DC-SIGN and VDR polymorphisms are associated with chronic form of paracoccidioidomycosis with oral manifestations.

Paracoccidioidomycosis (PCM) is a granulomatous disease caused by fungi of the species complex of the Paracoccidioides genus. One of the main clinical manifestations of PCM is the presence of oral lesions with the presence of epithelioid granulomas. In this work, we aimed to evaluate the frequency of SNPs in the TNF-α, JAK1, VDR, DC-SIGN and FcγRIIa genes in patients with chronic PCM and verify possible association of these SNPs with the organisation pattern of the granulomas in the oral lesions. A total of 66 samples of DNA were obtained from oral lesions biopsies and 106 DNA samples were obtained from healthy individuals. The individuals were genotyped for SNPs in DC-SIGN (rs4804803), FcγRIIa (rs1801274), JAK1 (rs11208534), TNF-α (rs1800629) and VDR (rs7975232) by real-time PCR and allele discrimination method. Granulomas were classified as loose or dense according to the histological pattern. In the VDR (rs7975232), the CC genotype (P < 0.001, OR = 5.94, 95% CI = 2.07-17.05), and the C allele (P = 0.027, OR = 2.71, 95% CI = 1.07-6.86), as well as the GG genotype in DC-SIGN (rs4804803) (P = 0.032, OR: 3.76, 95%, I = 1.06-13.38) are associated with an increased risk of oral PCM. Our data indicate that VDR and DC-SIGN genetics variations are related to the susceptibility of oral PCM in the group of patients analysed.

Lipopolysaccharide-induced acute lung injury in mice chronically infected by Schistosoma mansoni.

We used a murine model of Schistosoma mansoni (SM) infection and lipopolysaccharide (LPS)-induced endotoxicity to investigate if these conditions can interact to modify the pathological manifestations typically observed in each condition. Swiss mice were randomized into four groups: SAL, uninfected; SM, infected; LPS, uninfected + LPS; and SM + LPS, infected + LPS. S. mansoni infection developed over 120 days, after which blood samples and lungs were collected, peritoneal leukocytes were isolated and cultivated for 6 and 24 h after LPS inoculation (1 mL/kg). Infected animals presented marked granulomatous inflammation. LPS exposure transiently modified the profile of leucocyte migration into the lung tissue and increased NO production by isolated leukocytes, without inducing any acute effect on the structure of schistosomiasis granulomas. Beyond modifying lung morphology, S. mansoni and LPS interacted to modulate the circulating levels of cytokines. S. mansoni infection restricted INF-γ upregulation 6 and 24 h after LPS administration. Conversely, 24 h after inoculation, LPS increased IL-2 and IL-5 levels. Our findings indicate that LPS impaired the lung microenvironment by acutely disrupting inflammatory homeostatic mechanisms that control lung schistosomiasis. As schistosomiasis develops as a chronic condition, long-term exposure to endotoxins could aggravate the granulomatous process, an issue that requires further investigation.

Photodynamic inactivation of oral paracoccidioidomycosis affecting woman with systemic lupus erythematosus: An unusual case report.

Paracoccidioidomycosis (PCM) is a systemic disease caused by the dimorphic fungus Paracocdioides brasiliensis. The infection primarily reaches the lungs by the inhalation of fungi spores and later can disseminate to other organs causing secondary oral lesions. Systemic lupus erythematosus (SLE), on the other hand, is an autoimmune chronic inflammatory disease that affects various organ systems, including skin and oral cavity. Here we report a 39-year-old female patient bearing SLE and presenting an ulcerated lesion on the hard palate extending to the superior alveolar ridge, diagnosed as PCM. Itraconazole 200mg was prescribed and photodynamic therapy (PDT) was also instituted in a way to help dealing with the PCM infection while assisting such an immunocompromised patient to heal. PDT consisted of topically placing toluidine blue dye at 37.5mg/L for 5min, followed by low-level laser irradiation (660nm; 100J/cm2; 40mW of power; 100s per point). Forty days after beginning the treatment, the patient showed total regression of the oral lesion and absence of painful symptoms. The serologic test was performed again after six months of therapy and was negative; the patient continues to be followed periodically.

Cyclin D1 and Ki-67 expression correlates to tumor staging in tongue squamous cell carcinoma

BACKGROUND: The immunohistochemical expression of Cyclin D1 and Ki-67 were analyzed in tongue squamous cell carcinomas (SCC), relating them to the clinical and morphological exhibition of these tumors. MATERIAL AND METHODS: Twenty-nine patients fulfilled the inclusion criteria; clinical data included gender, age, ethnicity and use of licit drugs such as alcohol and tobacco. The TNM staging and histopathological differentiation grading was assessed for each case. In addition, T1 patients were gathered with T2 patients; and T3 patients were gathered with T4 patients to assemble two distinct groups: (T1/T2) and (T3/T4). RESULTS: The mean follow-up time was 24 months and 30% of the patients died as a consequence of the disease, while 23.3% lived with the disease and 46.7% lived lesion-free. T1 and T2 tumors showed statistically lesser Ki-67 and Cyclin D1 staining when compared to T3 and T4 tumors. CONCLUSIONS: Ki-67 and Cyclin D1 pose as auxiliary tools when determining the progression of tongue SCC at the time of diagnosis

Correlation between clinical and histopathological diagnoses in periapical inflammatory lesions.

AIM: The purpose of the present study was to evaluate the correlation between clinical and histopathological diagnoses of periapical inflammatory lesions, focusing mainly on cystic conditions. METHODS: Files dating from 1998 to 2006 at the Oral Pathology Laboratory, School of Dentistry, Alfenas Federal University, Brazil, were reviewed to identify cases with histopathological diagnoses of periapical inflammatory lesions. A total of 1788 files were analyzed, and 255 cases were identified with clinical diagnoses of periapical inflammatory lesions. RESULTS: The most prevalent clinical diagnosis was apical periodontal cyst (59%), followed by periapical granuloma (20%), and dentoalveolar abscess (2%). After histopathological analysis, 53% of the cases represented apical periodontal cyst, 42% periapical granuloma, and 5% dentoalveolar abscess. CONCLUSIONS: The outcomes of the present study show a high prevalence of periapical cysts among periapical inflammatory lesions. Moreover, this study highlights the importance of histopathological evaluation for the correct diagnosis of periapical inflammatory lesions.

Localized gingival enlargement associated with alveolar process expansion: peripheral ossifying fibroma coincident with central odontogenic fibroma.

BACKGROUND: Despite the common occurrence of localized gingival enlargements, which often represent reactive lesions, the temporal and spatial association of such a lesion with a central jaw lesion has not been reported. The purpose of this case report is to present the exceptional combination of a peripheral ossifying fibroma and a central odontogenic fibroma. The differential diagnosis and management of each lesion is reviewed. METHODS: A 45-year-old black female presented with a chief complaint of a painless protuberance in the left mandible of 1-year duration. Clinical and radiographic examination revealed a gingival enlargement localized between teeth #21 and #23 and a multilocular radiolucent lesion with radiopaque foci in the same area. Excisional biopsy of the gingival lesion and incisional biopsy of the central lesion were performed, and specimens were submitted for histopathological analysis. RESULTS: Biopsy of the gingival lesion revealed stratified squamous epithelium and highly cellular fibroblastic component presenting central areas of calcification, features consistent with a diagnosis of peripheral ossifying fibroma. The central lesion was characterized by cellular fibrous tissue admixed with rests of odontogenic epithelium and few calcification areas, features consistent with a diagnosis of central odontogenic fibroma/World Health Organization type. Subsequently, the central lesion was enucleated. After 1-year follow-up, no recurrence has been observed. CONCLUSIONS: The combination of a rare central lesion with a common gingival lesion may present unique diagnostic and therapeutic challenges. Clinician awareness regarding the possibility of such a combined presentation and its implications will help to ensure optimal treatment outcomes.

Immunohistochemical profile of canalicular adenoma of the upper lip: a case report

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Canalicular adenoma is an uncommon benign salivary gland neoplasm that has a marked predilection for occurrence in the upper lip. It is composed of columnar cells arranged in branching and interconnecting cords of single or double cell thick rows. This tumor has an excellent prognosis after conservative surgical treatment in all locations. In the present report we describe, using immunohistochemistry, the expression of cytokeratins (CK), S-100 protein and EMA in a canalicular adenoma that arose in the upper lip of a 55-year-old female. Cells of the canalicular adenoma showed an immunohistochemical profile that indicates an excretory duct origin: most of these cells positively expressed AE1/AE3 cytokeratins and S100 protein. A comparison of the immunohistochemical features of canalicular adenoma with other salivary gland neoplasms that share similar histological features is discussed