desquamative gingivitis

2. DESQUAMATIV
E GINGIVITIS
D.Hema
PG-I
Dept. of Periodontics

3. 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. INTRODUCTI
ON
4

5. 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

6. • 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

7. 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

8. 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

9. 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

10. EPIDEMIOLO
GY
Disorder Incidence
Mucous membrane pemphigoid 35-48%
Oral lichen planus 24- 45%
Pemphigus vulgaris 3-15%
Lupus erythematous 7.6 – 40%
10

11. 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

12. Endocrinal
imbalance
Estrogen deficiency in females
(menopause, following
hysterectomy and oopherectomy)
Testosterone deficiency in males
Chronic
infections
Tuberculosis
Chronic candidiasis
Histoplasmosis
12

13. 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

14. Glickman & Smulow:
3 forms of desquamative gingivitis
Mild Moderate
Severe
14

15. 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.

16. Desmosomes:
• Cadherins: desmoglein, desmocollin
• Catenins: desmoplakin, plakoglobin, plakophillin
Garrod et al. Desmosome structure, composition and function. Biochimica et Biophysica
Acta 1778 (2008) 572–587

17. Hemidesmosomes
Mihai et al. Immunopathology and molecular diagnosis of autoimmune bullous diseases. J.
Cell. Mol. Med. Vol 11, No. 3, 2007 pp. 462-481

18. 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

19. R. J. Nisengardt and R. S. Rogers. The Treatment of Desquamative Gingival
Lesions. 19

20. 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

21. Intraepithelial lesions
Target antigens of desmosomes implicated in intraepithelial lesions:

22. 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).

23. 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.

24. 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.

25. 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

26. 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

27. 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. DISEASES THAT
PRESENT
CLINICALLY AS
DESQUAMATIVE
GINGIVITIS

29. 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

30. 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

31. 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.

32. 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

33. 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.

34. • 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

35. 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

36. 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.

37. 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:

38. 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.

39. 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.

40. 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.

41. 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.

42. • 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

43. • 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

44. 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

45. 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.

46. 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

47. 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

48. 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.

49. 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

50. 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:

51. 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

52. 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.

53. 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

54. 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.

55. 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.

56. 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).

57. 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.

58. 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.

59. 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.

60. Lupus Erythematosus
Lupus erythematosus is an autoimmune disease with three
different clinical presentations:
1. systemic,
2. chronic cutaneous,
3. Subacute cutaneous.

61. 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

62. 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

63. • 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:

64. 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

65. Subacute Cutaneous Lupus Erythematosus:
• similar to DLE but lack the development of scarring and atrophy.

66. 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

67. 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.

68. 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.

69. 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.

70. 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

71. 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

72. 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.

73. • 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.

74. 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

75. 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.

76. 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

77. 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

78. 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

79. 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.

80. 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

81. 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:

82. Drug therapy has included
corticosteroids
Antibiotics
Immunosuppresive agents
Intravenous Immunoglobulis
Hormonal therapy
Vitamins

83. 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

84. 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

85. 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)

86. 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),

87. 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.

88. 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)

89. 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

90. 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

91. 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.

92. 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.

93. 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

94. 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.

95. • 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.

96. • 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.

98. HPA axis?
Exogeno
us
steroids

Impairs pt ability to
respond to stress.

99. 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.