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Revista Española de Cirugía Oral y Maxilofacial

On-line version ISSN 2173-9161Print version ISSN 1130-0558

Rev Esp Cirug Oral y Maxilofac vol.28 n.3 Barcelona May./Jun. 2006

 

PÁGINA DEL RESIDENTE

 

What should the diagnosis be?

¿Cuál es su diagnóstico?

A 56-year old female, with no personal medical history of interest, was referred to our unit with a lesion on the left border of her tongue that had been evolving for three months. It was painless and had been growing continually. There were no associated consumptive or feverish symptoms. Her medical history did not include smoking, alcohol use or any other toxic substances. There was no evidence of a focus of infection or of any spontaneous bleeding of the lesion, and she denied any previous trauma in the area.

During the physical examination several root remains were observed together with a lesion measuring 5 x 2.5 cm in diameter in the left ventro- lateral side of the tongue. The lesion was exophytic, with an erythematous base and a whitish surface and it protruded by 2 cm from the ventro-lateral side of the tongue. No other lesions were observed on the lingual surface. The neck examination did not reveal any clinically significant swelling (Fig. 1).

An incisional biopsy of the lesion was carried out under local anesthesia. The macroscopical examination reported a ring of mucosa with a surface that measured 1 x 0.6 cm and a depth of 0.5 cm. There were two lesions on the mucosal surface, one was raised and whitish with a warty appearance, and it measured 0.7 cm at its widest point. The second lesion was on the other side of the ring. It was whitish with papillomatous features and it measured 0.5 cm at its widest point.

The histological study by microscope reported a mucosal surface on the tongue with endo-exophytic transformation and ortho- and parakeratotic hyperkerastosis together with a polymorphonuclear and lymphocytic inflammatory infiltrate by the chorion with focal extension into the overlying epithelium. PAS positive fungal hyphae were identified that were related to Candida (Figs. 2 and 3).


Chronic hyperplastic candidosis of the oral mucosa

Candidiasis hiperplásica crónica de la mucosa oral

 

 

R. González-García1, J. Sastre-Pérez2, M.F. Muñoz-Guerra2, L. Naval-Gías2, F.J. Rodríguez-Campo2
C. Gamallo3, F.J. Díaz-González4

1 Médico Residente. Servicio de Cirugía Oral y Maxilofacial
2 Médico Adjunto. Servicio de Cirugía Oral y Maxilofacial
3 Médico Adjunto. Servicio de Anatomía Patológica
4 Jefe de Servicio de Cirugía Oral y Maxilofacial.
Hospital Universitario de la Princesa, Madrid, España.

Correspondence

 

 

With the diagnosis of verrucous hyperplasia with acute inflammation associated with Candida, anti-fungal medical treatment was administered. Once hepatic disease had been ruled out, Ketoconazole was prescribed at a dose of 200 mg orally per day for two weeks, together with oral rinses with nystatin and chlorhexidine.

After two weeks of anti-fungal treatment, the patient returned for follow-up. The lesion continued to persist and there were no apparent changes. Due to this persistence and following medical therapy failure, a decision was made to carry out a biopsy excision of the lesion with a CO2 laser under general anesthesia. The lesion was removed with minimal margins of healthy tissue. The surgical bed was vaporized and an oxycellulose pad was placed and proper hemostatic control was achieved. There were no complications during the immediate and late post-operative period, and complete functional recovery was achieved. The anatomopathologic study confirmed the initial biopsy findings, and a lesion that was identical to the previous one was reported, but this time fungal hyphae were not identified. The diagnosis was of lingual mucosa with warty hyperplasia and both acute and chronic inflammation. There were no signs of recurrence 12 months after surgery.

 

Discussion

Candida is found in the oral commensal microflora of 40% of healthy individuals.1 However, it can be responsible for fungal infections with local or systemic repercussions. The most common clinical manifestation is in the mucosa, although the systemic form can occur in immunodepressed patients.2 There are a series of local factors that favor candidiasis infection such as the use of prostheses, smoking, dry mouth, concomitant oral pathology and topical treatment with antibiotics and steroids.

Chronic Hyperplastic Candidosis (CHC) is a type of oral candidiasis infection with certain clinical and histological characteristics that serve as a base for its diagnosis. Other clinical forms of candidiasis consist of the pseudomembranous variety, the erythematous variety, and erythematous variety associated with dental prostheses, median rhomboid glossitis and angular cheilitis.

The histological examination of the CHC specimen showed parakeratosis of the mucosal surface epithelium, with Candida hyphal invasion. The presence of polymorphonuclear leukocytes in the epithelium that form microabscesses in the stratum corneum is a characteristic feature. In addition to this, the lamina propria showed chronic inflammatory cell infiltrate.3 Our case had the histological characteristics mentioned as well as an acute inflammatory component made up of polymorphonuclear leukocytes and chronic inflammation made up of lymphocytes. The epithelial and chorion involvement was in accordance with reports in the literature. The invasion of the epithelium by Candida hyphae in the initial biopsy contributed to the etiological diagnosis. The systemic anti-fungal therapy administered for the two weeks that followed the diagnosis was enough to eliminate the Candida in the lesion, but not the inflammatory component and the hyperplastic response.

With regard to the inflammatory response observed, it has been reported that the extension of the inflammatory infiltrate does not depend on the number of hyphae present in the specimen, but rather on the time over which the infection has been evolving, or on the properties of the Candida invasion.3 Current histopathological studies with modern staining techniques have shown that the presence of Candida albicans and Candida glabrata is common place in CHC biopsies.4 The presence of T lymphocytes in the lamina propria and underlying epithelium is typical, together with lymphocytes secreting IgA, all in conjunction with polymorphonuclear leukocytes recruited in the epithelium by T lymphocytes.

We believe that carrying out a diagnostic biopsy is necessary for those cases in which the cytological and microbiological studies are inconclusive and when the symptoms have not improved with medical treatment. In this particular case, active systemic anti-fungal treatment for Candida was given. This was therefore not an empirical treatment, as is indicated when awaiting the microbiological study results and when the suspected diagnosis is of a fungal infection. As the clinical presentation of this entity was of exophytic formations that had been growing slowly over various months, and as the localization on the tongue was ventrolateral, an epidermoid carcinoma of the oral mucosa with an exophytic growth pattern was suspected. With this diagnostic suspicion, an incisional biopsy was mandatory, and while the anatomopathological results were awaited no treatment was administered. The differential diagnosis with lesions of this type should lead the physician to rule of the possibility of a neoplasm, which would require rapid treatment. Once this has been ruled out, other therapeutic options can be considered.

We believe, in concordance with Zegarelli,5 that when dealing with lesions of the oral mucosa and when a fungal infection is suspected, establishing empirical treatment is fundamental, not only for obtaining an diagnosis due to clinical improvement and the disappearance of the lesion, but also in order to avoid delaying treatment while awaiting the results of the cultivation or the cytology exudate results. We believe, however, that in some CHC cases, an incisional biopsy is a priority as from the start, in order to avoid diagnostic errors in the event of possible squamous cell carcinoma with a similar clinical presentation. In this sense, the microscopic demonstration of fungal hyphae is indicative of Candida infection, regardless of whether this has been observed in the PAS swabs or in the interior of stratified squamous epithelium of a biopsy sample.

It is well known that the chronic forms of fungal infections are more resistant to therapy. In this sense CHC and rhomboid glossitis have a worse response to anti-fungal therapy than the erythematous and pseudomembranous varieties of candidiasis. A reduction of the size of CHC lesions in patients treated with anti-fungal medication has been reported. However, a high percentage of these lesions persist in spite of therapy.6,7 In our opinion, medical anti-fungal therapy before surgical treatment may be advisable for CHC cases. For small sized lesions a reduction of the size of the lesion can be expected. Surgical removal will thus be less aggressive and patient morbidity will be reduced. However, if progress is poor, surgical treatment should not be delayed given the possibility of neoplastic progression to squamous cell carcinoma.8,9 CHC lesions of a large size, such as the one in this case, can respond poorly to medical therapy and surgical treatment is eventually required. In this particular case, once the existence of malignancy had been ruled out, surgical excision was decided on while conserving the maximum volume of macroscopically normal tissue. We preferred using Laser CO2 with vaporization of the lesion bed and second intention healing so that tongue size was not reduced.

 

 

Correspondence:
Raúl González García
C/ Los Yébenes 35, 8 C
28047 Madrid, España
Email: raugg@mixmail.com

 

 

References

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3. Williams DW, Potes AJ, Wilson MJ, Matthews JB, Lewis MAO. Characterisation of the inflammatory cell infiltrate in chronic hyperplastic candidosis of the oral mucosa. J Oral Pathol 1997;26:83-9.        [ Links ]

4. Williams DW, Wilson MJ, Lewis MAO, Potes AJC. Identification of Candida species in formalin-fixed, paraffin-embedded oral mucosa by sequencing of ribosomal DNA. J Clin Pathol Mol Pathol 1996;49:23-8.        [ Links ]

5. Zegarelli DJ. Fungal infections of the oral cavity. Otolaryngol Clin N Am 1993;26:1069-89.        [ Links ]

6. Budtz-Jorgensen E. Histopathology, immunology, and serology of oral yeast infections. Acta Odontol Scand 1990;48:37.        [ Links ]

7. Holmstrup P, Axell T. Classification and clinical manifestations of oral yeast infections. Acta Odontol Scand 1990:48:57.        [ Links ]

8. Williamson DM. Chronic hyperplastic candidiasis and squamous carcinomaa. Br J Dermatol 1969;81:125-7.        [ Links ]

9. Eyre J, Nally FF. Oral candidosis and carcinoma. Br J Dermatol 1971;85:73-5.        [ Links ]

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