Key points P.2 Flashcards
Oral Lichen Planus (OLP)
Definition
Lichen planus (LP) is a chronic, inflammatory, mucocutaneous, immune-mediated condition with variable clinical presentations
Oral Lichen Planus (OLP)
Pathogenesis
OLP is characterized by a chronic T-cell inflammatory infiltrate with basal cell degeneration** including **vacuolar degeneration,** **hyperkeratosis** or **parakeratosis**, and **saw- tooth rete ridges
OLP
Types:
- The reticular lesions: the most recognized form of OLP, encompass white lesions, which appear as a network of connecting and overlapping lines referred to as Wickham striae, papules, or plaques
- The erosive form: of OLP may present with erythema caused by inflammation or epithelial thinning, or both, and ulceration/pseudomembrane formation with periphery of the lesion surrounded by reticular keratotic striae
If the erosive subtype of OLP only affects the gingival tissue, the descriptive clinical term desquamative gingivitis is used
OLP
Histopathological criteria
- Signs of “liquefaction degeneration” in the basal cell layer
- Degenerating keratinocytes may be seen in the area of the epithelium and connective tissue interface and have been termed colloid, cytoid, hyaline, or Civatte bodies
- Absence of epithelial dysplasia
- When the histopathological features are less obvious, the term “histopathologically compatible with” should be used
OLP
Vacuolar degeneration
- Vacuolar degeneration (also called liquefaction degeneration) is the intracellular vacuole formation in injured basal keratinocytes and separation of the plasma cell membrane from the underlying basement membrane
- If the injury is severe, the cell undergoes apoptosis and becomes a Civatte body (colloid body)
OLP
Clinical criteria
- Presence of bilateral, more or less symmetrical lesions
- Presence of a lacelike network of slightly raised gray- white lines (reticular pattern)
- Erosive, atrophic, bullous, and plaque-like lesions are only accepted as a subtype in the presence of reticular lesions elsewhere in the oral mucosa
- In all other lesions that resemble OLP but not complete with the aforementioned criteria, the term “clinically compatible with” should be used
OLP
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Oral lichenoid lesions
- oral lichenoid drug reaction
- oral lichenoid contact hypersensitivity reaction
- chronic graft-versus-host disease
- chronic ulcerative stomatitis
- lupus erythematosus
- The plaque-like OLP occurs more frequently is difficult to distinguish it from oral leukoplakia
- The gingival lesions caused by mucous membrane pemphigoid or pemphigus vulgaris may appear as “desquamative gingivitis”
Mucous Membrane Pemphigoid
Clinical Features - Oral Involvement
- Oral lesions present in 85% patients
- Intraoral sites are the gingiva (80%), buccal mucosa (58%), palate (26%), alveolar ridge (16%), tongue (15%), and lower lip (7%)
There are three broad patterns of intraoral involvement:
- desquamative gingivitis (DG)
- extra-gingival lesions, and
- a combination of the two
Notably, the gingivae are the most frequently affected site, while the lip, tongue, and floor of mouth are much less affected
Mucous Membrane Pemphigoid
Gingival lesions-Desquamative Gingivitis
Gingival lesions in MMP may be indistinguishable from LP, PV, or epidermolysis bullosa acquisita (EBA), and therefore histology** and **immunofluorescence are essential for diagnosis
Mucous Membrane Pemphigoid
Extra-Gingival Lesions
- Appear as erythematous patches or blisters that subsequently develop into erosions
- Ulcers are frequently chronic and may occasionally be associated with scarring
Mucous Membrane Pemphigoid
Diagnosis
The current gold standard diagnostic test for MMP is positive DIF for IgG, IgA, IgM, or C3 at the BMZ
Pemphigus
The condition known as pemphigus represents four related diseases of an autoimmune origin:
- Pemphigus vulgaris
- Pemphigus vegetans
- Pemphigus erythematosus
- Pemphigus foliaceus
Only the first two of these affect the oral mucosa
Pemphigus
There are two subtypes of pemphigus vulgaris:
- the mucocutaneous type, with extensive skin blisters and erosions in addition to mucosal involvement
- the mucosal-dominant type, with mucosal lesions but minimal skin involvement
Pemphigus
Etiology:
- Due to an abnormal production, for unknown reasons, of autoantibodies that are directed against the epidermal cell surface glycoproteins, desmoglein 3 and desmoglein 1
- These desmogleins are components of desmosomes and the autoantibodies attach to these desmosomal components, effectively inhibiting the molecular interaction that is responsible for adherence
- As a result of this immunologic attack on the desmosomes, a split develops within the epithelium, causing a blister to form
Pemphigus
Clinical Features
- Affect virtually any oral mucosal location
- Positive Nikolsky sign
- Patients rarely report vesicle or bulla formation intraorally, and such lesions can seldom be identified by the examining clinician, probably because of early rupture of the thin, friable roof of the blisters
- More than 50% of the patients have oral mucosal lesions before the onset of cutaneous lesions, sometimes by as much as 1 year or more
- Eventually, however, nearly all patients have intraoral involvement
Unlike cicatricial pemphigoid, the ocular lesions of pemphigus typically do not cause scarring and symblepharon formation
Pemphigus
Histopathologic Features
- Biopsy specimens of perilesional tissue show characteristic intraepithelial separation, which occurs just above the basal cell layer of the epithelium
- The cells of the spinous layer of the surface epithelium typically appear to fall apart, a feature that has been termed acantholysis, and the loose cells tend to assume a rounded shape
- A mild-to-moderate chronic inflammatory cell infiltrate in the underlying connective tissue
- The diagnosis of pemphigus vulgaris should be confirmed by direct immunofluorescence examination of fresh perilesional tissue
