Review article

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

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, denitive agreement on about the exact nature and correct classication of these manifestations is lacking in published studies. Controversy exists on the signicance 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

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

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 classication 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 ares 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 signicance of oral lesions of LE.

Oral lesions in lupus erythematosus

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

Classication of oral LE and correlation with cutaneous LE

Cutaneous manifestations of LE are divided in non-specic (non-diagnostic lesions) and specic (diagnostic lesions) [14]. Non-specic lesions usually indicate systemic disease with consequent cutaneous repercussions and include vasculitis, Raynauds phenomenon, non-scarring alopecia and livedo racemosa. Non-specic manifestations are not observed in the oral cavity. Specic LE lesions indicate lupus dermatitis (analogous to lupus arthritis, lupus nephritis, lupus serositis etc) and are represented by interface dermatitis. These are classied as cutaneous acute, subacute and chronic LE [14, 15]. These categories represent variants of the lupus process on the skin, with specic 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 classied. The greatest difculty 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
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(consequently no follicular pluggings, so typical of discoid LE) and scarring (atrophy) is difcult 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, inltrated, scaly and atrophic plaques with follicular plugging, mainly on the face, scalp, ears, and, more rarely, on the chest and arms (disseminated discoid LE) (gure 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 (gure 1B and C). Morphologic variants of chronic oral LE include the so-called honeycomb plaques (a clinical aspect of mucosal scarring) (gure 2A) [1] intensely keratotic white lesions (corresponding to verrucous CCLE) (gure 2B), and linear ssured, 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 (gure 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 (gure 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] (gure 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.
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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.

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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.

Figure 5. Acute cutaneous and oral LE: A) Acute cutaneous LE: typical erythematous and edematous buttery 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.

cutaneous LE (SCLE) includes psoriasiform (erythematopapulo-squamous) and polycyclic (erythema multiformelike) photosensitive eruptions and is more commonly associated to mild systemic disease (gure 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 (gure 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 (gure 3B).

Acute lesions
Acute cutaneous LE (ACLE) includes the classic malar edematous buttery lesion (gure 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 inammatory 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 (gure 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 specic acute or non-specic LE dermatitis [14] but histopathological and immunouorescence data [14-16] favor specic 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] (gures 6A and B). There is a rare variant of LE in which lesions have a widespread erosive bullous aspect

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 specic lupus dermatitis/mucositis or a non-specic 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, specic lupus lesions clinically and histopathologically (interface mucositis), without prognostic implications [18] (gure 7). Curiously, though, the same group of authors, in a latter review, stated that these ulcers are non-specic manifestations of SLE heralding serious disease. However, no explanation is offered on their nature or histopathological ndings [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 specic LE lesions), and separated from erythematous rash, discoid lesions, lupus paniculitis, bullous lesions (specic LE lesions). This classication probably provides unnecessary additional value to muco-cutaneous specic 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.
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B A C

Figure 7. Oral ulcers in LE represent ulcerated specic lupus interface mucositis: A) Palatal ulcerations in a patient with systemic LE. B) Histopathology of the same lesion revealed ulcerated supercial and deep perivascular mucositis with interface inammation, no signs of vasculitis are present. Except for the ulceration, this aspect is similar to gure 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 llings, 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).

Figure 8. Histopathology of oral LE (hematoxylin-eosin): A) Supercial and deep perivascular lymphocytic mucositis. B) Atrophy alternated with acanthosis, interface mucositis. C) Detail of gure 7B showing marked hydropic degeneration of the basal layer, necrotic basal keratinocytes and focal basement membrane thickening.

Histopathological aspects
Several studies have focused on the histopathological aspects (gures 8A-C) of cutaneous and mucosal lesions of
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 (gure 1B) Linear ulcers with keratotic striae. Honeycomb plaques (longstanding scarring lesions) (gure 2A). Intensely keratotic lesions (verrucous LE) (gure 2B). palatal discoid lesions (gure 1C). Labial discoid lesions (gure 3A). Squamous cell carcinoma may arise in longstanding scarring lesions (gure 3C).

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 inammatory inltrate 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 nding 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 ndings corresponded to an interface mucositis with a supercial and deep perivascular lymphocytic inammation; 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 nding in oral mucosa biopsies, not important for diagnosis). Foci with hydropic degeneration of the basal layer were evident.

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

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

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Table 2. Histopathological comparison between oral LE, oral LP and oral lichenoid drug reactions
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 inammatory inltrate of variable intensity with limited or widespread aggression to the basal keratinocytes. Inammatory inltrate is seen both in the supercial 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 inammatory inltrate. Lichenoid drug reactions Hyperkeratosis, granulosis, acanthosis and atrophy, marked spongiosis, hydropic degeneration (generally widespread necrosis up to suprabasal layers).

Epithelial alterations

Basement membrane (epithelial and vascular wall) Lamina propria

Widespread destruction of basement membrane by inammatory inltrate.

Heavy lymphocytic predominant Lymphocytic predominant lichenoid inltrate with presence of lichenoid inltrate, with presence of eosinophils. Inammatory Langerhans cells. inltrate 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 inammation 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 inltrates 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 ndings demonstrate that oral ulcers in SLE represent the ulcerated form of specic LE mucositis, probably without prognostic implications [18] (gure 7B), contrary to the view that these lesions could indicate systemic vasculitis and have prognostic implications [3, 11-13].

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 identied immuno-reactants are IgM and C3, the most common immuno-reactive patterns include colloid (apoptotic) bodies and continuous (linear) or granular basement membrane uorescence that can be found on up to 100% of biopsies studied [7, 8]. These ndings can also be found in other diseases and in sun damaged skin and thus are considered non-specic. IgG and IgA immuno-reactivity is most specic 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 inammation 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 denite evidence that oral LE lesions of any type may herald a worse outcome or systemic vasculitis. j
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Immunouorescence studies
Direct Immunouorescence (DIF) studies are often performed when diagnosing cutaneous and mucosal lesions of

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Acknowledgements. FAPESP grant 03/04880-3. Conict of interest: none.

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