Open access peer-reviewed chapter

Desquamative Gingivitis

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Hiroyasu Endo, Terry D. Rees, Hideo Niwa, Kayo Kuyama, Morio Iijima, Ryuuichi Imamura, Takao Kato, Kenji Doi, Hirotsugu Yamamoto and Takanori Ito

Submitted: October 28th, 2016 Reviewed: April 18th, 2017 Published: September 20th, 2017

DOI: 10.5772/intechopen.69268

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Desquamative gingivitis (DG) is characterized by erythematous, epithelial desquamation, 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.


  • gingival diseases/pemphigus/pemphigoid
  • benign mucous membrane/lichen planus
  • oral/hypersensitivity/autoimmune diseases

1. Introduction

Manifestations of desquamative gingivitis (DG) include erythematous gingiva, epithelial desquamation, 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 different 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 sensation [4, 5]. DG occurs more often in females than males; approximately 80% of the patients are female [48]. Most patients with DG are middle‐aged and older, although rare cases have 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 nonspecific 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, 48, 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 stomatitis [10, 19, 20], lichen planus pemphigoides [21, 22], plasmacytosis [23], plasma cell gingivitis [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 [3134], which was suggestive of mucocutaneous diseases including MMP [32, 33] or PV [34]. Contact stomatitis due to dental hygiene products, dental materials, or food flavorings and preservatives may mimic DG [1, 11, 25, 3539], while several systemic disorders, including Crohn’s disease [40], psoriasis [4143], sarcoidosis [44], and adverse drug reactions [38, 45], may possess some but usually not all of the clinical features of DG.

Figure 1.

Desquamative lesions on the attached gingiva. Gentle palpation with the periodontal probe elicited some desquamation of the gingival surface (positive Nikolsky’s sign).


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 potentially 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 would certainly deteriorate the quality of life for MMP patients. Early recognition and treatment of the lesions can prevent serious complications. Histopathological examination and direct immunofluorescence (DIF) testing of biopsied tissues are often required to determine the underlying etiology of DG [68, 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 nonspecific inflammatory response in suspected non‐autoimmune disorders such as LP, erythema multiforme, foreign body gingivitis, factitious 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 considered 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 final diagnosis since clinical features may be so similar [68, 10, 47, 48]. On the other hand, DIF findings 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 conditions [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 cutting edge. If a larger specimen is needed, the tip of the blade can be repositioned and the rolling stroke extended. The gingival epithelium 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 inflammatory disease of unknown etiology. LPcommonly occurs in middle‐aged and older people, and women are affected more frequently than men [53, 54]. The lesions are found in multiple regions including the skin, genitalia, or oral mucosa, although they are confined to the gingiva alone in some cases [5356] (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 [5355, 57] (Figures 46). For these reasons, erosive LP usually requires treatment. Histopathologically, specimens may demonstrate hyperortho‐ or hyperparakeratosis, degenerative changes to the basal cells, and band‐like subepithelial infiltrate composed of lymphocytes [11] (Figure 7). When available, DIF testing is also valuable in establishing the diagnosis, although DIF findings are only suggestive, rather than diagnostic, of LP [6, 10, 48, 58]. Characteristic DIF findings in oral LP include a linear pattern of anti‐fibrin or anti‐fibrinogen in the basement membrane zone and, to a lesser degree, the presence of IgM or IgG deposits in cytoid bodies [6, 10, 48, 58] (Figure 8).

Figure 2.

Desquamative gingivitis associated with oral lichen planus. Erythematous lesions on the attached gingiva.

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.

Figure 5.

Extraoral lesion associated with oral lichen planus. The reticular lesion was observed on the lip.

Figure 6.

Oral lichen planus patient. The examination revealed diffuse erythematous lesions on the gingiva (A and B). Lesions were also found on the buccal mucosa (C) and tongue (D).

Figure 7.

Hematoxylin‐eosin‐stained section of oral lichen planus. The basal layer liquefaction and shortened rete ridges were found. A band‐like infiltration of lymphocytes in the lamina propria was also observed.

Figure 8.

Direct immunofluorescence of oral lichen planus. A linear deposition of fibrinogen at the basement membrane zone was found.

3.2. Mucous membrane pemphigoid (MMP)

MMP is an autoimmune, subepithelial blistering disease that affects mucous membranes. Most patients with MMP are between 60 and 80 years of age [5961]. However, on relatively rare occasions, MMP has been reported in children [9]. Women are affected nearly two times more frequently than men [5961]. MMP can involve any oral mucosal site, although the gingiva is affected far more often than other oral tissues [52, 5962] (Figures 913). 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 affected [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, 6465]. Multiple target antigens of MMP were identified 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 caused by these antibodies may result in subepithelial blistering. Histopathologically, MMP is characterized by subepithelial bulla formation [11] (Figure 14). During DIF testing, the linear deposition of complement component C3, IgG, or other immunoglobulin is observed in a linear pattern along the basement membrane zone [48, 62] (Figure 15).

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.

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.

Figure 13.

Desquamative lesions on the attached gingiva associated with mucous membrane pemphigoid.

Figure 14.

Hematoxylin‐eosin‐stained section of mucous membrane pemphigoid. A subepithelial blister formation was found.

Figure 15.

Direct immunofluorescence of the mucous membrane pemphigoid. A linear deposition of IgG at the basement membrane zone was found.

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 [6871]. The disease is equally common in men and women [71], and it is a potentially life‐threatening disease [72]. Characteristics of the PV lesions are flaccid bulla formation, erosion, and ulceration in the skin or mucosa [1, 68] (Figures 1619). 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 affect the gingiva, and occasionally, the gingiva is the only site of involvement in early lesions [69, 7375]. Circulating PV autoantibodies in the serum are pathogenic, and they can cause acantholysis in the epithelium [76]. More than 50 proteins have been reported to specifically 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 membranes [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 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 intercellular spaces of the epithelium [48] (Figure 22).

Figure 16.

Desquamative gingivitis associated with pemphigus vulgaris. Eroded gingival surface with ragged edges was observed.

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.

Figure 19.

Pseudomembrane‐covered erosion of buccal mucosa associated with pemphigus vulgaris.

Figure 20.

Skin involvement in a desquamative gingivitis associated with pemphigus vulgaris.

Figure 21.

Hematoxylin‐eosin‐stained section of pemphigus vulgaris. Acantholys was recognized.

Figure 22.

Direct immunofluorescence of pemphigus vulgaris. An intercellular deposition of IgG was seen.

3.4. Contact hypersensitivity reactions as cause of DG

Localized or generalized DG is sometimes elicited by contact hypersensitivity reactions to various foodstuffs, preservatives, oral hygiene products, and dental restorative materials [11, 25, 3539, 81]. Toothpaste hypersensitivity reactions may occur in various oral or perioral 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 “fiery red gingiva” [35]. Epithelial sloughing is the most common irritant effect 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 is performed, these lesions present with non‐specific histopathologic findings with submucosal perivascular inflammatory cell infiltration [11, 35, 36]. The existence of focal granulomatous inflammation 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 reactions, the allergen should be identified and removed. To do so, patients should be questioned 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 confirm a specific 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 positive [35, 81]. However, diagnosis of contact hypersensitivity reactions may be confirmed 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.


4. Managing DG patients

The specific disease or disorder causing DG, the severity of the gingival lesions, the presence 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 therapy [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 concomitant 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 followed closely and referred to other experts immediately if they develop lesions elsewhere on the body. Management of the specific 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 effective therapeutic protocol should include non‐surgical periodontal therapy consisting of oral hygiene instruction, scaling, and root planting [2, 8489] (Figure 25). We believe that excessively vigorous scaling and root planting can be unnecessarily damaging to DG‐affected 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 demonstrated a correlation between compromised periodontal status and autoimmune bullous diseases affecting the mouth [9096]. There are several reports on periodontal surgery or dental implant therapy performed on patients having DG [1517, 73, 97100]. Tissue sloughing and a lack of tissue elasticity caused by active autoimmune bullous disease can disturb the manipulation of the mucosal flap. 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 fitting 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 effects on osseointegration. Penarrocha et al. [98] reported that implants can be successfully placed and used to support dental 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 prosthesis 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 flared‐up but were successfully treated with topical steroids. There was no evidence of potential implant failure as a result of these flare‐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.

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 effective plaque control (B).


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 disease. Histopathological examination and DIF testing are often required to establish the final 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.



DGDesquamative gingivitis
LPLichen planus
MMPMucous membrane pemphigoid
PVPemphigus vulgaris
DIFDirect immunofluorescence


  1. 1. Rees TD, Burkhart N. Desquamative Gingivitis [Internet]. 2016. Available from:‐us/professional‐education/ce‐courses/ce481 [Accessed: February 9, 2017]
  2. 2. Endo H, Rees TD. Diagnosis and management of desquamative gingivitis. In: Panagakos FS, Davies RM, editors. Gingival Diseases – Their Aetiology, Prevention and Treatment. Rijeka, Croatia: InTech; 2011. pp. 171-188. Available from:‐and‐management‐of‐desquamative‐gingivitis [Accessed: February 9, 2017]
  3. 3. Nisengard RJ, Levine RA. Diagnosis and management of desquamative gingivitis. Periodontal Insights. 1995;2:4-10
  4. 4. Lo Russo L, Fierro G, Guiglia R, et al. Epidemiology of desquamative gingivitis: Evaluation of 125 patients and review of the literature. International Journal of Dermatology. 2009;48:1049-1052
  5. 5. Leao JC, Ingafou M, Khan A, Scully C, Porter S. Desquamative gingivitis: Retrospective analysis of disease associations of a large cohort. Oral Diseases. 2008;14:556-560
  6. 6. Nisengard RJ, Neiders M. Desquamative lesions of the gingiva. Journal of Periodontology. 1981;52:500-510
  7. 7. Nisengard RJ, Rogers 3rd RS. The treatment of desquamative gingival lesions. Journal of Periodontology. 1987;58:167-172
  8. 8. Rinaggio J, Crossland DM, Zeid MY. A determination of the range of oral conditions submitted for microscopic and direct immunofluorescence analysis. Journal of Periodontology. 2007;78:1904-1910
  9. 9. Cheng YS, Rees TD, Wright JM, Plemons JM. Childhood oral pemphigoid: A case report and review of the literature. Journal of Oral Pathology & Medicine. 2001;30:372-377
  10. 10. Suresh L, Neiders ME. Definitive and differential diagnosis of desquamative gingivitis through direct immunofluorescence studies. Journal of Periodontology. 2012;83:1270-1278. DOI: 10.1902/jop.2012.110627
  11. 11. Rees TD. Desquamative gingivitis/mucocutaneous diseases commonly affecting the gingiva. In: Harpenau LA, Kao RT, Lundergan WP, Sanz M, editors. Hall’s Critical Decisions in Periodontology and Dental Implantology. 5th ed. Connecticut, USA: People’s Medical Publishing House; 2013. pp. 68-73
  12. 12. Kranti K, Seshan H, Juliet J. Discoid lupus erythematosus involving gingiva. Journal of Indian Society of Periodontology. 2012;16:126-128. DOI: 10.4103/0972‐124X.94621
  13. 13. Bassim CW, Fassil H, Mays JW, et al. Oral disease profiles in chronic graft versus host disease. Journal of Dental Research. 2015;94:547-554. DOI: 10.1177/0022034515570942
  14. 14. Ayangco L, Rogers 3rd RS. Oral manifestations of erythema multiforme. Dermatologic Clinics. 2003;21:195-205
  15. 15. Brain JH, Paul BF, Assad DA. Periodontal plastic surgery in a dystrophic epidermolysis bullosa patient: Review and case report. Journal of Periodontology. 1999;70:1392-1396
  16. 16. Buduneli E, Ilgenli T, Buduneli N, Ozdemir F. Acellular dermal matrix allograft used to gain attached gingiva in a case of epidermolysis bullosa. Journal of Clinical Periodontology. 2003;30:1011-1015
  17. 17. Hakki SS, Celenligil‐Nazliel H, Karaduman A, et al. Epidermolysis bullosa acquisita: Clinical manifestations, microscopic findings, and surgical periodontal therapy. A case report. Journal of Periodontology. 2001;72:550-558
  18. 18. Ricketts DN, Morgan CL, McGregor JM, Morgan PR. Kindler syndrome: A rare cause of desquamative lesions of the gingiva. Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontics. 1997;84:488-491
  19. 19. Lorenzana ER, Rees TD, Glass M, Detweiler JG. Chronic ulcerative stomatitis: A case report. Journal of Periodontology. 2000;71:104-111
  20. 20. Qari H, Villasante C, Richert J, Rees TD, Kessler H. The diagnostic challenges of separating chronic ulcerative stomatitis from oral lichen planus. Oral Surgery, Oral Medicine, Oral Pathology and Oral Radiology. 2015;120:622-627. DOI: 10.1016/j.oooo.2015.07.018
  21. 21. Sultan A, Stojanov IJ, Lerman MA, et al. Oral lichen planus pemphigoides: A series of four cases. Oral Surgery, Oral Medicine, Oral Pathology and Oral Radiology. 2015;120:58-68. DOI: 10.1016/j.oooo.2015.03.012
  22. 22. Mignogna MD, Fortuna G, Leuci S, Stasio L, Mezza E, Ruoppo E. Lichen planus pemphigoides, a possible example of epitope spreading. Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontics. 2010;109:837-843. DOI: 10.1016/j.tripleo.2009.12.044
  23. 23. Gupta SR, Gupta R, Saran RK, Krishnan S. Plasma cell mucositis with gingival enlargement and severe periodontitis. Journal of Indian Society of Periodontology. 2014;18:379-384. DOI: 10.4103/0972‐124X.134583
  24. 24. Mishra MB, Sharma S, Sharma A. Plasma cell gingivitis: An occasional case report. The New York State Dental Journal. 2015;81:57-60
  25. 25. Rees TD. Orofacial granulomatosis and related conditions. Periodontology 2000. 1999;21:145-157
  26. 26. Mignogna MD, Fedele S, Lo Russo L, Lo Muzio L. Orofacial granulomatosis with gingival onset. Journal of Clinical Periodontology. 2001;28:692-696
  27. 27. Gravitis K, Daley TD, Lochhead MA. Management of patients with foreign body gingivitis: Report of 2 cases with histologic findings. Journal of the Canadian Dental Association. 2005;71:105-109
  28. 28. Yalamanchili PS, Potluri S, Surapaneni H, Basha MH, Davanapelly P. Candidal infection of the gingiva mimicking desquamative gingivitis: A case report. Journal of Clinical and Diagnostic Research. 2016;10:ZD04‐ZD05. DOI: 10.7860/JCDR/2016/17413.7367
  29. 29. Porter SR, Bain SE, Scully CM. Linear IgA disease manifesting as recalcitrant desquamative gingivitis. Oral Surgery, Oral Medicine, Oral Pathology. 1992;74:179-182
  30. 30. O’Regan E, Bane A, Flint S, Timon C, Toner M. Linear IgA disease presenting as desquamative gingivitis: A pattern poorly recognized in medicine. Archives of Otolaryngology – Head and Neck Surgery. 2004;130:469-472
  31. 31. McGrath KG, Pick R, Leboff‐Ries E, Patterson R. Factitious desquamative gingivitis simulating a possible immunologic disease. The Journal of Allergy and Clinical Immunology. 1985;75:44-46
  32. 32. Heasman PA, MacLeod I, Smith DG. Factitious gingival ulceration: As presenting sign of Munchausen’s syndrome? Journal of Periodontology. 1994;65:442-447
  33. 33. Kotansky K, Goldberg M, Tenenbaum HC, Mock D. Factitious injury of the oral mucosa: A case series. Journal of Periodontology. 1995;66:241-245
  34. 34. Zonuz AT, Treister N, Mehdipour F, Farahani RM, Tubbs RS, Shoja MM. Factitial pemphigus‐like lesions. Medicina Oral Patologia Oral y Cirugia Bucal. 2007;12:E205‐E208
  35. 35. Endo H, Rees TD. Clinical features of cinnamon‐induced contact stomatitis. Compendium of Continuing Education in Dentistry. 2006;27:403-409; quiz 410, 421
  36. 36. Endo H, Rees TD, Sisilia F, et al. Atypical gingival manifestations that mimic mucocutaneous diseases in a patient with contact stomatitis caused by toothpaste. Journal of Implant and Advanced Clinical Dentistry. 2010;2:101-106
  37. 37. Lamey PJ, Lewis MA, Rees TD, Fowler C, Binnie WH, Forsyth A. Sensitivity reaction to the cinnamonaldehyde component of toothpaste. British Dental Journal. 1990;168:115-118
  38. 38. Rees TD. Drugs and oral disorders. Periodontology 2000. 1998;18:21-36
  39. 39. Singh B, Sharma A, Garg A. Herbal oral gel induced contact stomatitis along with desquamative gingivitis due to a coloring agent. Journal of Indian Society of Periodontology. 2015;19:569-572. DOI: 10.4103/0972‐124X.167165
  40. 40. Ayangco L, Rogers 3rd RS, Sheridan PJ. Pyostomatitis vegetans as an early sign of reactivation of Crohn’s disease: A case report. Journal of Periodontology. 2002;73:1512-1516
  41. 41. Jones LE, Dolby AE. Desquamative gingivitis associated with psoriasis. Journal of Periodontology. 1972;43:35-37
  42. 42. Yamada J, Amar S, Petrungaro P. Psoriasis‐associated periodontitis: A case report. Journal of Periodontology. 1992;63:854-857
  43. 43. Brice DM, Danesh‐Meyer MJ. Oral lesions in patients with psoriasis: Clinical presentation and management. Journal of Periodontology. 2000;71:1896-1903
  44. 44. Antunes KB, Miranda AM, Carvalho SR, Azevedo AL, Tatakis DN, Pires FR. Sarcoidosis presenting as gingival erosion in a patient under long‐term clinical control. Journal of Periodontology. 2008;79:556-561
  45. 45. Rees TD. Oral effects of drug abuse. Critical Reviews in Oral Biology & Medicine. 1992;3:163-184
  46. 46. Endo H, Rees TD, Allen EP, et al. A stab‐and‐roll biopsy technique to maintain gingival epithelium for desquamative gingivitis. Journal of Periodontology. 2014;85:802-809. DOI: 10.1902/jop.2014.130428
  47. 47. Sano SM, Quarracino MC, Aguas SC, et al. Sensitivity of direct immunofluorescence in oral diseases. Study of 125 cases. Medicina Oral Patologia Oral y Cirugia Bucal. 2008;13:E287‐E291
  48. 48. Mutasim DF, Adams BB. Immunofluorescence in dermatology. Journal of The American Academy of Dermatology. 2001;45:803-822; quiz 822-824
  49. 49. Siegel MA, Balciunas BA, Kelly M, Serio FG. Diagnosis and management of commonly occurring oral vesiculoerosive disorders. Cutis. 1991;47:39-43
  50. 50. Casiglia J, Woo SB, Ahmed AR. Oral involvement in autoimmune blistering diseases. Clinical Dermatology. 2001;19:737-741
  51. 51. Lo Russo L, Fedele S, Guiglia R, et al. Diagnostic pathways and clinical significance of desquamative gingivitis. Journal of Periodontology. 2008;79:4-24
  52. 52. Endo H, Rees TD, Niwa H, Kuyama K, Yamamoto H, Ito T. Desquamative gingivitis as an oral manifestation of mucous membrane pemphigoid: Diagnosis and treatment. In: Vega JP, editor. Advances in Dermatology Research. New York, USA: Nova Science Publishers; 2015. pp. 73-86. Available from: [Accessed: February 9, 2017]
  53. 53. Ingafou M, Leao JC, Porter SR, Scully C. Oral lichen planus: A retrospective study of 690 British patients. Oral Diseases. 2006;12:463-468
  54. 54. Mignogna MD, Lo Russo L, Fedele S. Gingival involvement of oral lichen planus in a series of 700 patients. Journal of Clinical Periodontology. 2005;32:1029-1033
  55. 55. Camacho‐Alonso F, Lopez‐Jornet P, Bermejo‐Fenoll A. Gingival involvement of oral lichen planus. Journal of Periodontology. 2007;78:640-644
  56. 56. Petruzzi M, De Benedittis M, Pastore L, Grassi FR, Serpico R. Peno‐gingival lichen planus. Journal of Periodontology. 2005;76:2293-2298
  57. 57. Endo H, Rees TD, Kuyama K, Matsue M, Yamamoto H. Successful treatment using occlusive steroid therapy in patients with erosive lichen planus: A report on 2 cases. Quintessence International. 2008;39:e162‐e172
  58. 58. Buajeeb W, Okuma N, Thanakun S, Laothumthut T. Direct immunofluorescence in oral lichen planus. Journal of Clinical and Diagnostic Research. 2015;9:ZC34‐ZC37. DOI: 10.7860/JCDR/2015/13510.6312
  59. 59. Ahmed AR, Hombal SM. Cicatricial pemphigoid. International Journal of Dermatology. 1986;25:90-96
  60. 60. Hanson RD, Olsen KD, Rogers 3rd RS. Upper aerodigestive tract manifestations of cicatricial pemphigoid. Annals of Otology, Rhinology & Laryngology. 1988;97:493-499
  61. 61. Lamey PJ, Rees TD, Binnie WH, Rankin KV. Mucous membrane pemphigoid. Treatment experience at two institutions. Oral Surgery, Oral Medicine, Oral Pathology. 1992;74:50-53
  62. 62. Chan LS, Ahmed AR, Anhalt GJ, et al. The first international consensus on mucous membrane pemphigoid: Definition, diagnostic criteria, pathogenic factors, medical treatment, and prognostic indicators. Archives of Dermatology. 2002;138:370-379.
  63. 63. Endo H, Rees TD, Kuyama K, Kono Y, Yamamoto H. Clinical and diagnostic features of mucous membrane pemphigoid. Compendium of Continuing Education in Dentistry. 2006;27:512-516; quiz 517-518
  64. 64. Higgins TS, Cohen JC, Sinacori JT. Laryngeal mucous membrane pemphigoid: A systematic review and pooled‐data analysis. Laryngoscope. 2010;120:529-536
  65. 65. Higgins GT, Allan RB, Hall R, Field EA, Kaye SB. Development of ocular disease in patients with mucous membrane pemphigoid involving the oral mucosa. British Journal of Ophthalmology. 2006;90:964-967
  66. 66. Calabresi V, Carrozzo M, Cozzani E, et al. Oral pemphigoid autoantibodies preferentially target BP180 ectodomain. Journal of Clinical Immunology. 2007;122:207-213
  67. 67. Bernard P, Antonicelli F, Bedane C, et al. Prevalence and clinical significance of anti‐laminin 332 autoantibodies detected by a novel enzyme‐linked immunosorbent assay in mucous membrane pemphigoid. JAMA Dermatology. 2013;149:533-540. DOI: 10.1001/jamadermatol.2013.1434
  68. 68. Chams‐Davatchi C, Valikhani M, Daneshpazhooh M, et al. Pemphigus: Analysis of 1209 cases. International Journal of Dermatology. 2005;44:470-476
  69. 69. Lamey PJ, Rees TD, Binnie WH, Wright JM, Rankin KV, Simpson NB. Oral presentation of pemphigus vulgaris and its response to systemic steroid therapy. Oral Surgery, Oral Medicine, Oral Pathology. 1992;74:54-57
  70. 70. Scully C, Paes De Almeida O, Porter SR, Gilkes JJ. Pemphigus vulgaris: The manifestations and long‐term management of 55 patients with oral lesions. British Journal of Dermatology. 1999;140:84-89
  71. 71. Sirois D, Leigh JE, Sollecito TP. Oral pemphigus vulgaris preceding cutaneous lesions: Recognition and diagnosis. Journal of the American Dental Association. 2000;131:1156-1160
  72. 72. Nair PS, Moorthy PK, Yogiragan K. A study of mortality in dermatology. Indian Journal of Dermatology, Venereology and Leprology. 2005;71:23-25
  73. 73. Endo H, Rees TD, Matsue M, Kuyama K, Nakadai M, Yamamoto H. Early detection and successful management of oral pemphigus vulgaris: A case report. Journal of Periodontology. 2005;76:154-160
  74. 74. Endo H, Rees TD, Hallmon WW, et al. Disease progression from mucosal to mucocutaneous involvement in a patient with desquamative gingivitis associated with pemphigus vulgaris. Journal of Periodontology. 2008;79:369-375. DOI: 10.1902/jop.2008.070258
  75. 75. Mignogna MD, Lo Muzio L, Bucci E. Clinical features of gingival pemphigus vulgaris. Journal of Clinical Periodontology. 2001;28:489-493
  76. 76. Anhalt GJ, Labib RS, Voorhees JJ, Beals TF, Diaz LA. Induction of pemphigus in neonatal mice by passive transfer of IgG from patients with the disease. The New England Journal of Medicine. 1982;306:1189-1196
  77. 77. Grando SA. Pemphigus autoimmunity: Hypotheses and realities. Autoimmunity. 2012;45:7-35. DOI: 10.3109/08916934.2011.606444
  78. 78. Amagai M, Klaus‐Kovtun V, Stanley JR. Autoantibodies against a novel epithelial cadherin in pemphigus vulgaris, a disease of cell adhesion. Cell. 1991;67:869-877
  79. 79. Amagai M, Tsunoda K, Zillikens D, Nagai T, Nishikawa T. The clinical phenotype of pemphigus is defined by the anti‐desmoglein autoantibody profile. Journal of The American Academy of Dermatology. 1999;40:167-170
  80. 80. Endo H, Rees TD, Kuyama K, Matsue M, Yamamoto H. Use of oral exfoliative cytology to diagnose desquamative gingivitis: A pilot study. Quintessence International. 2008;39:e152‐e161
  81. 81. Endo H, Rees TD. Cinnamon products as a possible etiologic factor in orofacial granulomatosis. Medicina Oral Patologia Oral y Cirugia Bucal. 2007;12:E440‐E444
  82. 82. Kuttan NA, Narayana N, Moghadam BK. Desquamative stomatitis associated with routine use of oral health care products. General Dentistry. 2001;49:596-602
  83. 83. Harpenau LA, Plemons JM, Rees TD. Effectiveness of a low dose of cyclosporine in the management of patients with oral erosive lichen planus. Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontics. 1995;80:161-167
  84. 84. Stone SJ, Heasman PA, Staines KS, McCracken GI. The impact of structured plaque control for patients with gingival manifestations of oral lichen planus: A randomized controlled study. Journal of Clinical Periodontology. 2015;42:356-362. DOI: 10.1111/jcpe.12385
  85. 85. Salgado DS, Jeremias F, Capela MV, Onofre MA, Massucato EM, Orrico SR. Plaque control improves the painful symptoms of oral lichen planus gingival lesions. A short‐term study. Journal of Oral Pathology & Medicine. 2013;42:728-732. DOI: 10.1111/jop.12093
  86. 86. Guiglia R, Di Liberto C, Pizzo G, et al. A combined treatment regimen for desquamative gingivitis in patients with oral lichen planus. Journal of Oral Pathology & Medicine. 2007;36:110-116
  87. 87. Orrico SR, Navarro CM, Rosa FP, Reis FA, Salgado DS, Onofre MA. Periodontal treatment of benign mucous membrane pemphigoid. Dentistry Today. 2010;29:100-102; quiz 102-103
  88. 88. Arduino PG, Lopetuso E, Carcieri P, et al. Professional oral hygiene treatment and detailed oral hygiene instructions in patients affected by mucous membrane pemphigoid with specific gingival localization: A pilot study in 12 patients. International Journal of Dental Hygiene. 2012;10:138-141. DOI: 10.1111/j.1601‐5037.2011.00527.x
  89. 89. Damoulis PD, Gagari E. Combined treatment of periodontal disease and benign mucous membrane pemphigoid. Case report with 8 years maintenance. Journal of Periodontology. 2000;71:1620-1629
  90. 90. Akman A, Kacaroglu H, Yilmaz E, Alpsoy E. Periodontal status in patients with pemphigus vulgaris. Oral Diseases. 2008;14:640-643
  91. 91. Arduino PG, Farci V, D’Aiuto F, et al. Periodontal status in oral mucous membrane pemphigoid: Initial results of a case‐control study. Oral Diseases. 2011;17:90-94. DOI: 10.1111/j.1601‐0825.2010.01709.x
  92. 92. Tricamo MB, Rees TD, Hallmon WW, Wright JM, Cueva MA, Plemons JM. Periodontal status in patients with gingival mucous membrane pemphigoid. Journal of Periodontology. 2006;77:398-405
  93. 93. Schellinck AE, Rees TD, Plemons JM, Kessler HP, Rivera‐Hidalgo F, Solomon ES. A comparison of the periodontal status in patients with mucous membrane pemphigoid: A 5‐year follow‐up. Journal of Periodontology. 2009;80:1765-1773
  94. 94. Pradeep AR, Manojkumar ST, Arjun R. Pemphigus vulgaris with significant periodontal findings: A case report. Journal of the California Dental Association. 2010;38:343-346
  95. 95. Ramon‐Fluixa C, Bagan‐Sebastian J, Milian‐Masanet M, Scully C. Periodontal status in patients with oral lichen planus: A study of 90 cases. Oral Diseases. 1999;5:303-306
  96. 96. Lo Russo L, Guiglia R, Pizzo G, Fierro G, Ciavarella D, Lo Muzio L, Campisi G. Effect of desquamative gingivitis on periodontal status: A pilot study. Oral Diseases. 2010;16:102-107
  97. 97. Lorenzana ER, Rees TD, Hallmon WW. Esthetic management of multiple recession defects in a patient with cicatricial pemphigoid. Journal of Periodontology. 2001;72:230-237
  98. 98. Penarrocha M, Larrazabal C, Balaguer J, Serrano C, Silvestre J, Bagan JV. Restoration with implants in patients with recessive dystrophic epidermolysis bullosa and patient satisfaction with the implant‐supported superstructure. The International Journal of Oral & Maxillofacial Implants. 2007;22:651-655
  99. 99. Altin N, Ergun S, Katz J, Sancakli E, Koray M, Tanyeri H. Implant‐supported oral rehabilitation of a patient with pemphigus vulgaris: A clinical report. Journal of Prosthodontics. 2013;22:581-586. DOI: 10.1111/jopr.12050
  100. 100. Esposito SJ, Camisa C, Morgan M. Implant retained overdentures for two patients with severe lichen planus: A clinical report. Journal of Prosthetic Dentistry. 2003;89:6-10
  101. 101. Toscano NJ, Holtzclaw DJ, Shumaker ND, Stokes SM, Meehan SC, Rees TD. Surgical considerations and management of patients with mucocutaneous disorders. Compendium of Continuing Education in Dentistry. 2010;31:344-350, 352-359; quiz 362, 364

Written By

Hiroyasu Endo, Terry D. Rees, Hideo Niwa, Kayo Kuyama, Morio Iijima, Ryuuichi Imamura, Takao Kato, Kenji Doi, Hirotsugu Yamamoto and Takanori Ito

Submitted: October 28th, 2016 Reviewed: April 18th, 2017 Published: September 20th, 2017