RESUMO
This study investigated the expression of extracellular matrix glycoproteins tenascin (TN) and fibronectin (FN) in pulp repair after capping with calcium hydroxide (CH), following different hemostasis protocols. Class I cavities with a pulp exposure were prepared in 42 human third molars scheduled for extraction. Different hemostatic agents (0.9% saline solution, 5.25% sodium hypochlorite and 2% chlorhexidine digluconate) were used and pulps were capped with CH cement. After 7, 30 or 90 days, teeth were extracted, formalin-fixed, and prepared for immunohistochemical technique. Hemostatic agents did not influence the expression of TN and FN. Both glycoproteins were found in the entire the pulp tissue and around collagen fibers, but were absent in the mineralized tissues. In the predentin, TN showed positive immunostaining and FN had a variable expression. Within 7 days post-treatment, a slightly more pronounced immunostaining on the pulp exposure site was observed. Within 30 days, TN and FN demonstrated a positive expression around the dentin barrier and at 90 days, a thin and linear expression of TN and FN was delimitating the reparative dentin. In conclusion, hemostatic agents did not influence TN and FN expression. Immunostaining for TN and FN was seen in different regions and periods, demonstrating their role in pulp repair.
Assuntos
Capeamento da Polpa Dentária , Fibronectinas/análise , Hemostáticos/uso terapêutico , Agentes de Capeamento da Polpa Dentária e Pulpectomia/uso terapêutico , Tenascina/análise , Adulto , Bis-Fenol A-Glicidil Metacrilato/química , Hidróxido de Cálcio/uso terapêutico , Clorexidina/análogos & derivados , Clorexidina/uso terapêutico , Colágeno/análise , Resinas Compostas/química , Polpa Dentária/química , Exposição da Polpa Dentária/terapia , Restauração Dentária Permanente/métodos , Dentina/química , Dentina Secundária/química , Seguimentos , Humanos , Cloreto de Sódio/uso terapêutico , Hipoclorito de Sódio/uso terapêutico , Extração Dentária , Adulto JovemRESUMO
This study investigated the expression of extracellular matrix glycoproteins tenascin (TN) and fibronectin (FN) in pulp repair after capping with calcium hydroxide (CH), following different hemostasis protocols. Class I cavities with a pulp exposure were prepared in 42 human third molars scheduled for extraction. Different hemostatic agents (0.9% saline solution, 5.25% sodium hypochlorite and 2% chlorhexidine digluconate) were used and pulps were capped with CH cement. After 7, 30 or 90 days, teeth were extracted, formalin-fixed, and prepared for immunohistochemical technique. Hemostatic agents did not influence the expression of TN and FN. Both glycoproteins were found in the entire the pulp tissue and around collagen fibers, but were absent in the mineralized tissues. In the predentin, TN showed positive immunostaining and FN had a variable expression. Within 7 days post-treatment, a slightly more pronounced immunostaining on the pulp exposure site was observed. Within 30 days, TN and FN demonstrated a positive expression around the dentin barrier and at 90 days, a thin and linear expression of TN and FN was delimitating the reparative dentin. In conclusion, hemostatic agents did not influence TN and FN expression. Immunostaining for TN and FN was seen in different regions and periods, demonstrating their role in pulp repair.
Este estudo investigou a expressão das glicoproteínas Tenascina (TN) e Fibronectina (FN) da matriz extracelular no reparo pulpar após capeamento com hidróxido de cálcio (HC), seguindo diferentes protocolos de hemostasia. Cavidades de classe I com exposição pulpar foram preparadas em 42 terceiros molares humanos indicados para extração. Diferentes agentes hemostáticos (solução salina a 0,9%, hipoclorito de sódio a 5,25% e clorexidina a 2%) foram usados e as polpas foram capeadas com cimento de HC. Após 7, 30 ou 90 dias, os dentes foram extraídos, fixados em formalina e preparados para análise imunoistoquímica. Os agentes hemostáticos não influenciaram a expressão de TN e FN. Ambas glicoproteínas foram encontradas em todo tecido pulpar, ao redor das fibras colágenas e estiveram ausentes nos tecidos mineralizados. Na pré-dentina, a TN mostrou forte imunoexpressão e a FN teve uma expressão variável. Após 7 dias, foi observada uma expressão levemente mais pronunciada no lugar da exposição pulpar. Aos 30 dias, a TN e a FN demonstraram uma expressão mais forte sob a barreira dentinária e aos 90 dias, uma expressão fina e linear da TN e FN apresentava-se delimitando a dentina reparativa. Em conclusão, os agentes hemostáticos não influenciaram e expressão da TN e da FN. A imunoexpressão da TN e FN foi observada em diferentes regiões e períodos, demonstrando o seu papel no reparo pulpar.
Assuntos
Adulto , Humanos , Adulto Jovem , Capeamento da Polpa Dentária , Fibronectinas/análise , Hemostáticos/uso terapêutico , Agentes de Capeamento da Polpa Dentária e Pulpectomia/uso terapêutico , Tenascina/análise , Bis-Fenol A-Glicidil Metacrilato/química , Hidróxido de Cálcio/uso terapêutico , Clorexidina/análogos & derivados , Clorexidina/uso terapêutico , Colágeno/análise , Resinas Compostas/química , Exposição da Polpa Dentária/terapia , Polpa Dentária/química , Restauração Dentária Permanente/métodos , Dentina Secundária/química , Dentina/química , Seguimentos , Cloreto de Sódio/uso terapêutico , Hipoclorito de Sódio/uso terapêutico , Extração DentáriaRESUMO
FUNDAMENTO: O Imatinib é um inibidor do receptor tirosina-quinase que foi confirmada como exercendo um efeito inibidor sobre a atividade do receptor do PDGF, fator de crescimento plaquetário (PDGFRα e PDGFRβ). OBJETIVO: Investigar o efeito protetor do Imatinib na fibrose miocárdica em acetato de deoxicorticosterona (DOCA)/ratos com hipertensão induzida por sal. MÉTODOS: Sessenta ratos Sprague-Dawley machos, uninefrectomizados foram distribuídos em três grupos: ratos controles (grupo CON): grupo deoxicorticosterona (grupo DOCA); grupo deoxicorticosterona e Imatinib (grupo DOCA IMA). A Pressão Arterial Sistólica (PAS) foi medida quinzenalmente. Foi estudada a porção apical do ventrículo esquerdo. Foram empregados: coloração vermelho sirius, coloração de hematoxilina-eosina, imuno-histoquímica e ensaio de western blot. RESULTADOS: A PAS nos grupos DOCA e IMA+DOCA foi maior que no grupo CON nos dias 14 e 28. Os animais do grupo DOCA apresentaram fibrose intersticial e perivascular grave no dia 28, e as expressões de PI, PIII, tenascina-C e fibronectina foram significativamente maiores que nos grupos DOCA+IMA e CON. Quando comparados com o grupo CON, os grupos DOCA e DOCA+IMA apresentaram resposta inflamatória de tecido miocárdico e infiltração de monócitos/macrófagos de diferentes graus. As expressões proteicas do PDGF-A, PDGF-C e PDGFRα foram significativamente maiores nos grupos DOCA e DOCA+IMA que no grupo CON, mas a expressão proteica do p-PDGFRα no grupo DOCA+IMA foi menor que no DOCA. CONCLUSÃO: O Imatinib pode exercer efeitos inibitórios sobre a fibrose miocárdica em ratos com hipertensão induzida por DOCA/sal, os quais podem ser atribuídos à inibição da atividade do PDGFR-α.
BACKGROUND: Imatinib is a tyrosine kinase receptor inhibitor that has been confirmed to exert inhibitory effect on the platelet derived growth factor PDGF receptor (PDGFRα and PDGFRβ) activity. OBJECTIVE: To investigate the protective effect of imatinib on the myocardial fibrosis in deoxycorticosterone-acetate (DOCA)/salt induced hypertensive rats. METHODS: Sixty male uninephrectomized Sprague-Dawley rats were assigned to three groups: control rats (CON group); deoxycorticosterone group (DOCA group); deoxycorticosterone and imatinib group (DOCA+IMA group). Systolic blood pressure (SBP) was measured biweekly. The apical portion of the left ventricle was studied. Sirius-Red staining, Hematoxylin-Eosin staining, immunohistochemistry and Western blot assay were employed. RESULTS: SBP in the DOCA group and DOCA+IMA group was higher than that in the CON group on day 14 and 28. Animals in the DOCA group showed severe interstitial and perivascular fibrosis on day 28, and the expressions of PI, PIII, tenascin-C and fibronectin were significantly higher than those in the DOCA+IMA group and CON group. When compared with the CON group, myocardial tissue inflammatory response and monocyte/macrophage infiltration of different degrees were observed in the DOCA group and DOCA+IMA group. Protein expressions of PDGF-A, PDGF-C and PDGFRα were signiflcantly higher in the DOCA and DOCA+IMA groups than those in the CON group, but the p-PDGFRα protein expression in the DOCA+IMA group was lower than that in the DOCA group. CONCLUSION: Imatinib can exert inhibitory effects on myocardial fibrosis in DOCA/salt induced hypertensive rats, which may be attributed to the inhibition of PDGFR-α activity.
Assuntos
Animais , Masculino , Ratos , Benzamidas/farmacologia , Fibrose Endomiocárdica/tratamento farmacológico , Piperazinas/farmacologia , Inibidores de Proteínas Quinases/farmacologia , Pirimidinas/farmacologia , Receptor alfa de Fator de Crescimento Derivado de Plaquetas/antagonistas & inibidores , Western Blotting , Benzamidas/uso terapêutico , Pressão Sanguínea/efeitos dos fármacos , Desoxicorticosterona , Modelos Animais de Doenças , Fibrose Endomiocárdica/patologia , Fibronectinas/análise , Fibronectinas/metabolismo , Fibrose/tratamento farmacológico , Fibrose/patologia , Hipertensão/induzido quimicamente , Hipertensão/fisiopatologia , Nefrectomia/métodos , Piperazinas/uso terapêutico , Inibidores de Proteínas Quinases/uso terapêutico , Pirimidinas/uso terapêutico , Ratos Sprague-Dawley , Receptor alfa de Fator de Crescimento Derivado de Plaquetas/metabolismo , Receptor beta de Fator de Crescimento Derivado de Plaquetas/antagonistas & inibidores , Receptor beta de Fator de Crescimento Derivado de Plaquetas/metabolismo , Resultado do Tratamento , Tenascina/análise , Tenascina/metabolismoRESUMO
BACKGROUND: Imatinib is a tyrosine kinase receptor inhibitor that has been confirmed to exert inhibitory effect on the platelet derived growth factor PDGF receptor (PDGFRα and PDGFRß) activity. OBJECTIVE: To investigate the protective effect of imatinib on the myocardial fibrosis in deoxycorticosterone-acetate (DOCA)/salt induced hypertensive rats. METHODS: Sixty male uninephrectomized Sprague-Dawley rats were assigned to three groups: control rats (CON group); deoxycorticosterone group (DOCA group); deoxycorticosterone and imatinib group (DOCA+IMA group). Systolic blood pressure (SBP) was measured biweekly. The apical portion of the left ventricle was studied. Sirius-Red staining, Hematoxylin-Eosin staining, immunohistochemistry and Western blot assay were employed. RESULTS: SBP in the DOCA group and DOCA+IMA group was higher than that in the CON group on day 14 and 28. Animals in the DOCA group showed severe interstitial and perivascular fibrosis on day 28, and the expressions of PI, PIII, tenascin-C and fibronectin were significantly higher than those in the DOCA+IMA group and CON group. When compared with the CON group, myocardial tissue inflammatory response and monocyte/macrophage infiltration of different degrees were observed in the DOCA group and DOCA+IMA group. Protein expressions of PDGF-A, PDGF-C and PDGFRα were significantly higher in the DOCA and DOCA+IMA groups than those in the CON group, but the p-PDGFRα protein expression in the DOCA+IMA group was lower than that in the DOCA group. CONCLUSION: Imatinib can exert inhibitory effects on myocardial fibrosis in DOCA/salt induced hypertensive rats, which may be attributed to the inhibition of PDGFR-α activity.
Assuntos
Benzamidas/farmacologia , Fibrose Endomiocárdica/tratamento farmacológico , Piperazinas/farmacologia , Inibidores de Proteínas Quinases/farmacologia , Pirimidinas/farmacologia , Receptor alfa de Fator de Crescimento Derivado de Plaquetas/antagonistas & inibidores , Animais , Benzamidas/uso terapêutico , Pressão Sanguínea/efeitos dos fármacos , Western Blotting , Desoxicorticosterona , Modelos Animais de Doenças , Fibrose Endomiocárdica/patologia , Fibronectinas/análise , Fibronectinas/metabolismo , Fibrose/tratamento farmacológico , Fibrose/patologia , Hipertensão/induzido quimicamente , Hipertensão/fisiopatologia , Mesilato de Imatinib , Masculino , Nefrectomia/métodos , Piperazinas/uso terapêutico , Inibidores de Proteínas Quinases/uso terapêutico , Pirimidinas/uso terapêutico , Ratos , Ratos Sprague-Dawley , Receptor alfa de Fator de Crescimento Derivado de Plaquetas/metabolismo , Receptor beta de Fator de Crescimento Derivado de Plaquetas/antagonistas & inibidores , Receptor beta de Fator de Crescimento Derivado de Plaquetas/metabolismo , Tenascina/análise , Tenascina/metabolismo , Resultado do TratamentoRESUMO
The aim of this study was to evaluate the changes caused by chronic diabetes in the rat ventral prostate and to establish a correlation between diabetes and the development of prostatic lesions. Male rats received alloxan (42 mg/kg b.w.) to induce diabetes. Ninety days after diabetes diagnosis, animals were sacrificed and the ventral prostate was removed and prepared for general and immunohistochemical analyses. The total area showing different types of lesions was estimated. Diabetes led to a decrease in the body and prostatic weights, as well as in testosterone levels. The prostate morphology and stereology showed high variation in the diabetic group. Some animals had light changes; the great majority had an intense epithelial atrophy; and other rats showed premalignant and malignant lesions in the prostate. Such epithelial atrophy was, in some samples, combined with chronic inflammation, similar to proliferative inflammatory atrophy (PIA). The diabetic group also presented high incidence of prostatitis, adenocarcinoma and prostatic intra-epithelial neoplasia (PIN). Samples with adenocarcinoma had poorly differentiated acini with high levels of cellular proliferation and nuclear atypia. These lesions exhibited an invasive feature showing Bcl-2-positive cells and interruptions in the basement membrane. An association of PIA, PIN and adenocarcinoma was detected in one sample. Reduced androgen levels have a synergic effect to insulin dysfunction promoting negative effects in the rat prostate. Diabetic individuals had a high incidence of prostatitis, and this inflammation could stimulate the incidence of other forms of prostatic pathology.
Assuntos
Adenocarcinoma/etiologia , Diabetes Mellitus Experimental/complicações , Neoplasias da Próstata/etiologia , Adenocarcinoma/sangue , Adenocarcinoma/patologia , Animais , Biomarcadores Tumorais/análise , Diabetes Mellitus Experimental/sangue , Diabetes Mellitus Experimental/patologia , Imuno-Histoquímica , Masculino , Próstata/patologia , Hiperplasia Prostática/sangue , Hiperplasia Prostática/patologia , Neoplasia Prostática Intraepitelial/sangue , Neoplasia Prostática Intraepitelial/patologia , Neoplasias da Próstata/sangue , Neoplasias da Próstata/patologia , Prostatite/sangue , Prostatite/patologia , Proteínas Proto-Oncogênicas c-bcl-2/análise , Ratos , Ratos Wistar , Tenascina/análise , Testosterona/sangueRESUMO
This study was conducted to analyze the participation of tenascin and fibronectin, components of the extracellular matrix, in different types of carcinoma ex pleomorphic adenoma (CXPA). Seventeen cases of CXPA, classified according to the presence of epithelial and myoepithelial cells and the degree of invasion-intracapsular, minimally, and frankly invasive carcinoma-were immunohistochemically labeled for tenascin and fibronectin. Normal salivary gland included in the specimens showed tenascin only around the excretory duct, and fibronectin slightly expressed all over the stroma of the gland. In reminiscent pleomorphic adenoma, tenascin and fibronectin were observed around tubular structures and in the stroma. Both tenascin and fibronectin were expressed in all the CXPA studied. In areas of in situ carcinoma of the intracapsular type, the expression of these extracellular matrix proteins was enhanced compared with areas of residual pleomorphic adenoma. In intracapsular and minimally invasive types of CXPA, some areas of the tumor border presented tenascin and no fibronectin, pattern that may represent the real invasive front. In frankly invasive CXPA type with only epithelial component, fibronectin was strongly observed in a fibrillar network pattern, and tenascin was only focal. In frankly invasive type with myoepithelial component, tenascin staining was very strong and diffuse. This study showed different patterns of expression of tenascin and fibronectin along the process of tumorigenesis and tumor progression in CXPA, a fact that might play a role in invasion properties of these tumors.
Assuntos
Adenoma Pleomorfo/metabolismo , Fibronectinas/metabolismo , Neoplasias das Glândulas Salivares/metabolismo , Tenascina/metabolismo , Adulto , Idoso , Idoso de 80 Anos ou mais , Feminino , Fibronectinas/análise , Humanos , Masculino , Pessoa de Meia-Idade , Tenascina/análiseRESUMO
O ameloblastoma é uma neoplasia odontogênica benigna comumente encontrada nos ossos maxilares. Histologicamente, mostra diversos padrões, incluindo a ameloblastoma plexiforme e folicular. Quando estes padrões histológicos coexistem com um ameloblastoma que exibe abundante desmoplasia, são então denominados de lesão æhíbrida" de ameloblastoma desmoplásico e convencional. No presente trabalho, nos propomos a relatar um caso de lesão híbrida de ameloblastoma desmoplásico e convencional destacando os aspectos imuno-histoquímicos relativos a expressão das proteínas da matriz extracelular (tenascina, fibronectina e colágeno I).
Ameloblastoma is a benign epithelial odontogenic tumor and is the most commonly encountered odontogenic tumor in the jaws. Histologically, ameloblastomas occur in different patterns, including plexiform pattern and follicular pattern. "Hybrid " lesion of ameloblastoma is a tumor variant in which histologically, areas of follicular or plexiform ameloblastoma coexist with characteristic areas of ameloblastoma exhibiting pronounced stromal desmoplasia (desmoplastic ameloblastoma). The purpose of this article is to present a case of "hybrid" lesion of desmoplastic ameloblastoma (AD) and conventional, and investigate extracellular matrix proteins such as tenascin, fibronectin, and type I collagen.
Assuntos
Humanos , Masculino , Adulto , Ameloblastoma/diagnóstico , Colágeno Tipo I/análise , Fibronectinas/análise , Neoplasias Mandibulares/diagnóstico , Tenascina/análise , Ameloblastoma/patologia , Ameloblastoma/cirurgia , Imuno-Histoquímica , Neoplasias Mandibulares/patologia , Neoplasias Mandibulares/cirurgiaRESUMO
Ameloblastoma is a benign epithelial odontogenic tumor and is the most commonly encountered odontogenic tumor in the jaws. Histologically, ameloblastomas occur in different patterns, including plexiform pattern and follicular pattern. "Hybrid" lesion of ameloblastoma is a tumor variant in which histologically, areas of follicular or plexiform ameloblastoma coexist with characteristic areas of ameloblastoma exhibiting pronounced stromal desmoplasia (desmoplastic ameloblastoma). The purpose of this article is to present a case of "hybrid" lesion of desmoplastic ameloblastoma (AD) and conventional, and investigate extracellular matrix proteins such as tenascin, fibronectin, and type I collagen.
Assuntos
Ameloblastoma/patologia , Neoplasias Mandibulares/patologia , Adulto , Ameloblastoma/química , Ameloblastoma/cirurgia , Colágeno Tipo I/análise , Fibronectinas/análise , Humanos , Imuno-Histoquímica , Masculino , Neoplasias Mandibulares/química , Neoplasias Mandibulares/cirurgia , Proteínas de Neoplasias/análise , Tenascina/análiseRESUMO
Immunoexpression of the extracellular matrix (ECM) proteins laminin, fibronectin, tenascin and types I, III and IV collagen was analyzed in the major and minor salivary glands of seven human fetuses at different gestational ages. The results showed the presence and localization of laminin, collagen IV and fibronectin around glandular structures at all stages of development. Tenascin was only detectable around excretory ducts. In the earliest stages of development, type I and type III collagen were presented as fine fibers delineating the glandular structures and delimiting the extension of the future lobule. As glandular development proceeded, the lobule was gradually filled with collagens and glandular tissue.
Assuntos
Proteínas da Matriz Extracelular/análise , Glândulas Salivares/embriologia , Anticorpos , Colágeno Tipo I/análise , Colágeno Tipo III/análise , Colágeno Tipo IV/análise , Feto , Fibronectinas/análise , Idade Gestacional , Humanos , Imuno-Histoquímica , Laminina/análise , Ductos Salivares/embriologia , Glândulas Salivares Menores/embriologia , Tenascina/análiseRESUMO
OBJECTIVE: Investigate the immunohistochemical distribution of fibronectin, tenascin, laminin and collagen IV in syndrome (SOKC) and non-syndrome odontogenic keratocysts (NSOKC). MATERIALS AND METHODS: Ten cases of SOKC and five of NSOKC were selected and streptoavidin-biotin technique was applied. The specimens were analyzed taking into account the following evaluation parameters: presence, continuity and thickness in the basement membrane and intensity, distribution and association with inflammatory cells in the cyst wall. RESULTS: Differences could be detected regarding tenascin, fibronectin and collagen IV between the SOKC and NSOKC. Tenascin was present in all cases along the basement membrane in SOKC and in five cases of NSOKC predominated negative areas. Furthermore, tenascin distribution was focal in the cyst wall in SOKC whereas in NSOKC it was diffuse. Concerning fibronectin, it was detected as a discontinuous band when present in SOCK and as a continuous band in NSOKC. Collagen IV was not present in the majority of the cases in SOKC. Negative areas for laminin predominated in the basement membrane in both groups. CONCLUSIONS: These findings show differences between the immunohistochemical expression of tenascin, fibronectin and collagen IV which might indicate a more aggressive biological behavior of SOKC as compared with NSOKC.