Solitary Langerhans cell histiocytosis in an adult: case report and literature review.

BACKGROUND: Langerhans cell histiocytosis (LCH) is a disease that often affects children, but can also occur in adults and smokers. Oral manifestations are unusual and are characterized by bone pain, tooth mobility, necrotic ulcers and local edema. The aim of this paper is to describe a clinical case of LCH in an oral cavity that mimicked oral squamous cell carcinoma. CASE PRESENTATION: A male, 63 years old, complaining about a "wound in the mouth" for 6 months, without any pain or spontaneous bleeding. His medical history was free of disease. The patient was a smoker for 33 years. Intraoral examination revealed a destructive ulcerative lesion around the upper left first and second molars that resembled an oral squamous cell carcinoma. Biopsy of the ulcerative lesion was performed and the microscopic features showed an inflammatory infiltrate rich in plasma cells. Based on this microscopical finding, the final diagnosis was periodontal disease associated with a proliferative non-neoplastic lesion. The patient was referred to a specialized dental surgeon and underwent periodontal therapy including surgical procedures. After that, according to follow-up with the patient, there were no signs of disease remission. The lesion increased in size, although the patient did not complain of any symptoms. A second biopsy was performed and the microscopic features again showed a rich inflammatory infiltrate with mononuclear cells and histiocytic cells, characterized by pale histiocytes with lobed nuclei, resembling a bean. A varying number of eosinophils also were observed, without any evidence of atypical cells present in this infiltrate. An immunohistochemical staining panel was done to determine the nature of this inflammatory infiltrate by using antibodies S-100, CD1a, CD-68 and CD45RO that were positive. These immunohistochemical findings were fundamental for the final diagnosis of LCH. The treatment included surgical extraction of all superior teeth, radiation and systemic corticoid therapies. After 8 years of treatment, the patient is free of disease. CONCLUSION: Although LCH is an unusual lesion in an oral cavity, it can be present. Biopsy and a histological exam are essential to establish the diagnosis. Immunohistochemicals were fundamental to exclude malignant lesion and to confirm the diagnosis of LCH.

Immune response in cervical lymph nodes from patients with primary oral squamous cell carcinoma.

BACKGROUND: Deficient immune response in the cervical lymph nodes of patients with head and neck squamous cell carcinoma may contribute to dissemination of metastatic neoplastic cells. This study evaluates the immune response in cervical lymph nodes from patients with primary oral cavity squamous cell carcinoma (OCSCC). METHODS: The density of immature (CD1a(+)) and mature (CD83(+)) dendritic cells (DCs), cytotoxic T lymphocytes CD8(+) /perforin(+) (CTLs), and Foxp3(+) regulatory T (Tregs) cells in the lymph nodes of patients with OCSCC without cervical lymph node metastases (LN1) (negative) (n = 10) were identified through immunohistochemistry. From patients with cervical lymph node metastases, samples were obtained of lymph nodes both with (LM2) (positive) (n = 10) and without (LN2) (negative) (n = 10) metastases. RESULTS: The results demonstrated that the number of CD1a(+) and Foxp3(+) cells was significantly higher in the LM2 group than in either the LN1 or the LN2 group. In addition, the number of CD8(+) /perforin(+) and CD83(+) cells was significantly lower in the LM2 group than in the other groups. CONCLUSION: The results of this study demonstrate a higher density of immature DCs and Tregs cells and a lower density of mature DCs and activated CTLs in metastatic than in non-metastatic lymph nodes. These findings might indicate an immunosuppressive microenvironment, which could be involved in the spread of neoplastic cells to cervical lymph nodes.

Oral squamous cell carcinoma versus oral verrucous carcinoma: an approach to cellular proliferation and negative relation to human papillomavirus (HPV).

Human papillomavirus (HPV) has been cited as a possible initiating agent in the pathogenesis of oral cancer. However, the literature tends to be both controversial and inconclusive about the prevalence of HPV and its potential for proliferation in oral squamous cell carcinoma (SCC). The aim of this study was to investigate the cellular proliferation and the presence of HPV in SCC and verrucous carcinoma (VC). Forty-seven samples of SCC were selected and divided into three groups: 39 SCC, 8 VC, and 9 of normal mucosa (control-CT). Quantitative analyses of all groups showed a greater expression of PCNA, followed by Ki-67 and cyclin B1. A significant difference was observed in cyclin B1 expression in the SCC group compared with VC. PCNA, Ki-67, and cyclin B1 were statistically significant when comparing the SCC and CT groups. However, when SCC and VC were compared, there was no difference in Ki-67 expression. Our results showed that only cyclin B1 had an association with histological grade, and that poorly differentiated tumors presented a higher expression of cyclin B1. Therefore, considerable differences in the cellular proliferation between SCC and VC were observed, and no correlation with HPV was established, since all samples were negative for HPV.

Association of CCL2 with lymph node metastasis and macrophage infiltration in oral cavity and lip squamous cell carcinoma.

AIMS/METHODS: We investigated the expression of CCL2 by immunohistochemistry in samples of oral cavity squamous cell carcinoma (OCSCC), lip squamous cell carcinoma (LSCC) and metastatic and nonmetastatic lymph nodes. The relationship of CCL2 with survival data was also evaluated. RESULTS: The percentage of CCL2+ cells in tumor parenchyma was similar in OCSCC and LSCC. In stroma, OCSCC showed a higher number of CCL2+ cells when compared with LSCC. In contrast, higher CD68+ macrophage counts were observed in LSCC. Low macrophage counts were significantly related to a greater proliferative index in tumoral cells. The density of CCL2+ nodal cells was significantly higher in metastatic lymph nodes when compared with nonmetastatic lymph nodes. When considering CCL2 in the parenchyma, the mean survival time for the patients with high CCL2+ cell counts was lower than that for patients with low CCL2+ cell counts. In contrast, in stroma, the mean survival time for the patients with high CCL2+ cell percentages was higher than for those with low CCL2+ cell percentages. CONCLUSION: Our findings suggest a role for CCL2 in the spreading of tumoral cells to the lymph node in OCSCC. Furthermore, the CCL2-independent macrophage infiltration may play a role in determining less aggressive behavior.