Circulating PV autoantibodies
Figure 9. Desquamative gingivitis associated with mucous membrane pemphigoid. Ulcerated gingival surface was
observed.
Figure 10. Desquamative gingivitis associated with mucous membrane pemphigoid. Ulceration of the palatal mucosa.
Insights into Various Aspects of Oral Health10

in the serum are pathogenic, and they can cause acantholysis in the epithelium [76]. More
than 50 proteins have been reported to specically react with pemphigus IgG autoantibodies
[77], but it has been determined that the principal autoantigens in pemphigus patients are
desmogleins, which are the components of desmosomes in the epidermis and mucous mem‐
branes [78, 79]. Almost all patients with PV lesions restricted to the oral mucosa have only
anti‐ desmoglein 3 antibody in the serum, whereas patients with advanced cases involving
Figure 11. Desquamative lesions featuring gingival erythema associated with mucous membrane pemphigoid.
Figure 12. Localized blister formation on the gingiva associated with mucous membrane pemphigoid.
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the oral mucosa and skin may have both anti‐desmoglein 3 and anti‐desmoglein 1 antibodies
[73, 74]. Histopathologically, PV is characterized by acantholysis and a suprabasilar split in
the epithelium [11] (Figure 21). Tzanck cells are often found in intraepithelial clefts [80]. In
the DIF examination of PV patients, the deposition of IgG and/or C3 is found in the intercel‐
lular spaces of the epithelium [48] (Figure 22).
Figure 13. Desquamative lesions on the aached gingiva associated with mucous membrane pemphigoid.
Figure 14. Hematoxylin‐eosin‐stained section of mucous membrane pemphigoid. A subepithelial blister formation was
found.
Insights into Various Aspects of Oral Health12

3.4. Contact hypersensitivity reactions as cause of DG
Localized or generalized DG is sometimes elicited by contact hypersensitivity reactions to
various foodstus, preservatives, oral hygiene products, and dental restorative materials [11,
25, 35–39, 81]. Toothpaste hypersensitivity reactions may occur in various oral or perioral
Figure 15. Direct immunouorescence of the mucous membrane pemphigoid. A linear deposition of IgG at the basement
membrane zone was found.
Figure 16. Desquamative gingivitis associated with pemphigus vulgaris. Eroded gingival surface with ragged edges
was observed.
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sites, but the gingiva was the most common site of onset [24, 35, 36, 39, 81] (Figure 23).
Erythema has been expressed as a “velvet‐like appearance of the gingiva” or “ery red gin‐
giva” [35]. Epithelial sloughing is the most common irritant eect associated with toothpastes
and mouthwashes [1, 2, 35, 82] (Figure 24). Allergy to dental restorative materials usually
causes localized DG in gingival or other mucosal tissues directly contacting the allergen
[1, 11]. Gingival contact hypersensitivity lesions are usually not biopsied. However, if a biopsy
Figure 17. Desquamative gingivitis associated with pemphigus vulgaris. Localized erosions of the palatal mucosa.
Figure 18. Mild erythema and ulceration of gingiva associated with pemphigus vulgaris.
Insights into Various Aspects of Oral Health14

is performed, these lesions present with non‐specic histopathologic ndings with submuco‐
sal perivascular inammatory cell inltration [11, 35, 36]. The existence of focal granuloma‐
tous inammation and/or multinucleated giant cells in the deep layer of the lamina propria
was also described in some cases studying contact hypersensitivity stomatitis [25, 81]. DIF
is not indicated because it is routinely negative [11]. To treat contact hypersensitivity reac‐
tions, the allergen should be identied and removed. To do so, patients should be questioned
Figure 20. Skin involvement in a desquamative gingivitis associated with pemphigus vulgaris.
Figure 19. Pseudomembrane‐covered erosion of buccal mucosa associated with pemphigus vulgaris.
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regarding the type(s) of oral hygiene products they use, and a 1–2‐week food diary may help
identify causative agents [35]. Patch testing may be required to identify the allergen or to
conrm a specic allergen in a dental hygiene product or in a dental restoration. Patients
are considered to have allergic reactions to a relevant allergen if their patch test results are
Figure 22. Direct immunouorescence of pemphigus vulgaris. An intercellular deposition of IgG was seen.
Figure 21. Hematoxylin‐eosin‐stained section of pemphigus vulgaris. Acantholys was recognized.
Insights into Various Aspects of Oral Health16

positive [35, 81]. However, diagnosis of contact hypersensitivity reactions may be conrmed
simply by the discontinuation of the causative agent(s) resulting in the remission of clinical
signs and symptoms [35, 36, 81].
Figure 23. Contact hypersensitivity reactions caused by toothpaste. Localized erythematous and edematous lesions were
found on the gingiva.
Figure 24. Contact hypersensitivity reactions caused by mouth rinse. Epithelial sloughing was noted.
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4. Managing DG patients
The specic disease or disorder causing DG, the severity of the gingival lesions, the pres‐
ence or absence of extraoral involvements, and the medical history of the patient are the
key factors in determining the selection of a topical or systemic immunosuppressive ther‐
apy [1, 2, 69, 83]. The patients diagnosed as having an autoimmune disease should be
closely followed because they may require immediate referral to other health care experts
especially if they develop extraoral lesions. After MMP is diagnosed from DG or con‐
comitant lesions, patients should undergo examination by medical specialists including
an ophthalmologist and an otolaryngologist, and the presence or absence of extraoral
lesions should be determined. PV patients with exclusively oral lesions should be fol‐
lowed closely and referred to other experts immediately if they develop lesions elsewhere
on the body. Management of the specic disease or disorder causing DG may best be
provided by a specialist in oral medicine, oral pathology, periodontics, or oral surgery,
but the dentist may still be responsible for maintaining the dental and periodontal health
of the patient. This is important because periodontal and dental considerations are often
observed in DG patients, but the literature contains minimal information regarding the
periodontal and dental management of these individuals. Plaque‐induced gingivitis is
almost universal in patients with symptomatic DG, and an eective therapeutic protocol
should include non‐surgical periodontal therapy consisting of oral hygiene instruction,
scaling, and root planting [2, 84–89] (Figure 25). We believe that excessively vigorous
scaling and root planting can be unnecessarily damaging to DG‐aected lesions, and we
prefer a sequential gingival management approach that features gentle supragingival and
slight subgingival debridement which can be repeated at two‐week intervals resulting
in gradual improvement in periodontal status until an acceptable level of periodontal
health has been achieved. The relationship between the existence of DG lesions and the
progression of periodontal diseases is inconclusive, although some but not all studies
Figure 25. Desquamative gingivitis associated with mucous membrane pemphigoid. The initial examination
revealed moderate erythema and swelling of the gingiva with plaque and calculus deposits (A). Treatment response.
The condition of the gingiva improved due to a topical corticosteroid therapy combined with eective plaque
control (B).
Insights into Various Aspects of Oral Health18

demonstrated a correlation between compromised periodontal status and autoimmune
bullous diseases aecting the mouth [90–96]. There are several reports on periodontal
surgery or dental implant therapy performed on patients having DG [15–17, 73, 97–100].
Tissue sloughing and a lack of tissue elasticity caused by active autoimmune bullous
disease can disturb the manipulation of the mucosal ap. Strict mucosal disease control
prior to surgery may reduce the surgical complications [101]. Implant therapy is likely to
enhance the quality of life in patients with systemic diseases and may help them maintain
long‐term masticatory function. Patients with DG are often unable to wear tissue‐borne
prostheses because of discomfort. This tissue irritation and oral pain can be increased if
the appliances are ill ing or damaged. A dental implant‐ supported prosthesis improves
the stabilization of the prosthesis, resulting in a higher degree of comfort. Published case
reports indicated that DG patients can be successfully managed with dental implants.
These reports suggest that the degree of disease control may be more important than
the nature of the disease itself in regard to the eects on osseointegration. Penarrocha
et al. [98] reported that implants can be successfully placed and used to support den‐
tal prostheses in patients with recessive dystrophic epidermolysis bullosa. A total of
38 implants were placed in six totally edentulous patients. Only one implant failed to
achieve osseointegration. The average follow‐up from implant placement was 5.5 years.
The implant‐supported prostheses were associated with improvements in the patients’
comfort and function, esthetics and appearance, taste, speech, and self‐esteem. Altin et
al. [99] presented a case of PV rehabilitation using a successful implant‐supported pros‐
thesis with a 32‐month follow‐up. They concluded that the implant treatment may be
considered as a good alternative to a tissue‐borne prosthesis in PV patients. Esposito et al.
[100] reported implant retained overdentures for two patients with severe oral LP. The
patients were often unable to wear tissue‐borne prostheses because of the discomfort.
There was good integration of the implants with no clinical or radiographic evidence of
bone loss, and the soft‐tissue/implant response was excellent. Lesions occasionally ared‐
up but were successfully treated with topical steroids. There was no evidence of potential
implant failure as a result of these are‐ups. Although these descriptions of successful
management using dental implants for patients with DG are promising, further studies
are needed since these were individual case reports.
5. Conclusion
DG is a clinical manifestation that is common to several diseases or disorders. It is important
to diagnose the diseases causing DG because the prognosis varies, depending on the dis‐
ease. Histopathological examination and DIF testing are often required to establish the nal
diagnosis. The patients diagnosed with autoimmune diseases such as MMP or PV should
be closely followed because they must be immediately referred to other experts when they
develop lesions on parts of their body other than the oral cavity.
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Abbreviations
Author details
Hiroyasu Endo1*, Terry D. Rees2, Hideo Niwa3, Kayo Kuyama4, Morio Iijima5, Ryuuichi
Imamura6, Takao Kato7, Kenji Doi1, Hirotsugu Yamamoto4 and Takanori Ito1
*Address all correspondence to: endo.hiroyasu@nihon‐u.ac.jp
1 Department of Oral Diagnosis, School of Dentistry at Matsudo, Nihon University, Matsudo,
Japan
2 Department of Periodontics, Texas A&M College of Dentistry, Dallas, Texas, USA
3 Department of Head and Neck Surgery, School of Dentistry at Matsudo, Nihon University,
Matsudo, Japan
4 Department of Oral Pathology, School of Dentistry at Matsudo, Nihon University, Matsudo,
Japan
5 Department of Removable Prosthodontics, School of Dentistry at Matsudo, Nihon
University, Matsudo, Japan
6 Department of Maxillofacial Orthodontics, School of Dentistry at Matsudo, Nihon
University, Matsudo, Japan
7 Department of Oral Implantology, School of Dentistry at Matsudo, Nihon University,
Matsudo, Japan
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Insights into Various Aspects of Oral Health20

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