RESUMO
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.
Assuntos
Moléculas de Adesão Celular/genética , Predisposição Genética para Doença , Lectinas Tipo C/genética , Doenças da Boca/genética , Doenças da Boca/patologia , Paracoccidioidomicose/genética , Paracoccidioidomicose/patologia , Receptores de Calcitriol/genética , Receptores de Superfície Celular/genética , Adulto , Alelos , Doença Crônica , Estudos de Coortes , Feminino , Granuloma/patologia , Histocitoquímica , Humanos , Masculino , Pessoa de Meia-Idade , Polimorfismo de Nucleotídeo Único , Reação em Cadeia da Polimerase em Tempo RealRESUMO
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.
Assuntos
Lesão Pulmonar Aguda/induzido quimicamente , Esquistossomose mansoni/complicações , Lesão Pulmonar Aguda/complicações , Análise de Variância , Animais , Doença Crônica , Citocinas/sangue , Modelos Animais de Doenças , Leucócitos/citologia , Leucócitos/metabolismo , Lipopolissacarídeos , Pulmão/patologia , Masculino , Camundongos , Óxido Nítrico/metabolismo , Distribuição AleatóriaRESUMO
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.
Assuntos
Doenças Periapicais/diagnóstico , Adulto , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Abscesso Periapical/diagnóstico , Abscesso Periapical/patologia , Doenças Periapicais/patologia , Granuloma Periapical/diagnóstico , Granuloma Periapical/patologia , Periodontite Periapical/diagnóstico , Periodontite Periapical/patologia , Cisto Periodontal/diagnóstico , Cisto Periodontal/patologia , Cisto Radicular/diagnóstico , Cisto Radicular/patologiaRESUMO
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.