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Oral lesions in lupus erythematosus:

Correlation with cutaneous lesions
Article in European journal of dermatology: EJD July 2008
DOI: 10.1684/ejd.2008.0388 Source: PubMed

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Review article
Marcello Menta Simonsen NICO1
Maria Apparecida
Constantino VILELA1
Evandro Ararigbia RIVITTI1
Silvia Vanessa LOURENO1,2
1

Department of Dermatology,
Hospital das Clnicas, Medical School;
University of So Paulo, Brazil
2
Department of Pathology, Faculdade de
Odontologia da Universidade de So Paulo,
Av Prof Lineu Prestes, 2227,
Cidade Universitria, So Paulo,
CEP: 05508-000, SP-Brazil

Reprints: S.V. Loureno

<sloducca@usp.br>

Article accepted on 5/12/2007

Eur J Dermatol 2008; 18 (4): 376-81

Oral lesions in lupus erythematosus:

correlation with cutaneous lesions
Oral lesions in the context of lupus erythematosus (LE) have long been
described. However, definitive agreement on about the exact nature and
correct classification of these manifestations is lacking in published
studies. Controversy exists on the significance of oral LE lesions regarding patient outcome. In this article, medical and dental literature on
clinical and histopathological aspects of oral LE lesions are reviewed
and critically discussed. A clinico-pathological correlation of oral lesions (interface mucositis-lupus mucositis) with cutaneous lesions (interface dermatitis-lupus dermatitis) is established, for those represent the
mucosal counterparts of cutaneous LE. Validity about widely used but
imprecise terms such as oral ulcers, ulcerative plaques, and others,
in the context of LE, is discussed, and the uncertain relationship of these
alterations to systemic disease with a worse outcome is commented.
Furthermore, insights about the nature, differential diagnosis, and prognosis of oral lesions in LE patients are presented.
Key words: lupus erythematosus, oral lesions

ral lesions occurring during the course of lupus

erythematosus (LE) have long been described in
dermatological, rheumatological and dental literature [1, 2]. Many attempts have been made to correlate
these manifestations with the prognosis of systemic LE
(SLE) (oral ulcerations are included among the American
College of Rheumatology criteria for systemic LE) [3], but
conclusions vary. Reproducible criteria in the classification
of oral lesions in LE are lacking and as a consequence,
comparison between existing studies is hampered.

petechial erythema [2, 3, 9-12]. Thus, in contrast to cutaneous LE, no uniformity exists in classifying oral LE lesions, and an adequate clinical categorization is lacking.
Additionally and yet more confusing, oral ulcerations in LE
patients have for a long time been considered as a sign of
vasculitis and predictors of severe systemic flares of the
disease [12, 13]. This misconception brings no light to the
knowledge of such lesions and has created myths among
physicians about the true significance of oral lesions of LE.

Classification of oral LE and correlation

with cutaneous LE

Different studies of oral lesions in the course of LE have

shown a frequency varying from 9 to 45% in systemic
disease and 3 to 20% in localized cutaneous disease [4-6].
Our group reported 26 patients with oral lesions among 188
LE patients studied, 13 of these had SLE according to the
ACR criteria. Nineteen patients were female and 7 were
male [7]. Burge et al. reported 10 female and 4 male
patients with oral lesions of LE, of these, 5 were considered
to have SLE and 9 had localized cutaneous LE [1]. In a
further study by our group, oral lesions were diagnosed in
46 patients, only 13 had SLE according to established
criteria [8]. A possible reason for the lower frequency of
oral lesions when compared with skin lesions may be the
lack of ultraviolet radiation incidence in the oral cavity in
contrast to the skin.
Clinical descriptions of oral LE lesions vary enormously in
the different studies. Terms used include: oral discoid
lesion, chronic plaque, lupus cheilitis, acute ulcer,
oral ulcer, red ulcer, ulcerative plaques, pebbly red
areas, honeycomb lesion, keratotic lesion white
keratotic plaques, purpuric lesions and diffuse palatal

Cutaneous manifestations of LE are divided in non-specific

(non-diagnostic lesions) and specific (diagnostic lesions)
[14]. Non-specific lesions usually indicate systemic disease
with consequent cutaneous repercussions and include vasculitis, Raynauds phenomenon, non-scarring alopecia and
livedo racemosa. Non-specific manifestations are not observed in the oral cavity.
Specific LE lesions indicate lupus dermatitis (analogous to
lupus arthritis, lupus nephritis, lupus serositis etc)
and are represented by interface dermatitis. These are classified as cutaneous acute, subacute and chronic LE [14, 15].
These categories represent variants of the lupus process on
the skin, with specific clinical, histopathological, genetic
and immunoserological features [14-16].
As with many other skin diseases with mucosal manifestations, oral lesions of LE represent the exact mucosal counterpart of skin lesions, and should be similarly classified.
The greatest difficulty in analyzing oral LE lesions lies in
the fact that mucosal clinical responses are morphologically more limited than their skin analogues: scales are not
observed due to moisture, there are no pilo-sebaceous units

376

EJD, vol. 18, n 4, July-August 2008

doi: 10.1684/ejd.2008.0388

Oral lesions in lupus erythematosus

(consequently no follicular pluggings, so typical of discoid LE) and scarring (atrophy) is difficult to assess because of better mucosal regeneration when compared to
skin. Moreover, some patients may present with exclusively oral lesions, making an immediate correlation with
cutaneous LE less obvious.

Chronic lesions
Chronic cutaneous LE (CCLE) includes, among others, the
classic discoid lesion. This is characterized by round, wellcircumscribed, infiltrated, scaly and atrophic plaques with
follicular plugging, mainly on the face, scalp, ears, and,
more rarely, on the chest and arms (disseminated discoid
LE) (figure 1A). Discoid lesions develop severe scarring in
most cases; scalp lesions typically show scarring alopecia.
Verrucous LE refers to intensely keratotic discoid lesions.
Other variants of CCLE include tumid, lupus panniculitis
and chilblain LE [14, 16, 17].
The commonest mucosal presentation of chronic LE is the
oral discoid lesion. The typical clinical picture is of a
well-demarcated, round or irregular red area that can be
atrophic or ulcerated, with white radiating keratotic striae
and telangiectases. This aspect represents the very same
lesion as the classic cutaneous discoid LE (figure 1B and
C). Morphologic variants of chronic oral LE include the
so-called honeycomb plaques (a clinical aspect of mucosal scarring) (figure 2A) [1] intensely keratotic white
lesions (corresponding to verrucous CCLE) (figure 2B),
and linear fissured, ulcerative and keratotic lesions that may

occur in buccal mucosa [10]. Most patients will have simultaneous cutaneous lesions, but exclusive mucosal manifestations are not rare. Isolated palatal lesions can be seen
(figure 1C). Pain is variable. Lesions are more often asymmetrically distributed in the oral cavity (palate, buccal
mucosa, tongue). This asymmetry is important in differential diagnosis since lesions of clinically similar diseases
such as oral lichen planus (LP) are almost always symmetric. Tumid and subcutaneous chronic LE have not been
described in the oral cavity.
Lip involvement is frequent. Clinical manifestations include well-demarcated discoid lesions or a diffuse cheilitis
[2]. Lesions typically tend to spread from the vermilion to
the surrounding lip skin, obscuring the limits of the vermilion (figure 3A and B). This feature is useful in differentiating LE from lichen planus of the lip and from other types of
cheilitis, as LP lesions are characteristically limited to the
vermilion area. The designation lupus cheilitis is used at
times [1, 2], but it may suggest a different or special
manifestation instead of a typical LE lesion on that location.
Squamous cell carcinoma may, rarely, arise in longstanding
scarring lesions of oral LE, as well as in long established
scars of other chronic mucosal diseases (LP, syphilis) [14,
16] (figure 3C).

Subacute lesions
Subacute LE represents a subtype of LE with characteristic
clinical, serological and prognostic features [14]. Subacute

Figure 2. Clinical aspects of longstanding oral discoid lesions:

A) Well-established scarring lesions often display a typical
honeycomb aspect. B) Longstanding intensely keratotic
plaque- this is akin to cutaneous verrucous LE.

C
Figure 1. Cutaneous and oral discoid LE: A) Typical discoid
LE-round plaques with keratosis, central atrophy and follicular plugging. B) Intra oral discoid lesion in the same patient
an erythematous round ulcer with surrounding keratotic striae.
C) Discoid lesions are common on the palate.
EJD, vol. 18, n 4, July-August 2008

Figure 3. Clinical aspects of lip lesions in LE: A) Discoid

lesion on the lip characteristically spreading from the vermilion to adjacent skin. B) Diffuse vermilion evolvement spreading to lip skin in a patient with subacute cutaneous LE.
C) Squamous cell carcinoma can develop on longstanding
scars of LE.

377

Figure 4. Subacute cutaneous and oral LE: A) Typical SCLE

lesions with marked photosensitivity. B) Red, round, discretely atrophic patches in the palate of the same patient. These
lesions are rare because SCLE is highly photo-sensitive.

cutaneous LE (SCLE) includes psoriasiform (erythematopapulo-squamous) and polycyclic (erythema multiformelike) photosensitive eruptions and is more commonly associated to mild systemic disease (figure 4A). Rowells
Syndrome refers to the coexistence of erythema multiforme and LE, but its identity is widely discussed. Subacute
LE lesions heal without scarring; vitiligo-like hypo pigmentation is common [14, 16, 17]. Although SCLE lesions
characteristically appear on sun-exposed areas, intra oral
manifestations may rarely be present. Lesions consist of
well-demarcated, round, red patches that on close inspection may appear slightly depressed. Due to moisture, scaling is not evident (figure 4B). Lip lesions may occur as
diffuse erythematous scaling plaques on the vermilion that
typically spread towards the skin of the lip and are almost
always associated with more generalized SCLE (figure 3B).

Acute lesions
Acute cutaneous LE (ACLE) includes the classic malar
edematous butterfly lesion (figure 5A), a corresponding
widespread eruption and bullous LE. These presentations
almost always indicate systemic LE, with its diagnostic
serological changes and manifestations in other organs.
These cutaneous lesions tend to heal without scarring since
inflammatory component is scarce [14-18]. Oral lesions in
the setting of systemically ill LE patients are very common.
There are many possible clinical presentations: circumscribed red macules, diffuse or palatal erythema, purpuric
macules (figure 5B), and erosions or ulcerations that may or
may not be symmetrically distributed in the mucosa [2, 14].
These can occasionally be present in the absence of skin
lesions.
There is still controversy as to whether bullous LE represents specific acute or non-specific LE dermatitis [14] but
histopathological and immunofluorescence data [14-16]
favor specific acute manifestation because they are diagnostic. Patients with bullous LE may present with linearly
arranged blisters along the lip vermilion or with intact or,
more often, ruptured blisters on the palate or buccal mucosa
[21] (figures 6A and B). There is a rare variant of LE in
which lesions have a widespread erosive bullous aspect

378

Figure 5. Acute cutaneous and oral LE: A) Acute cutaneous

LE: typical erythematous and edematous butterfly shaped
eruption on the face. B) Erythemato-purpuric macules on the
labial mucosa of the same patient. These represent the very
same lesions than on the skin, but on occasions they may be
seen without skin lesions.

similar to Stevens-Johnson disease or toxic epidermal

necrolysis, these patients usually present with hemorrhagic
crusts and erosions on the lips and mucous epithelial detachment. The question as to whether these manifestations
represent a hyper-acute type of specific lupus
dermatitis/mucositis or a non-specific indicator of severe
activity is still under debate [19, 20].
Oral ulcerations or ulcers in the setting of SLE have long
been considered to be predictors of systemic vasculitis and
worse prognosis [12, 13]. Jorizzo et al. proved that these
lesions represent, in fact, specific lupus lesions clinically
and histopathologically (interface mucositis), without
prognostic implications [18] (figure 7). Curiously, though,
the same group of authors, in a latter review, stated that
these ulcers are non-specific manifestations of SLE heralding serious disease. However, no explanation is offered on
their nature or histopathological findings [22]. Established
prognostic indexes for systemic LE in the rheumatological
literature, such as the Systemic Lupus Activity Measure
(SLAM) [11, 12], equivocally classify oral LE ulcers together with peri-ungueal erythema, photosensitive rash
and nail fold infarcts (mostly non specific LE lesions), and
separated from erythematous rash, discoid lesions, lupus
paniculitis, bullous lesions (specific LE lesions). This
classification probably provides unnecessary additional
value to muco-cutaneous specific LE lesions in establishing
systemic prognosis. These oral lesions of LE are summarized in table 1.

Figure 6. Clinical aspects of bullous LE: A) Linearly arranged

blisters along the vermilion. Similar lesions are present on the
skin of the lip. B) Ruptured blisters on the buccal mucosa.
EJD, vol. 18, n 4, July-August 2008

Figure 7. Oral ulcers in LE represent ulcerated specific lupus

interface mucositis: A) Palatal ulcerations in a patient with
systemic LE. B) Histopathology of the same lesion revealed
ulcerated superficial and deep perivascular mucositis with
interface inflammation, no signs of vasculitis are present.
Except for the ulceration, this aspect is similar to figure 8.

Clinical differential diagnosis

Clinical differential diagnosis of LE mucositis will depend
on the morphology of the lesion analyzed. The main differential diagnoses for keratotic discoid lesions are LP, lichenoid reactions to dental fillings, traumatic and smokers
keratoses, and verrucous carcinoma. Ulcerated discoid lesions should be differentiated from aphtha, erosive LP,
traumatic ulcers, deep mycoses, Langerhans cells histiocytosis and SCC (SCC can develop in old scarring LE lesions). Lip lesions may simulate contact cheilitis, factitious
cheilitis, actinic cheilitis, LP, psoriasis, erythema multiforme, pemphigus vulgaris and SCC. Erythematous or purpuric macules may resemble LP, erythema multiforme,
mucous patches of syphilis, petechiae of viral exanthem,
and negative pressure purpura (fellatio syndrome). Finally, differential diagnoses for oral bullous LE include
pemphigus vulgaris, mucous membrane pemphigoid, herpes simplex, varicella, and erythema multiforme with its
variants (Stevens-Johnson disease and toxic epidermal
necrolysis).

Histopathological aspects
Several studies have focused on the histopathological aspects (figures 8A-C) of cutaneous and mucosal lesions of

Figure 8. Histopathology of oral LE (hematoxylin-eosin):

A) Superficial and deep perivascular lymphocytic mucositis.
B) Atrophy alternated with acanthosis, interface mucositis.
C) Detail of figure 7B showing marked hydropic degeneration
of the basal layer, necrotic basal keratinocytes and focal basement membrane thickening.

LE [5, 7-9, 15, 16, 23, 24]. Characteristically, features of

cutaneous and mucosal LE are of perivascular and interface
dermatitis/mucositis.
Histopathological distinction between acute, subacute and
chronic cutaneous LE lies in the intensity of epithelial
affection, severity of follicular damage, nature and level of
the inflammatory infiltrate in the dermis [15, 16, 24]. The
histopathologic features of oral LE represent the mucosal
counterpart to the described aspects of cutaneous LE. The
most important differences lie in the absence of pilosebaceous units and the frequent finding of an absent epithelium that may be lost during the biopsy procedure or due
to the high frequency of ulcerated lesions inside the mouth
(marked basal cell liquefaction associated with mechanical
trauma). In a study of 46 oral LE patients by our group, the
most consistent findings corresponded to an interface mucositis with a superficial and deep perivascular lymphocytic
inflammation; edema in the lamina propria is constantly
present. The covering epithelium presented areas of acanthosis alternated with areas of atrophy. Occasional pseudoepitheliomatous hyperplasia was observed. Variable degrees of spongiosis were present (a common finding in oral
mucosa biopsies, not important for diagnosis). Foci with
hydropic degeneration of the basal layer were evident.

Table 1. Clinical presentations of oral LE lesions

Chronic lesions: discoid lesions
Note- lesions are almost always asymmetrically
distributed on buccal cavity.
Atrophic or ulcerated round lesions with
peripheral keratotic striae (figure 1B)
Linear ulcers with keratotic striae.
Honeycomb plaques (longstanding scarring
lesions) (figure 2A).
Intensely keratotic lesions
(verrucous LE) (figure 2B).
palatal discoid lesions (figure 1C).
Labial discoid lesions (figure 3A).
Squamous cell carcinoma may arise in
longstanding scarring lesions (figure 3C).

EJD, vol. 18, n 4, July-August 2008

Subacute lesions
Discrete red patches, (much rarer and
more discrete than cutaneous subacute LE)
(figure 4B).
Diffusely scaly labial patches (figure 3B).

Acute lesions
Erythemato-purpuric macules
(figure 5B).
Palatal erythema.
Petechiae.
Ulcerations (figure 7A).
Bullous LE: labial blisters (figure 6A),
intra-oral intact or ruptured blisters
(figure 6B).

379

Table 2. Histopathological comparison between oral LE, oral LP and oral lichenoid drug reactions

Epithelial alterations

Basement membrane
(epithelial and vascular
wall)
Lamina propria

Oral LE
Hyperkeratosis, granulosis,
acanthosis and atrophy, spongiosis,
hydropic degeneration (patchy or
widespread), colloid bodies,
hyperproliferation of basal layer,
sometimes with presence of
atypical keratinocytes.
Regular or focal thickening of
epithelial basement membrane
associated with thickening of
vascular wall.
Lymphocytic predominant
inflammatory infiltrate of variable
intensity with limited or widespread
aggression to the basal
keratinocytes. Inflammatory
infiltrate is seen both in the
superficial lamina propria
(lichenoid) and deep perivascular.
Vessel walls are prominent with
endothelial tumefaction. Edema and
variable deposits of mucin are
present.

Oral LP
Hyperkeratosis, granulosis,
acanthosis and atrophy, epithelial
cones in saw-tooth, spongiosis,
hydropic degeneration (patchy or
widespread). In severe cases,
complete destruction of basal layer
is seen.
Focal or widespread destruction of
basement membrane by
inflammatory infiltrate.

Widespread destruction of
basement membrane by
inflammatory infiltrate.

Heavy lymphocytic predominant

Lymphocytic predominant
lichenoid infiltrate with presence of lichenoid infiltrate, with presence
of eosinophils. Inflammatory
Langerhans cells.
infiltrate may be present around
vessels in mid and deep lamina
propria. Prominent interstitial
edema and vascular congestion are
present.

Basal necrotic keratinocytes, widespread or focal, were

frequent. Thickening of epithelial and vascular basement
membranes was visible on haematoxilin-eosin (HE) and
PAS stains [8, 9]. The presence of epithelial atypia is not
rare and has been observed by other authors [18]. This is
probably due to a hyperproliferative status of the mucosa as
demonstrated by our and previous studies using immunohistochemical labelling of cytokeratins [7, 25]. Occasional
interlobular minor salivary gland inflammation is present,
and this has been inappropriately labelled Sjgrens syndrome associated phenomenon [3, 22].
Histopathological changes in mucosal LE lesions must be
differentiated from similar alterations that may occur in
other instances of perivascular and interface mucositis,
such as lichen planus (LP), lichenoid mucositis and drug
reactions [16, 23]. Karjalainen et al. compared histopathological features of oral LE with those of LP and concluded
that the most important differences included: thicker basement membrane in LE (HE and PAS), edema in the lamina
propria more pronounced in LE, PAS positive thickening of
blood vessel walls in LE, deeper perivascular infiltrates in
LE, more pronounced epithelial atrophy in LP [9]. The
presence of mucin in the lamina propria is an important clue
in differentiating LE from LP [14, 16]. These differences
are summarized in table 2.
Jorizzo et al. [18] studied 10 patients diagnosed with SLE
who presented with oral ulcers. These authors demonstrated that all biopsies of these ulcers revealed interface LE
mucositis with no sign of vasculitis, these findings demonstrate that oral ulcers in SLE represent the ulcerated form of
specific LE mucositis, probably without prognostic implications [18] (figure 7B), contrary to the view that these
lesions could indicate systemic vasculitis and have prognostic implications [3, 11-13].

Immunofluorescence studies
Direct Immunofluorescence (DIF) studies are often performed when diagnosing cutaneous and mucosal lesions of

380

Lichenoid drug reactions

Hyperkeratosis, granulosis,
acanthosis and atrophy, marked
spongiosis, hydropic degeneration
(generally widespread necrosis up
to suprabasal layers).

LE [24, 26-28]. These are particularly useful in differential

diagnosis between LE and other possibly similar clinical
and histopathological conditions such as LP. The three
major classes of immunoglobulins IgG, IgA and IgM as
well as complement components may be found in basement
membrane zone deposits of cutaneous and oral LE, in a
linear and/or granular pattern [24, 26-28]. DIF in oral LE
lesions is frequently positive and the most commonly identified immuno-reactants are IgM and C3, the most common
immuno-reactive patterns include colloid (apoptotic) bodies and continuous (linear) or granular basement membrane
fluorescence that can be found on up to 100% of biopsies
studied [7, 8]. These findings can also be found in other
diseases and in sun damaged skin and thus are considered
non-specific. IgG and IgA immuno-reactivity is most specific for LE, typically in linear basement membrane pattern.
These are observed on up to 29% of oral lesions [26].

Conclusion
Oral lesions are not a rare event in the clinical context of
LE. These are better understood if considered as the mucosal counterpart of cutaneous LE (lupus dermatitis and
lupus mucositis), for they represent those very same
lesions in the mucosa. Identical to cutaneous LE, clinical
and histopathological subtypes of oral LE lesions represent
diversity in intensity and in chronological phases of interface inflammation on the mucosa [15, 29]. When compared
to cutaneous LE, differences concern mostly the anatomic
and functional peculiarities of oral tissues: lack of pilosebaceous units, lack of scaling due to moisture and frequent ulceration due to friction. These limitations make use
of strict clinical-pathological criteria essential for differentiating oral LE from other possibly similar conditions such
as LP, and other lichenoid eruptions such as drug reactions.
There is no definite evidence that oral LE lesions of any
type may herald a worse outcome or systemic vasculitis. j
EJD, vol. 18, n 4, July-August 2008

Acknowledgements. FAPESP grant 03/04880-3. Conflict

of interest: none.

References
1. Burge SM, Frith PA, Juniper RP, Wojnarowska F. Mucosal involvement in systemic and chronic cutaneous lupus erythematosus. Br J
Dermatol 1989; 121: 727-41.
2. Callen JP. Oral manifestations of collagen vascular disease.
Semin Cut Med Surg 1997; 16: 323-7.
3. Tan EM, Cohen AS, Fries JF, et al. The 1982 criteria for the
classification of systemic lupus erythematosus. Arthritis Rheum 1982;
25: 1271-7.
4. Tuffanelli D, Dubois E. Cutaneous manifestations of systemic lupus
erythematosus. Arch Dermatol 1964; 90: 377-86.
5. Johsson R, Heyden G, Westberg NG, Nyberg G. Oral mucosal
lesions in LE. A clinical, histopathological an immunopathological
study. J Rheumatol 1984; 11: 38-42.
6. Schiodt M. Oral manifestations of lupus erythematosus. Int J Oral
Surg 1984; 13: 101-47.
7. Loureno SV, Sotto MN, Vilela MAC, Carvalho FRG, Rivitti EA,
Nico MMS. Lupus erythematosus: clinical and histopathological
study of oral manifestations and immunohistochemical profile of
epithelial maturation. J Cutan Pathol 2006; 33: 657-62.
8. Loureno SV, Carvalho FRG, Boggio P, Sotto MN, Vilela MAC,
Rivitti EA, Nico MMS. Lupus erythematosus: clinical and histopathological study of oral manifestations and immunohistochemical profile
of the inflammatory infiltrate. J Cutan Pathol 2007; 34: 558-64.
9. Karjalainen TK, Tomich CE. A histopathologic study of oral mucosal lupus erythematosus. Oral Surg Oral Med Oral Pathol 1989;
67: 547-54.
10. Orteu CH, Buchanan JAG, Hutchison I, Leigh IM, Bull RH. Systemic lupus erythematosus presenting with oral mucosal lesions:
easily missed? Br J Dermatol 2001; 144: 1219-23.
11. Liang MH, Socher AS, Larson MG, Schur PH. Reliability and
validity of six systems for the clinical assessment of disease activity in
systemic lupus erythematosus. Arthritis Rheum 1989; 32: 1107-18.
12. Parodi A, Massone C, Cacciapuoti M, et al. Measuring the
activity of the disease in patients with cutaneous lupus erythematosus. Br J Dermatol 2000; 142: 457-60.
13. Ropes MW. In: Systemic lupus erythematosus. Cambridge,
Mass: Harvard University Press, 1976: 28.

EJD, vol. 18, n 4, July-August 2008

14. Costner MI, Sontheimer RD. Lupus erythematosus. In: Freedberg IM, Elisen AZ, Wolf K, Austen KF, Goldsmith LA, Katz SI, eds.
Fitzpatricks Dermatlogy in General Medicine. Mc Graw Hill, 2003:
1677-93.
15. Lee SS, Ackerman AB. Lupus dermatitis is an expression of
systemic lupus erythematosus. Dermatopathology: practical and conceptual 1997; 3: 346-7.
16. Crowson N, Magro C. The cutaneous pathology of lupus
erythematosus. J Cutan Pathol 2001; 28: 1-23.
17. Patel P, Werth V. Cutaneous lupus erythematosus: a review.
Dermatol Clin 2002; 20: 373-85.
18. Jorizzo J, Salisbury PL, Rogers III RS, Goldsmith SM, Shar GG,
Callen JP, Wise CM, Semble EL, White WL. Oral lesions in lupus
erythematosus: do ulcerative lesions represent a necrotizing vasculitis? J Am Acad Dermatol 1992; 27: 389-94.
19. Mandelcorn M, Shear NH. Lupus associated toxic epidermal
necrolysis: a novel manifestation of lupus? J Am Acad Dermatol
2003; 48: 525-9.
20. Stone TW, Stone MS, Racila D, Scofield RH, Sontheimer RD.
Toxic epidermal necrolysis-like and the spectrum of the acute syndrome of apoptotic panepidermolysis (ASAP): a case report, concept
review and proposal for a new classification of lupus erythematosus
vesicullobullous skin lesions. Lupus 2004; 13: 941-50.
21. Weinberg MA, Insler MS, Campen RB. Mucocutaneous features of autoimmune blistering diseases. Oral Surg Oral Med Oral
Pathol 1997; 84: 517-34.
22. Callen JP. Lupus erythematosus. In: Callen JP, Jorizzo JL,
Greer KE, Penneys NS, Piette WW, Zone JJ, eds. Dermatological
Findings of Systemic Disease. W.B. Saunders, 1995: 3-12.
23. Schiodt M. Oral discoid lupus erythematosus. III. A histopathologic study of sixty-six patients. Oral Surg Oral Med Oral Pathol
1984; 57: 281-93.
24. David-Bajar KM, Bennion SD, DeSpain JD, Golitz LE, Lee LA.
Clinical, histologic, and immunofluorescent distinctions betwwen
subacute cutaneous lupus erythematosus and discoid lupus erythematosus. J Invest Dermatol 1992; 99: 251-7.
25. Ichikawa E, Watanabe S, Takahashi H. Keratin and involucrin
expression in discoid lupus erythematosus and lichen planus. Arch
Dermatol Res 1997; 289: 519-26.
26. Schiodt M, Holmstrup P, Dabelsteen E, Ullman S. Deposits of
immunoglobulins, complement, and fibrinogen in oral lupus erythematosus, lichen planus, and leukoplakia. Oral Surg Oral Med Oral
Pathol 1981; 51: 603-8.
27. Burge SM, Frith PA, Millard PR, Wojnarowska F. The lupus band
test in oral mucosa, conjunctiva and skin. Br J Dermatol 1989; 121:
743-52.
28. Provost TT. Lupus Band Test. Int J Dermatol 1981; 20: 475.
29. Tebbe B, Mazur L, Stadler R, Orfanos CE. Immunohistochemical analysis of chronic discoid and subacute cutaneous lupus erythematosus. Relation to immunopathological mechanisms. Br J Dermatol
1995; 132: 25-31.

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