Background

Lichenoid dermatoses and tissue reactions are some of the most diverse clinical and histologic presentations in dermatology and pathology. The term interface dermatitis is sometimes used interchangeably. The prototypical lichenoid dermatitis is lichen planus. Yet, there are numerous diseases that have similar histology. The following list describes some of them but many dermatoses have a lichenoid inflammatory cell component.

Dermatomyositis
Erythema multiforme
Fixed drug eruptions
Graft-versus-host disease
Lichen planus
Lichen planus-like keratosis
Lichen nitidus
Lichen striatus
Lichenoid drug eruptions
Lupus erythematosus
Paraneoplastic pemphigus
Pityriasis lichenoides
Poikilodermas
Viral Exanthems

Lichenoid tissue reactions are characterized by epidermal basal cell damage. Killer T lymphocytes (CD8) attack the basal keratinocytes probably induced by ICAM-1 (Intercellular adhesion molecule-1) expression in the keratinocytes. The result is cell death leading to Civatte bodies, a result of apoptosis. Vacuolar alteration, also known as liquefaction degeneration results form intracellular edema leading to separation. With continued damage at the dermoepidermal junction, melanin transfer from melanocytes to keratinocytes is disrupted leading to release and phagocytosis by macrophages.

OUTLINE

Gross Appearance and Clinical Variants
Histopathological Features and Variants
Differential Diagnosis
Commonly Used Terms
Internet Links

CLINICAL VARIANTS	CHARCTERIZATION
ANNULAR LICHENOID DERMATATIS OF YOUTH
Annular lichenoid dermatitis of youth. Annessi G, Paradisi M, Angelo C, Perez M, Puddu P, Girolomoni G. Servizio di Istopatologia, Istituto Dermopatico dell'Immacolata, IRCCS, Via Monti di Creta 104, 00167 Rome, Italy.	J Am Acad Dermatol. 2003 Dec;49(6):1029-36. Abstract quote   BACKGROUND: Lichenoid dermatoses are composed of a wide spectrum of disorders with a common histopathologic interface pattern but diverse causes and pathophysiology. OBJECTIVE: We describe a series of young patients with a peculiar annular lichenoid dermatitis, the clinical appearance of which initially suggested diagnoses of morphea, mycosis fungoides, or annular erythema. RESULTS: The study involved 23 patients (median age 10 years; age range 5-22 years). Lesions consisted of persistent asymptomatic erythematous macules and round annular patches with a red-brownish border and central hypopigmentation, mostly distributed on the groin and flanks. Histology revealed a peculiar lichenoid dermatitis with massive necrosis/apoptosis of the keratinocytes limited to the tips of rete ridges, in the absence of dermal sclerosis and epidermotropism of atypical lymphocytes. The infiltrate was composed mainly of memory CD4(+) CD30(-) T cells with few B cells and macrophages. Analysis of T-cell receptor-gamma-chain gene rearrangement in skin biopsy specimens revealed polyclonality in all the 15 cases studied. Topical and systemic corticosteroids or phototherapy were effective in most patients with relapse after treatment withdrawal. CONCLUSIONS: We suggest that this is a distinctive inflammatory condition, and we propose to term it "annular lichenoid dermatitis of youth."
PEDIATRIC
Lichenoid eruptions in children. Tilly JJ, Drolet BA, Esterly NB. New York University School of Medicine, Medical College of Wisconsin, Milwaukee, USA.	J Am Acad Dermatol. 2004 Oct;51(4):606-24. Abstract quote   Lichenoid eruptions are quite common in children and can result from many different origins. In most instances the precise mechanism of disease is not known, although it is usually believed to be immunologic in nature. Certain disorders are common in children, whereas others more often affect the adult population. Lichen striatus, lichen nitidus, Gianotti-Crosti syndrome, and lichen spinulosus are examples of lichenoid lesions that are more common in children than adults. Distinguishing these diseases is necessary for prediction of the course of the eruption and for optimal management. In most cases, certain clinical characteristics enable the clinician to reach a diagnosis, whereas in other cases biopsy is required for a definitive answer. Many of these lesions are self-limited and only require symptomatic treatment, although corticosteroids can hasten resolution in certain disorders. Discontinuation of the medication is often sufficient for resolution of lichenoid drug eruptions.

 

HISTOPATHOLOGICAL VARIANTS

CHARACTERIZATION

Lichenoid and granulomatous dermatitis. Magro CM, Crowson AN. Department of Pathology, Cell Biology, and Anatomy, Medical College of Thomas Jefferson University, Philadelphia, PA, USA.

Int J Dermatol 2000 Feb;39(2):126-33 Abstract quote BACKGROUND: The prototypic lichenoid eruptions, lichen planus (LP), lichenoid drug eruptions, secondary syphilis, and collagen vascular disease, are defined histologically by a band-like lymphocytic infiltrate in close apposition to the epidermis. We describe a novel form of lichenoid dermatitis with a granulomatous component. DESIGN: Skin biopsies from 40 patients demonstrating a band-like lymphocytic infiltrate with concomitant granulomatous inflammation were encountered over 4 years. Clinicians were contacted to elucidate underlying triggers and medical illnesses. RESULTS: A lichenoid dermatitis, a linear eruption, vasculitis, annular erythema, and erythroderma were among the clinical presentations. A drug-based etiology was implicated in 14 cases: the drugs included antibiotics, lipid-lowering agents, anti-inflammatory drugs, antihistamines, hydroxychloroquine sulfate, and angiotensin-converting enzyme inhibitors. Over one-third of patients with drug-related eruptions had other medical illnesses associated with cutaneous granulomatous inflammation, namely rheumatoid arthritis (RA), Crohn's disease, hepatitis C, diabetes mellitus, and thyroiditis. A microbial trigger was implicated in 12 patients in the context of infective id reactions to herpes zoster, Epstein-Barr virus (EBV), or streptococci, or active infections by Mycobacterium tuberculosis, M. leprae, fungi, and spirochetes. The remainder had hepatobiliary disease and RA without obvious exogenous triggers, cutaneous T-cell lymphoma (CTCL), and idiopathic lichenoid eruptions (i.e. LP, lichen nitidus, and lichen striatus). One patient with LP had underlying multicentric reticulohistiocytosis. The histiocytic infiltrate assumed one or more of five light microscopic patterns: (i) superficially disposed loose histiocytic aggregates; (ii) cohesive granulomata within zones of band-like lymphocytic infiltration with or without deeper dermal extension; (iii) a diffuse interstitial pattern; (iv) scattered singly disposed giant cells; and (v) granulomatous vasculitis. Additional features included lymphocytic eccrine hidradenitis in those patients with drug reactions, hepatobiliary disease, and antecedent viral illnesses, tissue eosinophilia and erythrocyte extravasation in drug hypersensitivity, granulomatous vasculitis in patients with microbial triggers, drug hypersensitivity or RA, and lymphoid atypia in lesions of CTCL or drug hypersensitivity. CONCLUSIONS: The cutaneous lichenoid and granulomatous reaction may reflect hepatobiliary disease, endocrinopathy, RA, Crohn's disease, infection, or a drug reaction. One-fifth of cases represent idiopathic lichenoid disorders. Lymphoproliferative disease or pseudolymphomatous drug reactions must be considered in those cases showing lymphoid atypia.

DIFFERENTIAL DIAGNOSIS

Epidermal Changes	Dermal Histologic Pattern	Additional Clues	Diagnosis
Interface-Vacuolar	Superficial Perivascular Dermatitis
	Lymphocytes predominate	Ballooning and individual necrotic keratinocytes-normal cornified layter	Erythema multiforme
		Ballooning and individual necrotic keratinocytes-parakeratosis	Mucha-Haberamann disease (PLEVA)
		Ballooning and individual necrotic keratinocytes-prominent granular layer	Graft vs. Host disease
		Ballooning and individual necrotic keratinocytes-necrotic keratinocytes in papillary dermis also	Effects of nitrogen mustard on mycosis fungoides, patch/plaque
		No ballooning and few, if any, necrotic keratinocytes-cornified layer normal	Drug eruption (one type)
		No ballooning and few, if any, necrotic keratinocytes-basement membrane sometimes thickened, smudged interface, thinned epidermis	Discoid lupus erythematosus Dermatomyositis
		No ballooning and few, if any, necrotic keratinocytes-sclerosis in upper part of dermis	LSEA (Morphea)
		No ballooning and few, if any, necrotic keratinocytes-melanophages in papillary dermis	Postinflammatory pigmentary alteration
	Eosinophils and neutrophils predominate	Ballooning and individual necrotic keratinocytes-cornified layer normal	Fixed drug eruption, superficial
Interface-Lichenoid
	Lymphocytes predominate	Jagged epidermal hyperplasia, wedged hypergranulosis, compact orthokeratosis	Lichen planus
		Esoinophils sometimes, focally thinned epidermis, focal parakeratosis	Lichen planus-like drug eruption Lichenoid photodermatitis
		Individual necrotic keratinocytes, ballooning, spongiosis, pallor in the upper part of the epidermis, and parakeratosis	Mucha-Habermann disease
		Lymphocytes along adnexal structures in reticular dermis, individual necrotic keratinocytes	Lichen striatus
		Thinned epidermis, prominent granular layer, parakeratosis	Graft vs. host reaction
		Extravasated erythrocytes and/or siderophages	Lichenoid purpura of Gourgerot and Blum
		Necrotic keratinocytes, focal parakeratosis, residuum of solar lentigo sometimes	Lichen planus-like keratosis
		Coronoid lamellae	Disseminated superficial actinic porokeratosis
		Lymphocytes within epidermis, scant spongiosis	Mycosis fungoides, plaque
	Histiocytes predominate	Discrete foci in papillary dermis	Lichen nitidus
		Discrete foci and, sometimes, confluence of foci in reticular dermis	Sarcoidosis
	Langerhans' cells predominate	Large cells, crenated outlines of large pale nuclei, abundant amphophilic cytoplasm	Letterer-Siwe disease
	Superficial and Deep Perivascular Dermatitis
Interface-Vacuolar
	Lymphocytes predominate	Basement membrane sometimes thickened, smudged interface, thinned epidermis	DLE
		Individual necrotic keratinocytes, ballooning, parakeratosis	Mucha-Habermann disease
	Neutrophils and eosinophils prominent	Individual necrotic keratinocytes, ballooning	Fixed drug eruption
Interface-Lichenoid
	Lymphocytes predominate	Eosinophils sometimes, focal parakeratosis	Lichenoid drug eruption
		Individual necrotic keratinocytes sometimes	Lichenoid photodermatitis
		Individual necrotic keratinocytes, ballooning, spongiosis	Mucha-Habermann disease
		Thickened basement membrane, smudged appearance of interface, thinned epidermis focally	DLE
		Thinned epidermis, prominent granular layer, parakeratosis	Graft vs. host reaction
		Abnormal lymphocytes in wedge shaped infiltrate, often plasma cells, eosinophils, and neutrophils, as well as small lymphocytes	Lymphomatoid papulosis
		Lymphocytes in epidermis, scant spongiosis	Mycosis fungoides, plaque stage
	Neutrophils, eosinophils, and plasma cells prominent	Abnormal lymphocytes in wedge shaped infiltrate	Lymphomatoid papulosis
Ballooning Interface
	Lymphocytes predominate	Individual necrotic keratinocytes, normal cornified layer	Erythema multiforme
		Individual necrotic keratinocytes, prominent granular layer, parakeratosis	Graft vs. host reaction
	Eosinophils and neutrophils prominent	Individual necrotic keratinocytes, ballooning, normal cornified layer	Fixed drug eruption, superficial
		Individual necrotic keratinocytes, spongiosis, neutrophils as solitary units within epidermis	Toxic shock syndrome

Henry JB. Clinical Diagnosis and Management by Laboratory Methods. Twentieth Edition. WB Saunders. 2001.
Rosai J. Ackerman's Surgical Pathology. Ninth Edition. Mosby 2004.
Sternberg S. Diagnostic Surgical Pathology. Fourth Edition. Lipincott Williams and Wilkins 2004.
Robbins Pathologic Basis of Disease. Sixth Edition. WB Saunders 1999.
DeMay RM. The Art and Science of Cytopathology. Volume 1 and 2. ASCP Press. 1996.
Weedon D. Weedon's Skin Pathology Second Edition. Churchill Livingstone. 2002
Fitzpatrick's Dermatology in General Medicine. 5th Edition. McGraw-Hill. 1999.
Weiss SW and Goldblum JR. Enzinger and Weiss's Soft Tissue Tumors. Fourth Edition. Mosby 2001.

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Last Updated October 18, 2004

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