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Desquamative gingivitis 5th seminar

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desquamative gingivitis

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Desquamative gingivitis 5th seminar

  1. 1. DESQUAMATIV E GINGIVITIS D.Hema PG-I Dept. of Periodontics
  2. 2. CONTENTS Introduction Definition History Epidemiology Classification Epithelial Biology Etiology Pathogenesis Clinical presentation Clinical features Diseases that Present Clinically as Desquamative Gingivitis Effect of desquamative gingivitis on periodontal status Diagnosis of Desquamative Gingivitis: A Systematic Approach Management Conclusion References 3
  4. 4. Periodontal therapy involves not only the tx of plaque induced diseases but also varous nonplq induced conditions. And one of those conditions is desquamative gingivitis. Periodontal therapy involves not only the diagnosis and treatment of plaque associated diseases but also various non plaque related diseases. The International workshop for classification of periodontal diseases and conditions noted that the periodontist may be called upon to manage these non-plaque related mucocutaneous disorders either alone or as a part of treatment team consisting of physicians, dentists or other allied health care professionals. Among the oral manifestations which have long baffled dentists, chronic desquamative gingivitis is one of the most interesting and persistent
  5. 5. • Desquamation  from Latin desquamare, 'to scrape the scales off a fish‘  skin peeling,  shedding of the outermost membrane or layer of a tissue, such as the skin or mucosa. 6
  6. 6. DEFINITIO N • “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.” 7
  7. 7. HISTOR Y 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. 8
  8. 8. 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. 9Oles, R.D. Chronic desquamative gingivitis. J Periodont 38:485 Nov-Dee
  9. 9. EPIDEMIOLO GY Disorder Incidence Mucous membrane pemphigoid 35-48% Oral lichen planus 24- 45% Pemphigus vulgaris 3-15% Lupus erythematous 7.6 – 40% 10
  10. 10. CLASSIFICATI ON Based on etiological considerations, desquamative gingival lesions are classified as (modified classification of McCarthy and others) Dermatoses Lichen planus Cicatricial pemphigoid Bullous pemphigoid Pemphigus vulgaris Psoriasis Linear IgA disease 11
  11. 11. Endocrinal imbalance Estrogen deficiency in females (menopause, following hysterectomy and oopherectomy) Testosterone deficiency in males Chronic infections Tuberculosis Chronic candidiasis Histoplasmosis 12
  12. 12. Idiopathic Drug reactions (lichenoid reactions) • Toxic antimetabolites • Allergic- barbiturates, antibiotics etc Conditions mimicking DG • Crohn disease • Chronic ulcerative stomatitis • Plasma cell gingivitis • Grafts versus host disease • Factitious lesions • Kindler syndrome • Wegener granulomatosis • Foreign body gingivitis 13
  13. 13. Glickman & Smulow: 3 forms of desquamative gingivitis Mild Moderate Severe 14
  14. 14. EPITHELIAL BIOLOGY The integrity of oral epithelium is mainly dependent on the cells and the cellular junctions. Cellular junctions: 1. Occluding junctions 2. Communicating junctions 3. Anchoring junctions: • Cell-cell: Desmosomes Adherens junction • Cell-matrix: Hemidesmosomes Focal adhesions KV Arun. Molecular biology of periodontium. 1st Ed. 2010.
  15. 15. Desmosomes: • Cadherins: desmoglein, desmocollin • Catenins: desmoplakin, plakoglobin, plakophillin Garrod et al. Desmosome structure, composition and function. Biochimica et Biophysica Acta 1778 (2008) 572–587
  16. 16. Hemidesmosomes Mihai et al. Immunopathology and molecular diagnosis of autoimmune bullous diseases. J. Cell. Mol. Med. Vol 11, No. 3, 2007 pp. 462-481
  17. 17. ETIOLOGY • Various etiological factors contribute to the development of desquamative gingivitis. • Encompass autoimmune/immune mediated, infectious, neoplastic, hematologic, reactive, nutritional and idiopathic causes. • Approximately, 50% of oral mucosal diseases are localized to gingiva causing desquamative gingivitis, although other intraoral and extraoral sites may be involved. S. Sangeetha et al. The molecular aspects of oral mucocutaneous diseases: A review. International Journal of Genetics and Molecular Biology Vol. 3(10), pp. 141-148, November 2011
  18. 18. R. J. Nisengardt and R. S. Rogers. The Treatment of Desquamative Gingival Lesions. 19
  19. 19. PATHOGENESI S • An immunologic phenomenon has been recognized as an important pathogenic mechanism responsible for the initiation and/or progression of autoimmune diseases such as mucocutaneous lesions.  Epitope spreading. • Epitope spreading  the development of immune responses to endogenous epitopes secondary to the release of self antigens during a chronic autoimmune or inflammatory response. S. Sangeetha et al. The molecular aspects of oral mucocutaneous diseases: A review. International Journal of Genetics and Molecular Biology Vol. 3(10), pp. 141-148, November 2011
  20. 20. Intraepithelial lesions Target antigens of desmosomes implicated in intraepithelial lesions:
  21. 21. Subepithelial lesions Proteins Diseases BP 230 Cicatricial pemphigoid BP 180 Cicatricial pemphigoid, bullous pemphigoid α6, β4 Cicatricial pemphigoid, junctional epidermolysis bullosa Laminin 5 (epiligrin) Cicatricial pemphigoid, junctional epidermolysis bullosa Type VII collagen Epidermolysis bullosa dystrophica, Epidermolysis bullosa acquisita Target antigens of hemidesmosomes implicated in subepithelial blistering disorders (Bagan, 2005).
  22. 22. Intrepithelial/subepithelial clefts acantholysis/dissolution of ep- basal lamina junc. Activates immune system (complement, attracts immune cells). Formation of Ag-Ab complexes intercellulary or at the ep-basal lamina interface. Auto-antibodies formed against self-Ag.
  23. 23. CLINICAL PRESENTATION 24 • 1.5–2.5% of population. • females > males. • 3rd or 4th decade of life (can be seen in younger individuals). • Asymptomatic; when symptomatic their complaints range from burning sensation to severe pain.
  24. 24. CLINICAL FEATURES Mild Form Diffuse erythema. Condition is usually painless. Some blanching may be seen. Patients may complain of intolerance to hot and spicy foods. 25
  25. 25. Moderate Form Patchy distribution of bright red and gray areas. Smooth, shiny, soft gingiva. Burning sensation, sensitivity to temperature. Inhalation of air may be painful. Massaging the gingiva results in peeling of the epithelium with bleeding on brushing. 26
  26. 26. Severe Form Wide areas of the oral cavity involved. Surface epithelium appears shredded. Blowing of air causes a bubble in gingival epithelium. Very painful. Constant dry, burning sensation. 27
  28. 28. Lichen Planus 31  Immunologically mediated mucocutaneous disorder, T-cells trigger apoptosis of epithelial cells.  Mostly seen: Middle aged & older women.  The skin lesions of LP appear as small , angular, flat topped papules.  Oral lesions: 1. Reticular 2. Patch 3. Atrophic 4. Erosive 5. Bullous most common reticular & erosive
  29. 29. Reticular: •Asymptomatic & B/L. •Has interlacing white lines on erythematous background. Whickams striae •Involves buccal mucosa, lateral & dorsal aspects of tongue, hard palate, alveolar ridge, gingiva. Erosive: •Painful •Atrophic, erythematous & ulcerated areas with fine white radiating striae at the borders, •Sensitive to heat, acid & spicy foods. 32
  30. 30. Gingival Lesions: Approx. 7% to 10% of patients with OLP. Four distinctive patterns: Keratotic lesions: raised white lesions, papules/ linear- reticular lesions/ plaquelike configurations. Erosive/ ulcerative lesions: Extensive erythematous areas patchy distribution focal or diffuse Vesicular / bullous lesions: raised, fluid-filled lesions uncommon and short lived quickly rupture Atrophic lesions: Atrophy of tissues epithelial thinning erythema confined to the gingiva.
  31. 31. Histopathology: • Hyperkeratosis, • Hydropic degeneration of the basal layer, • Saw-tooth rete pegs; • Lamina propria exhibits dense, bandlike infiltrate primarily of T lymphocytes; • Civatte bodies colloid bodies seen at ep.-CT interface • E/M: separation of basal lamina from basal layer
  32. 32. Immunopathology: DIF: linear fibrillar (“shaggy”) deposits of fibrin in the basement membrane zone, • scattered immunoglobulin staining cytoid bodies in the upper areas of the lamina propria. IIF: negative. Differential Diagnosis: • Lichenoid mucositis • Oral lichen planus of gingival tissues without white striations MMP, PV • less common possibilities  linear IgA disease and chronic ulcerative stomatitis.
  33. 33. • Mild cases: use of vacuum-formed custom trays Rx: Lidex (0.05% fluocinonide) gel Rx: Nystatin oral pastilles (100,000 IU) • Recalcitrant cases: Rx: Protopic (0.1% tacrolimus) ointment • Severe or refractory cases: Intralesional injections of triamcinolone acetonide (10 to 20 mg) or short-term regimens of 40 mg prednisone daily for 5 days followed by 10 to 20 mg daily for an additional 2 weeks. Antifungal therapy. Treatment
  34. 34. Pemphigoid The term pemphigoid  number of cutaneous, immune mediated, subepithelial bullous diseases that are characterized by a separation of the basement membrane zone. 1. Bullous pemphigoid NON-SCARRING 2. Mucous membrane pemphigoid SCARRING 3. Pemphigoid (herpes) gestations
  35. 35. Bullous Pemphigoid: 38 • Chronic, autoimmune, subepidermal bullous disease with tense cutaneous bullae that rupture and become flaccid. • Oral Lesions:  Reported to occur secondarily in up to 40% of cases.  Gingiva- Erythematous and Desquamate  Painful.  Negative Nikolsky sign Coalescing cutaneous bullae Rupture serpiginous ulcers.
  36. 36. 39 • Subepithelial clefting with epithelial separation from the underlying lamina propria, leaving an intact basal layer. • No evidence of acantholysis. Histopathology: • Characterized by: 1. Immunoglobulin G (IgG) Complement 3 (C3) immune deposits along the epithelial basement membranes. 2. Circulating IgG antibodies to the epithelial basement membrane. • DIF + in 90% to 100% of patients • IIF + in 40% to 70% of patients. Immunofluorescence:
  37. 37. Treatment:  Designed to control its signs and symptoms.  Primary Tx moderate dose of systemic prednisone.  Steroid-sparing strategies  • prednisone plus other immunomodulatory drugs • used when high doses of steroids are needed or when the steroid alone fails to control the disease.  For localized lesions high-potency topical steroids or tetracycline with or without nicotinamide can be effective.
  38. 38. Mucous Membrane Pemphigoid (Cicatricial Pemphigoid): 41 • A chronic vesiculo-bullous autoimmune disorder of unknown cause. • Predominantly affects women, fifth decade of life. • Rarely been reported in young children. • Involves the oral cavity, the conjunctiva, mucosa of the nose, vagina, rectum, esophagus, and urethra. 20% cases showed skin involvement. • Five subtypes: 1. oral pemphigoid, 2. anti-epiligrin pemphigoid, 3. anti-BP antigen mucosal pemphigoid, 4. ocular pemphigoid, 5. multiple-antigens pemphigoid.
  39. 39. Pathogenesis of the lesion Attraction of PMNs to the area Elaboration of chemotactic factors Complement activation Antigen/antibody complexing at the BMZ Release of proteolytic enzymes that ultimately dissolve or cleave the basement membrane zone, usually at the lamina lucida level (Eversole, 1994). 2 major antigenic determinants: bullous pemphigoid 1 and 2 (BP1 and BP2). epiligrin (laminin-5), and β4 integrins.
  40. 40. Ocular Lesions: • The initial lesion is characterized by unilateral conjunctivitis that becomes bilateral within 2 years. • Symblepharon: adhesions of eyelid to eyeball. • Ankyloblepharon: Adhesions the edges of the eyelids may leading narrowing of the palpebral fissure. • Small vesicular lesions may develop on the conjunctiva, which may eventually produce scarring, corneal damage, and blindness.
  41. 41. • Presence of desquamative gingivitis, typically with areas of erythema, desquamation, ulceration, and vesiculation of the attached gingiva. • The bullae tend to have a relatively thick roof • Rupture within 2 to 3 days, leaving irregularly shaped areas of ulceration. • Healing of these lesions may take 3 weeks or more. Oral Lesions: Lesions are confined to the gingival tissues, where they produce a typical desquamative gingivitis appearance
  42. 42. • Subepithelial clefting with epithelial separation from the underlying lamina propria, leaving an intact basal layer. • A mixed inflammatory infiltrate (i.e., lymphocytes, plasma cells, neutrophils, and scarce eosinophils) is observed in the underlying fibrous connective tissue. Histopathology: Immunofluorescence • DIF: Linear deposits of C3 with or without IgG at the basement membrane zone in almost all cases. • C3 deposits confined along the basement membrane. • IIF: Basement membrane zone (IgG) antibodies in 10% of cases
  43. 43. Treatment: • Mild cases: • Rx: Lidex (0.05% fluocinonide) gel • Rx: Temovate (0.05% clobetasol propionate) TID for 6 months. • Severe or refractory cases: Refer to dermatologist for management with prednisone (20 to 30 mg/day); • concomitant use of azathioprine may be needed; dapsone, sulfonamide, and tetracycline are other alternatives • High risk: IV ig
  44. 44. Pemphigus Vulgaris • A group of autoimmune bullous disorders that produce cutaneous and mucous membranes blisters. • Other types: pemphigus foliaceus, pemphigus vegetans, pemphigus erythematosus. • potentially lethal chronic condition 10% mortality rate. • Female predilection, after 4th decade. • Also been reported in unusually young children and newborns.
  45. 45. Pathogenesis of PV • Circulating autoantibodies are responsible for disruption of intercellular junctions and loss of cell-cell adhesion. • Auto antibodies directed against desmoglein 3ORAL; DSG1CUTANEOUS. • Early studies implicated complement in the acantholysis which follows antibody binding (Jordan et al., 1974; Kawana et al., 1984,1985). • Plasminogen activator (PA) production by keratinocytes has been implicated in acantholysis. (Hashimoto et al., 1983; et al., 1985), Pemphigus foliaceus-Antibodies directed against Dsg 1 (Hashimoto al., 1990; Calvanico et al., 1991) Drug-induced pemphigus.Penicillamine and captopril can produce. Paraneoplastic pemphigus antigenically distinct from pemphigus vulgaris, and it is associated with underlying malignancies
  46. 46. Intraoral manifestations • Intraepithelial separation • Bullae soon rupture-Painful erosions with ragged borders. • Gingival lesions can occur and, along with other oral lesions, may represent the first manifestations of the disease. • Positive Nikolsky’s sign Orlowski WA et al, J Periodontol 1983, Markitziu A et al Oral Surg Oral Med OralPathol 1983
  47. 47. Histologic Features • Intraepithelial clefting” • Acantholysis and suprabasilar bullae formation. • Basal cells lining the floor of the bullae-"tombstone" pattern • Acantholytic keratinocytes (Tzank cells) - blister fluid. • Dense mononuclear lymphocytic infiltration.
  48. 48. Immunofluoroscence: DIF • Intercellular deposits in the epithelium; IgG in all cases and C3 in most cases. • Chicken wire” or “fish net” appearance. IIF • Less sensitive • Helpful in monitoring the disease
  49. 49. D/D: If the oral lesions of pemphigus vulgaris are restricted to the gingival tissues, then erosive lichen planus, pemphigoid, LAD, and chronic ulcerative stomatitis should be ruled out. Treatment:
  50. 50. Chronic Ulcerative Stomatitis first reported in 1990. clinically presents with chronic oral ulcerations. predilection for women during 4th decade of life. Oral Lesions: • Painful • solitary small blisters and erosions with surrounding erythema • mainly on the gingiva and the lateral border of the tongue. • The buccal mucosae and hard palate may also present similar lesions
  51. 51. Histopathology: • Hyperkeratosis, acanthosis, liquefaction of the basal cell layer with areas of subepithelial clefting. • The underlying lamina propria exhibits a lymphohistiocytic chronic infiltrate in a bandlike configuration. Immunofluorescence: DIF • typical stratified epithelium–specific antinuclear Ab. • nuclear deposits of IgG with a speckled pattern, basal cell layer of epithelium. • fibrin deposits at the epithelial- connective tissue interface. IDIF • presence of stratified epithelium– specific antinuclear antibodies.
  52. 52. Treatment: • Mild cases topical steroids (e.g., fluocinonide, clobetasol propionate) topical tetracycline • For severe cases a high dose of systemic corticosteroids • Recalcitrant cases Hydroxychloroquine sulfate 200-400 mg/ day
  53. 53. Linear Immunoglobulin A Disease • linear IgA dermatosis • Uncommon mucocutaneous disorder with female predilection. • Etiology: drug-induced LAD triggered by ACE inhibitors has been reported. • Clinical presentation:  Pruritic vesiculobullous rash.  Characteristic plaques/ crops with an annular presentation surrounded by a peripheral rim of blisters affect the skin.  Mucosal involvement ranges from 50% to 100% of the cases published.  Mimic lichen planus both clinically and histologically.
  54. 54. 57 Oral Lesions: • vesicles, painful ulcerations or erosions, and erosive gingivitis or cheilitis. • Hard and soft palates > tonsillar pillars > buccal mucosa > tongue > gingiva. • Rarely, oral lesions may be the only manifestation of LAD. • oral lesions of LAD have been clinically reported as desquamative gingivitis.
  55. 55. Immunofluorescence: Linear deposits of IgA are observed at the epithelial–connective tissue interface. Differential Diagnosis: includes erosive lichen planus, chronic ulcerative stomatitis, pemphigus vulgaris, bullous pemphigoid, and lupus Microscopic examination and immunofluorescence studies are necessary to establish the correct diagnosis. Treatment: The primary treatment combination of sulfones and dapsone. Small amounts of prednisone (10 mg/day to 30 mg/day). OR tetracycline (2 g/day) + nicotinamide (1.5 g/day). Refractory ulcerations Mycophenolate (1 g twice daily) + prednisolone (30 mg daily).
  56. 56. Dermatitis Herpetiformis • chronic condition that usually develops in young adults between the ages of 20 and 30 years. • Male predilection • Currently, evidence indicates that it is a cutaneous manifestation of celiac disease. • Etiology: tissue transglutaminase seems to be the autoantigen in the intestine, the skin, and sometimes the mucosae celiac disease.
  57. 57. Clinically: Bilateral and symmetric pruritic papules/vesicles Oral lesions: range from painful ulcerations preceded by the collapse of ephemeral vesicles or bullae to erythematous lesions.
  58. 58. Histopathology: focal aggregates of neutrophils and eosinophils among deposits of fibrin at the apices of the dermal pegs. Immunofluorescence: DIF IgA and C3 are present at the dermal papillary apices. 80% of patients have anti-endomysial and gliadin antibodies. Treatment: A gluten-free diet celiac disease and dermatitis herpetiformis. Oral dapsone to alleviate symptoms promptly.
  59. 59. Lupus Erythematosus Lupus erythematosus is an autoimmune disease with three different clinical presentations: 1. systemic, 2. chronic cutaneous, 3. Subacute cutaneous.
  60. 60. Systemic Lupus Erythematosus: • Females 10 : 1 • Affects kidneys, skin and mucosa • Fever, weight loss and • arthritis • Oral lesions are present in up to 40% of patients. • malar area with a distribution rash
  61. 61. Oral lesions: • hyperkeratotic plaques reminiscent of lichen planus appear on the buccal and palate. Immunofluorescence: • Ig and C3 deposits at the dermal–epidermal interface. • Antinuclear antibodies of cases, • deoxyribonucleic acid and extractable nuclear antigen antibodies 50% of patients
  62. 62. • Has no systemic signs or symptoms, lesions limited to the skin / mucosa. • chronic scarring, atrophy- producing lesion that may develop into hyper/hypo pigmentation or of the healing area. • In the oral cavity, lichen- planus–like plaques on the palate and the buccal mucosa. • The gingiva may be affected and present clinically as desquamative gingivitis. Chronic Cutaneous Lupus Erythematous/ DLE:
  63. 63. Histopathology: hyperkeratosis, Alternating acanthosis and atrophy, hydropic degeneration of the basal layer of the epithelium. lamina propria  chronic inflammatory cell infiltrate similar to that observed with lichen planus. Immunofluorescence: Same as SLE
  64. 64. Subacute Cutaneous Lupus Erythematosus: • similar to DLE but lack the development of scarring and atrophy.
  65. 65. Treatment: • depends on the severity and extent of the disease; • range from topical steroids to NSAIDS, • For chronic cutaneous lupus erythematosus: topical steroids cutaneous and oral lesions. • for severe systemic organ involvement:  moderate to high doses of prednisone.  Immunosuppressive drugs (e.g., cytotoxic agents such as cyclophosphamide and azathioprine)  plasmapheresis alone or with steroids.  rituximab  long-term remissions. • For patients who are resistant to topical therapy: systemic antimalarial drugs may be used, with good results
  66. 66. Erythema Multiforme Acute bullous and macular inflammatory mucocutaneous disease. young adults (20 and 40 years) Etiology: Allergic/hypersensitivity reactions. Medications Bacterial or viral infections Other triggers-Benign and malignant tumours, Crohns disease, sarcoidosis and infective mononucleosis Etiopathology: Deposition of immune complexes in the superficial microvascular supply of skin and mucosa (type II Immune reaction) / Cell mediated immunity (type IV). Complement fixation→ Leukocytic destruction of vascular walls and small vessel occlusion.→ Ischemic necrosis of the epithelium & connective tissue.
  67. 67. Clinical features: • mild condition (EM minor) • severe and possibly life- threatening condition (EM major or Stevens–Johnson syndrome). • An underdiagnosed type of erythema multiforme is the oral form • Target or “iris” lesions with central clearing are the hallmark of erythema multiforme.
  68. 68. Oral lesions: • multiple large, shallow, painful ulcers with an erythematous border. • chewing and swallowing are impaired. • buccal mucosa > tongue > labial mucosa > floor of the mouth > hard and soft palates > gingiva. • Lesions confined to gingiva presenting as DG are rare. • Hemorrhagic crusting of the vermilion border of the lips may occur.
  69. 69. Histopathology: • liquefaction degeneration of ep. • intraepithelial microvesicles • without the acantholysis (pemphigus). • hyperplasia, and necrotic keratinocytes • Degenerative changes basement membrane. • lamina propria is indistinct because of a dense inflammatory cell infiltrate & Edema
  70. 70. Immunofluorescence: NEGATIVE Treatment: no specific treatment for erythema multiforme. For mild symptoms systemic and local antihistamines topical anesthetics debridement of lesions with an oxygenating agent are adequate. In patients with bullous or ulcerative lesions and severe symptoms corticosteroids are considered the drug of choice, although their use is controversial and not completely accepted
  71. 71. Drug Eruptions • Drug  allergen:sensitizes the tissues. • Stomatitis medicamentosa: Eruptions in the oral cavity that result from sensitivity to drugs that have been taken by mouth or parenterally. • Stomatitis venenata / contact stomatitis: The local reaction from the use of a medicament in the oral cavity (e.g., stomatitis as a result of topical penicillin use). • Manifestations: multiform.  Vesicular and bullous lesions  pigmented / nonpigmented macular lesions  Erosions deep ulceration with purpuric lesions.  seen in different areas of the oral cavity, with the gingiva often being affected.
  72. 72. • Development of gingival lesions caused by contact allergy: Mercurial compounds in dental amalgam. Pyrophosphates and flavoring agents like cinnamon in tartar control toothpastes. • Intense erythema of the attached gingival tissues Comparitive of plasma cell gingivitis. Management: • clinical history source of the gingival disturbance. • Elimination of the offending agent  resolution of the gingival lesions within a week, • If removal of the offending medication is not possible, topical corticosteroids and topical tacrolimus can be used to treat the lesions.
  73. 73. Miscellaneous Conditions that Mimic Desquamative GingivitisHeterogeneous conditions that may masquerade as desquamative gingivitis.  Factitious lesions,  candidiasis,  Graft versus- host disease,  Wegener’s granulomatosis,  foreign body gingivitis,  Kindler syndrome,  squamous cell carcinoma
  74. 74. Effect of desquamative gingivitis on periodontal status • From a theoretic point of view, disorders causing DG may have potential harmful outcomes on the development and progression of plaque- related periodontal disease. • These potential injuries may be related to both direct and indirect relationships.  Indirect effect: symptomps associated with DG prevent proper oral hygiene  plaque  periodontal disease.  Direct effect: may also be plausible based on the possible shared pathogenetic mechanisms ⁄ mediators. • Ramon-Fluixa et al, 1999: observed that no significant differences were present between an OLP group of patients and a control group with regard to different periodontal indices. • Akman et al, 2008: periodontal status is worse in patients affected by pemphigus vulgaris (PV). L Lo Russo et al. Effect of desquamative gingivitis on periodontal status: a pilot study. Oral Diseases (2010) 16, 102–107.
  75. 75. Diagnosis of Desquamative Gingivitis: A Systematic Approach • Desquamative gingivitis is only a clinical term and not a diagnosis per se. • The following discussion represents a systematic approach to elucidate the disease that is triggering desquamative gingivitis:  Clinical History  Clinical Examination  Biopsy  microscopic examination  immunofluoroscence  Management
  76. 76. Clinical History Complete data regarding symptoms associated with the condition as well as historical aspect. • When did it start (acute or chronic)? • Aggrevating & alleviating fators? • Are the lesions recurrent? If yes, how often do they recur? • How long does it take for each lesion to heal? • Extraoral involvement? • has patient had fever, malaise, lymphadenopathy? (positive response may indicate an infections agent) • are there are any other systemic problems? • Medications being used? • Family history
  77. 77. Clinical Examination • Recognition of pattern of disease: focal/multifocal • If only gingiva involved other areas also. Nikoliskys sign –slight rubbing of the skin results in exfoliation of the outermost layer, forming a blister within minutes. +  Pemphigus, MMP -  lichen planus, BP Asboe-Hansen sign: extension of a blister to adjacent unblistered skin when pressure is put on the top of the bulla. Kobners phenomenon: appearance of lesion along the line of trauma/injury. LP, SLE, Psoriasis Auspitz sign: Psoriasis
  78. 78. Biopsy • Incisional biopsy is best to begin microscopic and immunological evaluation. • A perilesional biopsy should avoid areas of ulcerations because necrosis and epithelial denudation hamper diagnostic process. • Mostly perilesional tissues also show immunoflourescence. • In some lesions such as lichen planus, subacute lupus erythematosus only lesion tissue can be used.
  79. 79. H&E staining and light microscopic Immunoflourescence For direct Immunoflourescence : Unfixed frozen sections are incubated with a variety of flourescein labelled anti - human serum (antiIgG, antiIgA, anti IgM, anti- fibrin, anti- c3 etc.,) Indirect Immunoflourescence : Unfixed frozen section from oral or esophageal animal mucosa are first incubated with the patients serum to allow attachment of any serum antibodies to mucosa MICROSCOPIC EXAMINATION
  80. 80. After the diagnosis is established, the dentist must choose the optimum management for the patient. This is accomplished in accordance with three factors: (1) the practitioner’s experience; (2) the systemic impact of the disease; (3) the systemic complications of the medications. Overview Of Management Elimination of potential factors Suppressing the inflammatory reaction Using specific therapies for the underlying diseases Management of lesions by:
  81. 81. Drug therapy has included corticosteroids Antibiotics Immunosuppresive agents Intravenous Immunoglobulis Hormonal therapy Vitamins
  82. 82. Corticosteroids: Impair immunological competence. Suppress hypersensitisation and allergic phenomena Suppress recruitment of leucocytes at sites of contact with Ag. Regulation of protein synthesis Transcription of specific mRna binding to specific sites on the chromatin Migration into the nucleus Structural changes in steroid receptor complex Binds to a high affinity cytoplasmic receptor protein Corticosteroid penetrates cells MOA at cellular level
  83. 83. Topical Corticosteroids : Triamcinolone, Fluocinonide ,Clobetasol gel Beclomethasone dipropionate spray (inhaler) Hydrocortisone hemi succinate Topical creams or pastes in suitable customized tray or veneer (Carozzo et al;Northwood:Sci reviews 1996) Systemic corticosteroids Prednisone 10-40 mg. Long-term complications (steroid)  Osteoporosis, impaired wound healing  Premature cataract formation  Behavioral changes  Chemically-induced diabetes mellitus, HTN  Infections  Myopathy and muscle wasting, weight gain  Gastric ulceration and bleeding.  Suppression of HPA axis adrenal crisis impaired stress response
  84. 84. Immunosuppressive agents : Cyclosporine, Griseofulvin, Azathioprine , Methotrexate, Cyclophosphamide (Lever WF.et al . Am J Dermatopathol 1979; GorlinRJ et al . Gerodontics 1985) Drug Combinations Prednisone + Azathioprine or cyclophosphamide. Additional immunoregulatory benefit & Steroid-sparing properties Tetracycline Anticollagenase effects Inhibit PMN chemotaxis and random PMN migration. Inhibit complement-induced inflammatory responses to BM antigen- antibody complexes Help maintain the cohesion of the epithelial connective tissue junction. Systemic doxycycline improves Dg in LP (Ronbeck Oral surg Oral Med Oral Path oral radiol Endodontic 1990)
  85. 85. Intravenous Immunoglobulins: • Proved successful and safe in steroid-resistant PV. (Mobini et al., 1995; Bewley and Keefe, 1996; Bystryn and Steinman, 1996; Sibaud et al., 2000) Hormonal therapy: • Ziskin, 1937: established the ability of estrogen to stimulate connective tissue & to produce hyperkeratinization and hyperplasia of the oral epithelium. • He also showed that testosterone propionate produces a stimulating action on epithelium and connective tissue with a resultant benefit to the gums. • Yih et al: do not support the use of estrogen in the treatment of idiopathic CDG, might be because the ER expression in the gingiva is probably not related to the presence or absence of estrogen as well as the side effects of estrogen. Other Drugs: • Gold (Penneys et al., 1976; Salomon and Saurat, 1986), • Etretinate (Orfanos and Bauer, 1983), • prostaglandin E2 (Morita et al., 1995),
  86. 86. Plasmapheresis: Selective removal of large volumes of plasma which includes antibodies. used for tx of bullous pemphigoid, epidermolysis bullosa acquisita, lupus erythematosus, and pemphigus. Photopheresis: Extracorporeal photopheresis involves the exposure of the patient's mononuclear cells to 8-methoxypsoralen and ultraviolet A light to induce apoptosis of the T-cells.
  87. 87. Other tx: - proteinase inhibitors (Dobrev et al., 1996), -chimeric molecules for specific recognition and elimination of the autoimmune B-cells (Proby et al., 2000), -suggestions for targeting Dsg 3-specific T-cells for the eventual modulation of the T-cell-dependent production of pathogenic autoantibodies (Hertl and Riechers, 1999), -suggestions for a novel avenue for the development of a steroidal treatment for using the anti-acantholytic activity cholinergic agonists (Grando, 2000)
  88. 88. Control of dental plaque and local irritants (Damoulis PD et al J Periodontol 2000). Oral hygiene maintainance using soft brush with gentle brushing, use of floss or waterpik, & antiseptic mouth rinses. Caustic mouthwashes avoided. Dietary changes with avoidance of spicy food. Emphasis on oral hygiene, along with frequent SRP Multidisciplinary consultation Periodontal therapy : during periods of remission or if condition is not vesicular. Doubling of systemic steroid therapy to avoid adrenal shock during stressful periodontal treatment. Prophylactic antibiotics must be prescribed. Antifungals to prevent candidiasis Periodontal Management
  89. 89. TREATMENT OF DESQUAMATIVE GINGIVITIS WITH FREE GINGIVAL GRAFT 97 Comparison of surgical side(rt) with medication therapy side (lt) Recurrence of desquamation After 9 months Mehdi Vatankhah et al. Treatment of Desquamative Gingivitis with Free Gingival Graft: A Case Report. Dent Res Dent Clin Dent Prospect 2010; 4(1):33-36
  90. 90. Treatment of DG with tissue engineered human cultured gingival epithelial sheets. Okuda K1, Momose M, Murata M, Saito Y, lnoie M, Shinohara C, Wolff LF, Yoshie H. Treatment of chronic desquamative gingivitis using tissue-engineered human cultured gingival epithelial sheets: a case report. Int J Periodontics Restorative Dent. 2004 Apr;24(2):119-25.
  91. 91. Yilmaz HG, Kusakci-Seker B, Bayindir H, Tözüm TF. Low-Level Laser Therapy in the Treatment of Mucous Membrane Pemphigoid: A Promising Procedure. J Periodontol. 2010 Aug;81(8):1226-30. Treatment of DG with LLLT• A patient presented with MMP was successfully treated with the application of local corticosteroids and LLLT using an 810-nm diode laser. • The lesions were treated by LLLT over a period of 7 days using a continuous waveform for 40 seconds and an energy density of 5 J/cm2. Clinical condition at 12 months after LLLT. Clinical condition at 1 week after at the first visit LLLT may improve healing after the application of a local corticosteroid for a period of 12 months.
  92. 92. CONCLUSIO N In patients with suspicious desquamative lesions of the gingiva, it is imperative to establish a definitive diagnosis via histopathologic and immunologic findings. The goal of treatment should focus on eradication of the lesions prior to any periodontal therapy, following a conservative approach. These diseases may not be limited to the oral cavity, and it is crucial that appropriate consultations are made to ensure optimal patient care. The Periodontist has a unique opportunity to make the diagnosis and then refer the patient to a medical specialist for treatment. Thus a thorough understanding of these conditions is necessary so as to provide complete care to our patients . 100
  93. 93. REFEREN CES 101 • Newman Takei, Klokkevold Carranza. Desquamative Gingivitis. Carranza’s Clinical Periodontology. 12th ed. • Oles, R.D. Chronic desquamative gingivitis. J Periodont 38:485 Nov-Dec 1967. • R. J. Nisengardt and R. S. Rogers. The Treatment of Desquamative Gingival Lesions. J Periodontol. 1987 Mar;58(3):167-72 • NA Robinson,D Wray. Desquamative gingivitis: A sign of mucocutaneous disorders – a review. Australian Dental Journal 2003;48:4. • Gizem KARAGÖZ, Kıvanç BEKTAŞ-KAYHAN, Meral ÜNÜR. DESQUAMATIVE GINGIVITIS: A REVIEW. Istanbul Univ Fac Dent 2016;50(2):54-60.
  94. 94. • Garrod et al. Desmosome structure, composition and function. Biochimica et Biophysica Acta 1778 (2008) 572–587. • KV Arun. Molecular biology of periodontium. 1st Ed. 2010. • Mihai et al. Immunopathology and molecular diagnosis of autoimmune bullous diseases. J. Cell. Mol. Med. Vol 11, No. 3, 2007 pp. 462-481 • S. Sangeetha et al. The molecular aspects of oral mucocutaneous diseases: A review. International Journal of Genetics and Molecular Biology Vol. 3(10), pp. 141-148, November 2011 • Floris van Minden. Use of female sex hormone in the treatment of chronic desquamative gingivitis. J Am Dent Assoc. 1946 Oct;33:1294-7 • Yih WY, Richardson L, Kratochvil FJ, Avera SP, Zieper MB. Expression of estrogen receptors in desquamative gingivitis. J Periodontol. 2000 Mar;71(3):482-7.
  95. 95. • L Lo Russo et al. Effect of desquamative gingivitis on periodontal status: a pilot study. Oral Diseases (2010) 16, 102–107. • Mehdi Vatankhah et al. Treatment of Desquamative Gingivitis with Free Gingival Graft: A Case Report. Dent Res Dent Clin Dent Prospect 2010; 4(1):33-36. • Okuda K, Momose M, Murata M, Saito Y, lnoie M, Shinohara C, Wolff LF, Yoshie H. Treatment of chronic desquamative gingivitis using tissue-engineered human cultured gingival epithelial sheets: a case report. Int J Periodontics Restorative Dent. 2004 Apr;24(2):119-25. • Yilmaz HG, Kusakci-Seker B, Bayindir H, Tözüm TF. Low-Level Laser Therapy in the Treatment of Mucous Membrane Pemphigoid: A Promising Procedure. J Periodontol. 2010 Aug;81(8):1226-30.
  96. 96. HPA axis? Exogeno us steroids  Impairs pt ability to respond to stress.
  97. 97. Management of patients who are on long term steroid therapy? • Administration of prophylactic steroids in pts on steroid therapy is a common practice. • However, Shapiro et al, found that pt.s using 5-20mg/day steroids maintain some adrenal reserves after immediate termination of steroids. • Higher dosesuppress adrenal glands when used for more than 2-3 weeks, but its ability to respond to stress may return quickly after termination of steroid therapy. • Hopkins et al: recovery of HPA axis following exposure to exogenous GCs requires 6-12 months. • For pt. who are currently on steroid therapy: no supplements needed, if their usual dose is taken within 2 hr prior to surgery. • Supplements are needed:  For pts undergoing lengthy, major surgical procedure,  Expected to have significant blood loss  Who have extremely low adrenal function For these individuals, physician consultation and steroid supplementation is indicated. Periodontal Tx of medically compromised patients.