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Year : 2009  |  Volume : 21  |  Issue : 1  |  Page : 37-41 Table of Contents   

Discoid lupus erythematosus: A case report with review of the literature

1 Department of Oral Medicine and Radiology, A. B. Shetty Memorial Institute of Dental Sciences, Deralakatte, Mangalore, Karnataka, India
2 Department of Oral Medicine and Radiology, Mahatma Gandhi Dental College, Jaipur, India

Date of Web Publication14-Nov-2009

Correspondence Address:
C K Sreejan
Department of Oral Medicine and Radiology, A. B. Shetty Memorial Institute of Dental Sciences, Deralakatte, Mangalore, Karnataka
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0972-1363.57777

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Discoid lupus erythematosus (DLE) is the most common form of chronic cutaneous lupus erythematosus. Classic DLE lesions begin as red-purple macules, papules or small plaques and rapidly develop a hyperkeratotic surface. Most patients with untreated classic DLE lesions suffer indolent progression to large areas of cutaneous dystrophy and scarring alopecia that can be psychosocially devastating. A 68-year-old male patient presented with non-healing ulcers of the mouth since 6 months and skin lesions since 2 months. Examination revealed erythematous, disc-like, scaly plaques over the face, nose and scalp, showing signs of healing accompanied by scarring and hypopigmentation. Histopathologic examination verified a diagnosis of DLE. Topical steroids and antifungals were applied to the lesions twice daily for 2 weeks. After 2 weeks of application, all lesions regressed significantly. Follow-up is important and necessary every 6 months because DLE is considered as a pre-cancerous condition and for the early detection of systemic lupus erythematosus and to minimize scarring. The recent advances in the diagnostic criteria and treatment have also been highlighted.

Keywords: American college of rheumatology, discoid lupus erythematosus, hypopigmentation, scarring alopecia and systemic lupus erythematosus

How to cite this article:
Sreejan C K, Gopakumar R, Babu S, Roopashri R K. Discoid lupus erythematosus: A case report with review of the literature. J Indian Acad Oral Med Radiol 2009;21:37-41

How to cite this URL:
Sreejan C K, Gopakumar R, Babu S, Roopashri R K. Discoid lupus erythematosus: A case report with review of the literature. J Indian Acad Oral Med Radiol [serial online] 2009 [cited 2023 Jan 28];21:37-41. Available from: http://www.jiaomr.in/text.asp?2009/21/1/37/57777

   Introduction Top

Discoid lupus erythematosus (DLE) is a chronic, scarring, atrophy producing photosensitive dermatosis. DLE may occur in patients with systemic lupus erythematosus (SLE) and in some patients (<5%) with DLE, progress to SLE.

Worldwide, the prevalence of lupus erythematosus (LE) ranges from 17 to 48 cases per 100,000 populations. The highest prevalence of LE occurs in persons aged 40-60 years and is approximately 10 times higher in women than in men. [1]

Malignant degeneration of chronic lesions of LE is possible, leading to non-melanoma skin cancer. Oral mucosal lesions are considered to be a pre-malignant condition.

   Case Report Top

A 68-year-old male presented with a complaint of non-healing ulcers in the mouth since 6 months associated with pain and burning sensation. Gradual onset associated with erythema and burning sensation followed by blistering that ruptured within 2-3 days led to ulceration of the region. There was no history of prodromal symptoms of fever or malaise. Initially, lesions were noted over the dorsum of the tongue followed by involvement of the palate and buccal and labial mucosae associated with difficulty in swallowing. Two months later, he noticed similar lesions over the skin, predominantly on the trunk and scalp regions, which healed within 7-14 days.

The patient consulted a skin specialist 3 months back and was under treatment with topical corticosteroids and anticandidal mouth rinses. Skin lesions showed signs of healing with hypopigmentation, but the intraoral lesions persisted.

Past medical history revealed that the patient is a known diabetic since 14 years and is under medication. Family history was non-contributory.

The patient has a poor oral hygiene, with a habit of chewing areca nut, lime and tobacco about five to six times a day for a period of 20 years, which he stopped since 1 year.

On general physical examination, the patient was poorly nourished and weak, with signs of pallor. Review of systems revealed no significant abnormalities.

Examination of the trunk revealed multiple, well-defined, roughly round erosive lesions measuring approximately 1 Χ 2 cm in dimension.

Head and neck examination, as shown in [Figure 1], revealed discrete erosive lesions over the cheek, nose and scalp, measuring approximately 0.5 Χ 1 cm in diameter. Scalp lesions causing scarring alopecia should be noted [Figure 2]. [Figure 3] illustrates erythematous, disc-like, scaly plaques showing signs of healing accompanied by scarring and hypopigmentation.

The bilateral submandibular lymph nodes are palpable, single in number, tender, firm, mobile and measuring approximately 1 cm in diameter.

Intraoral examination revealed painful restricted mouth opening with multiple superficial discrete ulcerations along the upper and lower labial mucosa, buccal mucosa, soft palate and vestibule. Diffuse, irregular ulcers covered by a pseudomembraneous slough were noted [Figure 4] and [Figure 5].

On palpation, the ulcers are tender and bleed on slight provocation. Multiple fibrotic bands are felt along the bilateral buccal mucosa and circumorally. The tongue appears to be depapillated, with areas of fissuring and erythema.

Hard tissue examination revealed poor periodontal health, with generalized mobility and attrition of the teeth.

Based on history and clinical examination, a provisional diagnosis of DLE was made. Differential diagnosis of SLE and other autoimmune blistering mucocutaneous disorders was considered.

   Histopathological Examination Top

[Figure 6] illustrates the histopathological section obtained from the incisional biopsy of a skin lesion, which revealed epidermal hyperkeratosis and focal keratotic plugging. Mild atrophy of the stratum malphigii and mild degeneration of the basal layer were also seen. The dermis showed mild edema and few scattered aggregates of mononuclear chronic inflammatory cells in the form of lymphocytes and plasma cells, features suggestive of DLE.

[Figure 7] illustrates the histopathological section obtained from the incisional biopsy of an ulcer from the buccal mucosa, showing stratified squamous epithelium with subepithelial connective tissue. The epithelium showed severe dysplasia in the form of pleomorphism, nuclear atypia and loss of polarity and the basement membrane at one area appeared to be disrupted. The subepithelial tissue had a dense chronic inflammatory cell infiltrate consisting of lymphocytes, plasma cells and macrophages, features suggestive of severe epithelial dysplasia.

   Treatment Given Top

On the first visit, an immediate palliative treatment for intraoral lesions with topical antibiotics and analgesics along with multivitamins, proteins and antioxidant supplements was given. Skin lesions were treated with topical corticosteroids.

Follow-up examination after 5 days showed a mild regression of the symptoms and was advised with intraoral topical corticosteroids to be applied over the affected areas twice daily for 2 weeks along with topical antifungal therapy.

[Figure 8] and [Figure 9] illustrate signs of healing intraoral and skin lesions on the subsequent visit after 2 weeks.

   Discussion Top

DLE is a type of LE that is mainly confined to the skin and has minimal systemic involvement. The characteristic cutaneous lesions of DLE begin as erythematous, edematous, scaling papules that spread centrifugally and coalesce into plaques, the size of which varies from a few millimeters to a few centimeters. Lifting of the scales produces a carpet-tack appearance revealing dilated pilosebaceous orifices occupied by horny plugs. The healing of a lesion takes place in the center, producing atrophy, scarring, telangiectasia and pigmentary changes. Scarring alopecia is a significant finding.

Mucosal surface is affected in about 24% of the DLE patients, lesions appearing as chronic plaques or lichen planus-like oral lesions, ulcerations, cheilitis and plaque-like palatal lesions. [2]

DLE is slightly more common in African Americans than in whites or Asians. Patients with DLE probably have a genetic pre-disposition, which tends to run in the families. The pathophysiology of DLE is not well understood. It has been suggested that a heat shock protein is induced in the keratinocyte following ultraviolet (UV) light exposure or stress, and this protein may act as a target for gamma (delta) T-cell-mediated epidermal cell cytotoxicity. [3] In some patients with DLE, sunlight and cigarette smoking may make the lesions to appear.

Patients may manifest any symptom of SLE. Therefore, the history should include an assessment for symptoms of pleuritis, pericarditis, neurologic involvement and renal involvement.

Patients with DLE are often divided into two subsets: Localized and widespread. Localized DLE occurs when the head and neck only are affected, whereas widespread DLE occurs when other areas are affected.

Diagnostic criteria for DLE

  1. One or more cutaneous lesions in the form of an erythematous, disc-like, patch or plaque with some or all of the following features: Scales, follicular plugs, scarring, atrophy, telangiectasia, central hypopigmentation and peripheral hyperpigmentation.
  2. Skin biopsy of an established lesion showing features compatible with a diagnosis of LE.
  3. An absence of significant extracutaneous symptoms and signs at initial presentation, e.g., fever, arthralgia, Raynaud's phenomenon and diffuse alopecia.
  4. Normal systemic examinations except for the presence of skin and mucous membrane lesions.
  5. An absence of significant laboratory abnormalities at initial visits.
  6. Clinical features and results of investigations did not meet the American College of Rheumatology's revised classification criteria for SLE at initial visits. [2]
The diagnosis of DLE can be confirmed by the histopathological examination of a biopsy from an established lesion. Using direct immunofluorescence, immunoglobulin (Ig) G and IgM deposits can be seen at the dermoepidermal junction in 80% of the cases but for old lesions, this test can be negative. Hence, examination of a lesion for immunoreactants can be a useful test to support the diagnosis and cannot be used to confirm or rule out the diagnosis.

The treatment of DLE aims at avoiding exacerbating factors and the palliative suppression of lesions. Patients sensitive to sunlight need to wear a UVA/UVB-15 protective sunscreen daily and a hat while outdoors.

Topical steroid is the first-line drug for localized cutaneous and mucosal lesions. Intralesional cortisone injections, systemic corticosteroids, calcineurin inhibitors, pimecrolimus cream or tacrolimus ointment, aminoquinoline antimalarials, [4],[5],[6],[7] dapsone or imiquimod 5% may also be used along with topical antifungal therapy. Topical hydroquinone is used for the treatment of hyperpigmentated scars.

More recently, biological therapies with agents like etanercept and tumor necrosis factor have demonstrated an overall decline in the disease activity. Efalizumab, a monoclonal antibody and a T-cell modulator has also shown a good response in patients with DLE. [8]

Follow-up is important and necessary every 6 months as DLE is considered as a pre-cancerous condition and for the early detection of SLE and to minimize scarring.

   Conclusion Top

The DLE-associated cutaneous and oral lesions have a significant impact on the dental management of these complex patients and the oral lesions often are challenging to resolve. Appropriate treatment ranges from topical steroids to potent systemic immunosuppressive therapy. Nevertheless, with appropriate training and an understanding of the complex manifestations of LE, management can be provided by the dental practitioner.

   Acknowledgments Top

We would like to thank all the staff members of the Department of Oral Medicine and Radiology and the Dean, A. B. Shetty Memorial Institute of Dental Sciences, Mangalore.

   References Top

1.Available from: http://www.emedicine.com; December 11, 2008.  Back to cited text no. 1      
2.Tang WY, Chan LY, Lo KK. Discoid lupus erythematosus in Hong Kong Chinese: A review of 12 cases. Hong Kong Med J 1996;2:239-46.  Back to cited text no. 2      
3.Kuechle MK, Elkon KB. Shining light on lupus and UV. Arthritis Res Ther 2007;9:101.  Back to cited text no. 3  [PUBMED]  [FULLTEXT]  
4.Brennan MT, Valerin MA, Napeρas JJ, Lockhart PB. Oral manifestations of patients with lupus erythematosus. Dent Clin N Am 2005;49:127-41.  Back to cited text no. 4      
5.Neville B W, Damn DD, Allen CM, Bouquot JE. Oral and maxillofacial pathology. 2 nd ed. London: W B Saunders Co. Ltd; 2002.  Back to cited text no. 5      
6.Rajendran R, Shivapathasundaram. Shafer′s Textbook of Oral pathology. 5 th ed. Philadelphia: W B Saunders Co. Ltd; 2005.  Back to cited text no. 6      
7.Jayakumar ND, Jaiganesh R, Padmalatha O, Sheeja V. Systemic lupus erythematous. Indian J Dent Res 2006;17:91-3.  Back to cited text no. 7  [PUBMED]  Medknow Journal  
8.Usmani N, Goodfield M. Efalizumab in the treatment of discoid lupus erythematosus. Arch Dermatol 2007;143:873-7.  Back to cited text no. 8      


  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9]


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