Demystifying immunopathology and clinical presentation in common desquamative gingivitis

Dhanapal Raghu, Mochamad Arief Erry, Kondreddy Kameshwari, Arunachalam Rajeev

AIMST Dental Institute, Malaysia

Received: 12 – 04 – 2022

Revised: 30 – 04 – 2022

Accepted: 26 – 05 – 2022

Address for correspondence: Dr. Raghu Dhanapal MDS, (Oral Pathology), Associate Professor, AIMST Dental Institute, AIMST University, Jalan Semeling, Bedong, Kedah state, Malaysia, Pincode – 08100

This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-Noncommercial ShareAlike 4.0 license, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms

How to cite this article: Dhanapal R, Mochamad A E, Kondreddy K, Arunachalam R. Demystifying immunopathology and clinical presentation in common desquamative gingivitis. J Oral Biomed Sci 2022; 1: 62-5


Desquamative gingivitis is associated with certain inflammatory and immune conditions which includes a spectrum of autoimmune disorders, hypersensitivity reactions and granulomatous disorders. The autoimmune disorders and hypersensitivity reactions are the most common causative factors for the occurrence. This manuscript is an overview of the etiopathogenesis and clinical presentation in these common desquamative gingivitis associated lesions. The importance’s of the coordinated multispecialty approach in diagnosis, categorizing of the clinical presentation and treatment is emphasized in this review.

Keywords:  Desquamative gingivitis, Autoimmune disorders


Desquamative gingivitis is a chronic disorder which manifests as epithelial desquamation, associated with a spectrum of autoimmune disorders and hypersensitivity reactions. The most common autoimmune disorders manifesting as desquamative gingivitis are mucous membrane pemphigoid and oral lichen planus, followed by pemphigus.(1) The hypersensitive reactions also are desquamative in nature, which includes contact allergy and erythema multiforme. (2), (3), (4)

Literature states that extent of periodontitis in sites associated with desquamative gingivitis comparatively severe compared to areas without desquamative gingivitis. Areas with desquamative gingivitis can be associated with poor oral hygiene and hence a reservoir of plaque. Periodontal inflammation could possibly act as trigger for autoimmune reactions or act as sustaining factor for the persistence of autoimmunity. Oral lesions can be the first clinical manifestation. (5) The plaque is not causative factor of the desquamative gingival lesion; it can be an autoimmune or hypersensitive reaction.  The better understanding of the immunopathology will help understand the clinical manifestations and establish the final diagnosis.

Autoimmune disorders

Autoimmune disorders commonly affecting the gingiva mucosa include mucous membrane pemphigoid and oral lichen planus, which accounts for about 80% of desquamative gingival lesions. The other rare lesions include pemphigus, pemphigus lesions commonly manifests first in the oral cavity.

Mucous membrane pemphigoid

In mucous membrane pemphigoid the auto reactive T helper cell detect the self-antigens as foreign, cause autoimmune reaction to antigens in the basement membrane zone. The autoreactive T-helper cells cause the B-lymphocyte to produce autoantibodies. The auto antibodies found in mucous membrane pemphigoid include IgG and IgA, directed to BP230, BP180, laminin 5, laminin 6, type VII collagen, Integrin α6 and β4. The self-antigen more commonly associated with mucous membrane is BP 230. This characterized as subepithelial vesicle or bullae.(6), (7)

Oral lichen planus (OLP)

OLP in contrast to other lesions is commonly associated with antigen specific cytotoxic destruction of the epithelial cells in the basal layer. Main mechanism includes cytotoxic T-cell induced apoptosis of the basal epithelial cells in response to specific antigen. The other mechanism proposed, is auto-reactivity in T-cells because an altered immune recognition of basal epithelial cells leading to apoptosis. Apoptosis of basal epithelial cells can be mediated by TNF α or granzymes.(8)


Autoantibodies are mainly produced against desmogleins 1 and 3. In rare condition, they are formed against desmocollins and the intracellular plaque component of cell junctions i.e., desmoplakin, envoplakin, and periplakin. The autoantibody against self-antigens leads to acantholysis of the intra-epithelial junctions, forming an intra-epithelial vesicle or bullae.(7), (9), (10)

Hypersensitivity reactions

Erythema Multiforme (EM)

Minor and major subtypes tend to have a varied immunopathology, minor variant is associated with Type III hypersensitivity reaction (antigen antibody complex mediated damage) and the major variant is caused by autoimmunity. Hypersensitivity reaction leads to vasculitis in minor EM. Autoantibodies are directed against the desmoplakin. The vasculitis & autoimmunity to desmoplakin elucidates the erythematous lesions & vesicular eruptions in erythema multiforme.(11), (12)

Drug or contact allergy

Allergen induced desquamative gingivitis represents the type IV hypersensitivity reaction or delayed hypersensitivity. It manifests after exposure to allergen in comparatively long number of days, and be from months to years. It manifests as areas of atrophy in mucosa. (13)

Clinical parameters

Desquamative gingivitis can be first site of onset of the life threatening systemic diseases. The diverse clinical presentation in desquamative gingivitis can be erythema, blisters, hyperkeratosis and ulcerations.

Clinical features

The predominant symptoms are warmth, tenseness, tingling, itchiness, burning, and pain. Erythema and oedema of the marginal and attached gingiva are clinically observed predominantly in the frontal areas. It presents as a erythema which is diffuse and nominal desquamation.(14)

Mucous membrane pemphigoid

It occurs in individuals in age group of 50-60 years. Mucosal site commonly affected is the oral cavity and conjunctiva; it tends to heal without scar. Gingival lesions are erythematous and associated with loss of stippling; gingiva is one of the most common sites of occurrence.


The vesicular lesion commonly manifests in the fourth to sixth decade, with a gender equal predilection in both the males and females. It has a higher predominance in the Jewish population, genetic predisposition in HLA genes. Mucosal lesions of the oral region are the first site of occurrence. On the gingiva, it manifests as an erythematous lesion and positive for Nikolsky’s sign. (15)

Oral Lichen planus

Desquamative gingivitis in lichen planus is caused by the subtype atrophic lichen planus. Gingival lesions are characterised by central erosive lesions with peripheral white striae (Wickham’s striae). Gingival lesion can occur concomitantly with vulvovaginal lesions, which is termed vulvovaginal gingival syndrome (16), (17)

Erythema Multiforme

Mucosal lesions are common in the major variant of Erythema Multiforme (EM). Demographic distribution in this acute autoimmune disorder is young male patients. It is commonly associated with encrustations on the lips and gingival lesions, the gingival lesions constitute about 18% of lesions intra-orally. It can also present as polymorphous erosive erythematous lesions.(2)

Contact Allergy

Burning sensation of the gums is a characteristic symptom in contact allergy. Clinical presentation is an erythematous erosive gingival lesion commonly in proximity to the allergen. (3), (4)

The stepwise analysis for the diagnosis is imperative for conclusive diagnosis. The initial step includes demographic data and clinical history. There is a female predilection; pemphigus tends to have an ethnic predilection for Jews.  History should include drug history, recent restoration and severity of the lesions; pemphigus tends to manifest with severe symptoms. Next step is clinical examination of oral and extra-oral sites for characteristic clinical features of lesions. Mucous membrane pemphigoid is commonly associated with desquamative gingivitis with irregular erythematous patches & bullae, extra-oral mucosal lesions are also common. Typical clinical signs observed are Wickham’s straie in OLP, Nicolsky’s sign in pemphigus and target lesions in EM.  Last step in diagnosis is perilesion tissue biopsy for analysis of histopathology and immunofluorescence. (11), (13), (14)

Arduino et al’s clinical criteria for diagnosis is based on lesion size and performed under good dental light, with a calibrated probe in millimetres (PCPUNC15; Hu-Friedy, Chicago, IL, U.S.A.). Clinical assessment should be on both aspects of the gingival mucosa (six times vestibular and six times buccal), one for each sextant of the upper and lower gingiva.

Clinical criteria:

Score 0: no detectable gingival lesions present

Score 1: only white lesions

Score 2: mild erythema (< 3 mm from gingival margins)

Score 3: one or more bullae, or clinically obvious erythema (> 3 mm from gingival


Score 4: erosion or ulcer

In the event of presence of multiple features, the higher index can be chosen. The scores can range from 0 to 48 (considering both vestibular and oral sites), with higher results indicating more severe clinical disease.(18)

Plaque control in patients with severe desquamative gingivitis can be best done using sonic tooth brushes. (19) The topical steroids help reduce the severity of the local condition. The treatment approach should help improve the quality of life and a multi-disciplinary treatment approach is mandatory.(20)


The correlation between the clinical and pathological parameter renders the final diagnosis. The dental practitioner can have co-ordinated treatment plan after consultation with a dermatologist, periodontist and oral pathologist.

Conflict of interest: None

Financial support and sponsorship: Nil


  1. Scully C, Porter SR. The clinical spectrum of desquamative gingivitis. Semin Cutan Med Surg. 1997 Dec;16(4):308–13.
  2. Ayangco L, Rogers RS. Oral manifestations of erythema multiforme. Dermatol Clin. 2003 Jan;21(1):195–205.
  3. Staines KS, Felix DH, Forsyth A. Desquamative gingivitis, sole manifestation of tosylamide/formaldehyde resin allergy. Contact Dermatitis. 1998 Aug;39(2):90–90.
  4. Silvestre JF, Albares MP, Blanes M, Pascual JC, Pastor N. Allergic contact gingivitis due to eugenol present in a restorative dental material. Contact Dermatitis. 2005 Jun;52(6):341.
  5. Bystryn JC, Rudolph JL. Pemphigus. The Lancet. 2005 Jul;366(9479):61–73.
  6. Bagan J, Muzio L, Scully C. Number III Mucous membrane pemphigoid. Oral Dis. 2005 Jul;11(4):197–218.
  7. Oostingh G, Sitaru C, Kromminga A, Dormann D, Zillikens D. Autoreactive T cell responses in pemphigus and pemphigoid. Autoimmun Rev. 2002 Oct;1(5):267–72.
  8. Roopashree MR, Gondhalekar RV, Shashikanth MC, George J, Thippeswamy SH, Shukla A. Pathogenesis of oral lichen planus – a review: Pathogenesis of oral lichen planus. J Oral Pathol Med. 2010 Nov;39(10):729–34.
  9. Sinha AA. The Genetics of Pemphigus. Dermatol Clin. 2011 Jul;29(3):381–91.
  10. Mihai S, Sitaru C. Immunopathology and molecular diagnosis of autoimmune bullous diseases. J Cell Mol Med. 2007 May;11(3):462–81.
  11. Leuci S, Ruoppo E, Adamo D, Calabria E, Mignogna MD. Oral autoimmune vesicobullous diseases: Classification, clinical presentations, molecular mechanisms, diagnostic algorithms, and management. Periodontol 2000. 2019 Jun;80(1):77–88.
  12. Issrani R. Etiopathogenesis of Erythema Multiforme – A Concise Review. Adv Dent Oral Health [Internet]. 2017 Sep 6 [cited 2022 Aug 22];5(4). Available from:
  13. Sciuca AM, Toader MP, Stelea CG, Maftei GA, Ciurcanu OE, Stefanescu OM, et al. Desquamative Gingivitis in the Context of Autoimmune Bullous Dermatoses and Lichen Planus—Challenges in the Diagnosis and Treatment. Diagnostics. 2022 Jul 20;12(7):1754.
  14. Karagöz G, Bektaş Kayhan K, Ünür M. DESQUAMATIVE GINGIVITIS : A REVIEW. J Istanb Univ Fac Dent [Internet]. 2016 Apr 12 [cited 2022 Aug 22];50(2). Available from:
  15. Navarro CM, Sposto MR, Onofre MA, Scully C. Gingival Lesions Diagnosed as Pemphigus Vulgaris in an Adolescent. Case Report. J Periodontol. 1999 Jul;70(7):808–12.
  16. Romero W, Giesen L, Navajas-Galimany L, Gonzalez S. Erosive lichen planus: a therapeutic challenge. An Bras Dermatol. 2016 Feb;91(1):84–6.
  17. Lucchese A, Dolci A, Minervini G, Salerno C, DI Stasio D, Minervini G, et al. Vulvovaginal gingival lichen planus: report of two cases and review of literature. ORAL Implantol. 2016 Jun;9(2):54–60.
  18. Arduino PG, Broccoletti R, Sciannameo V, Scully C. A practical clinical recording system for cases of desquamative gingivitis. Br J Dermatol. 2017 Jul;177(1):299–301.
  19. Antonucci G, Gambino A, Carcieri P, Cabras M, Broccoletti R, Arduino PG. Use of an electric toothbrush in patients affected by autoimmune desquamative gingivitis: evaluation of biological parameters. Front Physiol [Internet]. 2019 [cited 2022 Aug 22];10. Available from:
  20. Saito A, Makiishi T. Chronic desquamative gingivitis and oral health-related quality of life. J Dermatol Case Rep. 2009 Nov 28;3(3):81.