Desquamative gingivitis (DG) is a descriptive term used to indicate epithelial desquamation, erythema, erosion, and/or vesiculobullouslesions of the attached and marginal gingiva that can progress to ulceration.DG can be localized ormore widespread and spread to alveolar mucosa.
DG occurs more often in females than males; approximately 80% of the patients are female.Most patients with DG are middle‐aged and older although rare cases have been observed in children.
Diseases Associated with Desquamative Gingival Lesions:
(R. J. Nisengard et al)
|Dermatoses (75-88%)||Oral Lichen Planus (OLP) (40-75%)|
CicatricialPemphigoid (CP) (9-45%)
Pemphigus Vulgaris (PV) (3-15%)
Erythema Multiforme (EM) (2%)
Graft-Versus-Host Disease (2%)
Lupus Erythematosus (2%)
Paraneoplastic Pemphigus (PNP) (1%)
EpidermolysisBullosaAcquisita (EBA) (1%)
Aphthous Ulcers, Behcet’s Syndrome (Sklavounou et al.)
|Endocrine imbalance||Estrogen deficiencies following oophorectomy and in postmenopausal womenTestosterone imbalanceHypothyroidism|
|Abnormal response to bacterial plaque|
|Chronic infections||Tuberculosis Chronic candidiasis Histoplasmosis|
|Irritant and allergic contact dermatitis||MouthwashesToothpastes (Sodium Lauryl Sulphate)Dental MaterialsCosmeticsChewing GumCinnamonDrugs: Barbiturates, Antibiotics|
|Conditions mimicking DG||Crohn disease Chronic ulcerative stomatitis Plasma cell gingivitis Grafts versus host disease Factitious lesions Kindler syndrome Wegener granulomatosis|
Epitope (determinant) spreading is the development of immune responses to endogenous epitopes secondary to the release of self-antigens during a chronic autoimmune or inflammatory response.
- Epitope spreading results from injuries in autoimmune dermatoses
- Intramolecular (intra-protein) epitope spreading: Pemphigus Vulgaris, Epidermolysis bullosaa quisita, Bullous pemphigoid
- (inter-protein) epitope spreading: Pemphigus vulgaris conversion to pemphigus foliaceus
- Epitope spreading results from injuries in inflammatory dermatoses and other inflammatory diseases:Lichen planus associated with BP
Reduced oral hygiene leads to accumulation of microorganism around the teeth in close proximity to the gingiva forming dental plaques.
This accumulation leads to release of proinflammatory cytokines such as IL-1 and TNF-α and leads to recruitment of inflammatory cells and periodontal inflammation upregulate matrix metalloproteases thatcauses breakdown of collagen and lead to loss of periodontal attachment and bone destruction.
Clinical Presentation of Desquamative Gingivitis:
Glickman &SmulowClassification of Severity:
|Occasional intolerance to hot and spicy foods||Burning sensation and sensitivity to temperature||Constant dry and burning sensation|
|Usually painless||Inhalation of air may bepainful||Very painful|
|Diffuse erythema. Some blanching may be seen.||Patchy distribution ofbright red and grayareas. Smooth, shiny, softGingiva Massaging the gingivaresults in peeling of theepithelium with bleedingon brushing.||Blowing of air causes a bubble in gingival epithelium|
Principle: In patients with active blistering, firm sliding pressure with a finger separates normal appearing epidermis, producing erosion.
Method: This is done by applying lateral pressure with the index finger which provides the shearing force to disrupt the intercellular adhesion in clinical Nikolsky’s sign. If the weakening of the intercellular adhesion is present but not marked, then the same shearing force may produce minimal damage at the cellular level which can be demonstrated only microscopically. As microscopic Nikolsky’s sign sometimes spans only a few cells, serial sections may be required to avoid missing a cleavage.
A typical Tzanck cell is a large round keratinocyte with a hypertrophic nucleus, hazy or absent nucleoli and abundant basophilic cytoplasm. The basophilic staining is deeper peripherally on the cell membrane (“mourning edged” cells) due to the cytoplasm’s tendency to get condensed at the periphery leading to a perinuclear halo.
A biopsy specimen should be obtained from all patients with desquamative gingivitis because the establishment of a correct diagnosis is critical, especially since the clinical characteristics are lessdistinct than those on elaborate skin.Immunofluorescence, both direct and indirect, should be performed for all patients where an autoimmune bullous disease is suspected both for diagnosis and possibly for monitoring of disease response to therapy.
Traditional Recommendations for gingival biopsy:
The biopsy specimen must be at least 3 mm with the first specimen taken from the edge of the erosion and must be formalin fixed and sent for routine histopathology. The second biopsy specimen should be perilesional, with the specimen being placed in transport medium and sent for direct immunofluorescence microscopic evaluation.
If a gingival biopsy is required, one should be careful to take the following steps into consideration:
- The specimen should be taken apical to the free gingival margin, since most marginal areas are inflamed and the inflammatory process may mask the histopathologic features necessary to establish the correct diagnosis.
- Local anesthesia is achieved being careful to avoid direct injection into the biopsy site to prevent hemorrhage, cellular distortion and epithelial disruption in the biopsy area.
- Often it is necessary to submit tissue samples for both histologic and direct immunofluorescence evaluation since the pathologic process may represent an autoimmune.
- Oral lichen planus has autoimmune properties found within lesions but lacks the systemic immunologic features confirming autoimmunity. Nevertheless, immunofluorescence studies of oral lichen planus may be indicated because a linear pattern of anti-fibrinogen at the basement membrane zone and the presence of immunoglobulins in cytoid bodies are supportive of the diagnosis.
- Other mucocutaneous diseases such as chronic ulcerative stomatitis, lichen planuspemphigoides, graft versus host disease, and discoid lupus erythematosus may mimic the clinical and histological features of oral lichen planus so DIF results may be of great value in supporting the diagnosis of OLP.
- Traditional biopsy protocol calls for incorporating lesional and perilesional tissue in the biopsy procedure. However in DG, lesional sites often have lost their surface epithelium and the perilesional area immediately adjacent to the lesion is extremely friable. This coupled with the trauma of the biopsy itself may result in epithelial sloughing and diagnostic failure. No significant difference in DIF findings between the perilesional area (within 1 cm of the lesion) (66.1%) and distant sites (beyond 1 cm of the lesions) (64.7%). Separate H&E and DIF biopsies are preferable to the traditional practice of splitting a single biopsy for the two analyses.
- Traditional Punch biopsy
- Stab-and-roll biopsy
Transport Medium for Immunoflourescence:
- 0.9% Nacl in liquid nitrogen
- Michel’s medium: Buffer 0.81gm Potassium Citrate, 0.0625 gm N-ethylmaleimide, 0.123 gm Magnesium Sulphate in100 ml distilled water and 55 gm of Ammonium Sulphate is added and allowed to dissolve before use. pH is adjusted to 7.0-7.2 with 1M KOH.
- Direct Immunoflourosence (DIF): DIF is a one step histological procedure to identify in vivo antibodies bound to tissue antigen. The tissue sample is overlaid with fluorescein isothiocyanate (FITC) conjugates with antiIgM, antiIgG, antiIgA, antiC3 and anti-fibrin.
- Indirect Immunoflourosence (IIF): IIF is a two step technique for detection of circulating antibodies in body fluid. Tissue substrate is allowed to react in serially diluted patient serum and overlaid with FITC conjugates. Control sera of known positive and negative antibody reactivity are tested simultaneously.
- Salt split Technique
- Antigen Mapping Method
- Double Staining Method
- Complement binding indirect Immunoflourosence : It is a three step technique in which normal tissue substrate is incubated in plasma which has been heated in 56°C to destroy the complement fixing activity of antigen-antibody complex. Then the tissue substrate is incubated in fresh serum and the antigen antibody bund in first step can activate complement that give rise to numerous C3 molecules bound to the antigen antibody complex. The tissue substrate is then incubated in fluorescein antihmanC3 antibody.
Recommended article Get to know about periodontal diseases