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| Year : 2006 | Volume
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| Issue : 2 | Page : 91-3 |
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| Systemic lupus erythematosus |
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ND Jayakumar, R Jaiganesh, O Padmalatha, V Sheeja
Department of Periodontitis, SIMATS, Chennai, India
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 Abstract | | |
Desquamative gingival lesions are non-plaque induced inflammatory gingival lesions. It is a clinical description and not a diagnosis. These desquamative lesions represent oral manifestations of various dermatoses. Systemic lupus erythematous (SLE), one of the rare dermatoses shows desquamative lesions as the oral manifestation. We here with report a case of SLE with oral lesions involving gingiva of a 36 year old female patient. The clinical presentation, histological features, and investigatory findings are discussed. Keywords: SEE, desquamative gingival lesion, dermatoses
How to cite this article:
Jayakumar N D, Jaiganesh R, Padmalatha O, Sheeja V. Systemic lupus erythematosus. Indian J Dent Res 2006;17:91 |
| Introduction | |  |
Desquamative lesions of the gingiva are non-plaque induced inflammatory gingival lesions. The term desquamative gingivitis is a clinical description and not a diagnosis [1]. It is used for conditions in which the gingiva appears red and desquamation of surface epithelium of attached gingiva is seen. Usually the whole of the attached gingiva of varying number of teeth is affected [1]. These desquamative lesions represent oral manifestations of various dermatoses which include lichen planus, pemphigus, erythema multiforme, lupus erythematosus, mucus membrane pemphigoid, bullous pemphigoid or scleroderma. Other conditions that must be considered when gingival desquamative lesions are present include endocrine imbalances, chronic infections and drug reactions [2]. The purpose of this paper is to report a case of rare desquamative lesion in regard to clinical, histopathologic and immunologic features.
| Case report | | |
A 36-year-old female came to the hospital with the complaint of burning sensation in the gums for the past one month. Burning sensation in the gums started one month back spontaneously, not associated with pain and aggravated on taking spicy foods and relieved gradually. She also had bleeding gums for the past one month while brushing and eating.
Her past medical history revealed that she had vesicles on the skin of lower limbs three months back and had undergone treatment for the same. She had joint pain for the past six months, pain during micturition, pain in the ear for the past six months and she has frequent respiratory tract infections. There was no relevant drug history or significant family history. She had not received any dental treatment before. Her personal history reveals that she had no inexpedient habits and she used only soft brush with non medicated paste.
On extra oral examination, there was no facial asymmetry and no lymphadenopathy. Intra oral examination of the buccal mucosa revealed an erythematous area measuring 1x1 cm 2 sub with white radiating lines seen in relation to maxillary third molar region. The white lines were not scrappable. Tongue, palatal mucosa and floor of the mouth were normal.
Examination of the gingiva revealed reddish marginal gingiva, attached gingiva and interdental papilla in both maxillary anterior and mandibular right and left posterior region. Grayish white areas were seen in attached gingiva of maxillary anteriors and mandibular posteriors [Figure 1,2]. It was firm and resilient in consistency. Bleeding on probing was present in the maxillary anterior and posterior gingiva and mandibular posterior gingiva, There were no periodontal pocket, furcation involvement and mobility. Based on the history and clinical features, the differential diagnosis included lichen planus, lupus erythematosus and Wegener's granulomatosis. The biopsy of the gingivawas done under local anesthesia in the maxillary anterior and mandibular posterior region. Biopsy was not considered for the lesion, which was present on the buccal mucosa distal to the maxillary third molar region, due to the difficulty in access to that region. Specimens were sent for histopathological examination. Slides were prepared for H and E staining and periodic acid Schiff (PAS) staining.
| Histopathology | | |
H and E section showed hyperparakeratinized squamous epithelium with hyperplastic, confluent rete ridges and pseudo epitheliomatous hyperplasia and focal areas of basal cell degeneration. Parakeratin plugging was seen in few areas. The underlying connective tissue had diffuse, moderate, inflammatory cell infiltrate with lymphocytes, few plasma cells and macrophages. Connective tissue showed mature collagen bundles with moderate vascularity. Histopathologicfeatures were not suggestive of lichen planus or Wegener's granulomatosis [Figure 3, 4]. PAS staining showed basement membrane thickening [Figure - 5].
As the histology was non-specific, complete hematological and urine examination and anti-nuclear antibody (ANA) and anti-neutrophil cytoplasmic antibody (ANCA) were advised. Hematological examination included total WBC count, differential white blood cell count, erythrocyte sedimentation rate, hacmatocrit, bleeding time and clotting time were within normal limits. Urine examination was negative for albumin and sugar. While ANCA was negative, ANA was positive.
| Diagnosis | | |
Based on the criteria proposed by AmericanAcademy of Rheumatologists for SEE [3] such as skin lesion, arthritis, renal function, respiratory function oral lesions and ANA test positivity, the lesion was diagnosed as systemic lupus erythematosus.
| Discussion | | |
Lupus erythematosus is a connective tissue disease which has two main forms, discoid lupus erythematosus and systemic lupus erythematosus. Either of these two can give rise to oral lesions which may appear similar to those of oral lichen planus[1]. Discoid lupus erytematosus is a skin disease with muco cutaneous lesions indistinguishable clinically from those of systemic lupus erythematosus [2].
Systemic lupus erythematosus (SEE) is a serious multisystem disease with variety of cutaneous and oral manifestations. It is an auto immune disease, where the patient develops auto antibodies to many of their cells and cell components and tissues [3]. Some of the manifestations appear to result from deposition of antigen antibody complex in the tissues. SEE often presents in non-specific, vague fashion, frequently with periods of remission and exacerbation. The age of onset is about 30 years in females and 40 years in males. Females are more commonly affected (F: M = 8:1) [4].
Cutaneous manifestations are erythematous patches on the face which coalesce to form a roughly symmetrical pattern over the cheeks across the bridge of the nose in a butterfly distribution. Skin over the neck, arms, shoulders and fingers are also affected. Patient may complain of itching or burning sensation. Some may present with areas of hyperpigmentation.
Involvement of various organs including the kidney, heart, lungs and CNS occurs. Joint pains and arthritis are common manifestations. Kidneys are affected in 40-50 % of patients and 50 % of SEE patients develop warty vegetations affecting the heart valves [3].
Oral lesions of SEE develop in 20-50% of patients. The oral mucosamay be involved either prior to or following the development of skin lesions or even in the absence of skin manifestations [5]. Oral lesions begin as erythematous areas, without induration and with white spots. The margins of the lesions are not sharply demarcated but frequently show the formation of narrow zone of keratinization. Hyperemia with edema will be there and there maybe a tendency for bleeding [5].
In this case, with H and E stain, lichen planus was ruled out, as the characteristic histopathologic feature of lichen planus such as saw tooth rete pegs and sub epithelial band of lymphocytes were absent. The characteristic histopathologic features of Wegener's granulomatosis such as dense inflammatory infiltrate with scattered giant cells and vascular changes were absent. Anti nuclear cytoplasmic antibody (ANCA), the confirmatory test for Wegener's granulomatosis was further negative. In this case, the histopathologic features were non-specific, but the contributory finding of basement membrane thickening with PAS staining is suggestive of systemic lupus erythematosus. Further investigation with ANA test which was positive is suggestive of systemic lupus erythematusus.
Normally antibodies present in the blood repel invaders in our body, such as virus, bacteria and other microbes. However ANA are antibodies detectable in the blood, that have the capability of binding to certain structures within the nuclei of cells [8]. ANA's are directed against several nuclear antigens and can be grouped into four categories, namely, antibodies to DNA, antibodies to histories, antibodies to non historic proteins bound to RNA and antibodies to nucleolar antigens.
The most commonly utilized method is indirect irmnunofluorescence, which detects a variety of nuclear antigens, including DNA, RNA and proteins (generic ANA). ANAs detected by this technique are present not only in SEE but also in other auto immune conditions like Hasbimoto's thyroiditis, rheumatoid arthritis and Sjogren's syndrome. The immuno-fluorescence test for ANA is sensitive for the detection of SEE, but it is 95% specific for SEE.
In the present case, the medical history revealed the presence of skin lesions in lower extremities three months back, joint pains, frequent respiratory tract infections and pain during micturition for the past six months. Along with medical history, the clinical appearance of oral lesions, histopathology and special investigations especially ANA, contributed to the diagnosis of systemic lupus erythematosus.
| Treatment | | |
Patient with systemic lupus erythematosus should avoid excessive exposure to sunlight because ultraviolet light may precipitate disease activity. For oral lesions, topical corticosteroids are effective and along with that systemic corticosteroids are prescribed. For cases that are resistant to topical steroid therapy, systemic antimalarial drugs may produce a response. In the present case, Triamcinolone with ora base topical steroid and along with that Prednisolone 5mg tablet twice daily was prescribed.
| References | | |
| 1. | Cawson RA, Odell EW: Essentials of oral pathology and oral medicine (6 fsub edition), Churchill Livingstone, London, pages 191 192, 301-302, 1997.  |
| 2. | Carranza, Newman, T'akei: Clinical Periodontology and Implant dentistry (9'° sub edition), Harcourt Asia Pvt Ltd, India, pages 328-329, 2003. |
| 3. | Neville BW, Damn DD, Allen CM, Bouquot JE: Oral and Maxillofacial Pathology (1"ed.), WB SaundersCo.Ltd, London, pages 580-583,1995. |
| 4. | ShaferWG,HineMK,Levy BM:Atextbookoforal pathology (4 `" ed.), WB Saunders Co. Ltd, Philadelphia, pages 841-845, t993. |
| 5. | Rhodes NL: The review of oral manifestations of systemic lupus erythematosus, Quintessence international, 21:461-465,1990. |
| 6. | Berger: Lupus Erythematosus, Brit Med J, 320: 1495,2000. |
| 7. | Burge SM et al : Mucosal involvement in systemic and chronic lupus erythematosus, Brit J Dermatol, 121:727-741,1989. |
| 8. | Swarsh: Hutchison's clinical methods (19'°sub edition), ELBS London. |
Correspondence Address:
N D Jayakumar
Department of Periodontitis, SIMATS, Chennai
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0970-9290.29883
Figures
[Figure - 1], [Figure - 2], [Figure - 3], [Figure - 4], [Figure - 5] |
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