Made available in DSpace on 2014-12-17T15:32:29Z (GMT). No. of bitstreams: 1 KaruzaMAP_Tese.pdf: 829792 bytes, checksum: 60cd145c0f060b54f7dfbb5463648200 (MD5) Previous issue date: 2010-02-25 / Coordena??o de Aperfei?oamento de Pessoal de N?vel Superior / The Giant Cell Lesions, both the Central Giant Cells Lesions (CGCL) as the Peripheral Giant Cells Lesions (PGCL), correspond to a group of oral lesions that are histologically similar entities; however they show a variable clinical behaviour. The purpose of this study was to compare the immunohistochemical expression of bone resorption factors RANK (Receptor Activator of Nuclear Factor kappa B), RANKL (Receptor Activator of Nuclear Factor kappa B Ligand) and OPG (Osteoprotegerin) between CGCL and PGCL. Additionally, these bone resorption factors were examined in terms of aggressiveness of these lesions. The sample consisted of 61 cases, 30 cases of PGCL and 31 CGCL (16 non-aggressive and 15 aggressive). The analysis was performed by quantification of mononuclear cells (MO) and giant multinucleated cells (CG) immunopositive to anti-RANK, anti-RANKL and anti-OPG antibodies in 10 fields. Moreover, according to the proportion between the amount of cells positive for RANKL and OPG, the cases were categorized into: RANKL>OPG, OPG>RANKL e RANKL=OPG. CGCL showed a higher amount of MO (p=0.002) and total cells (p=0.003) both positives to RANKL compared with the PGCL. Additionally, the CGCL revealed a significant association with the ratio of RANKL>OPG (p=0.001). Analysis of the bone resorption factors revealed no significant differences between aggressive and non-aggressive CGCL (p>0.05). It was observed a positive correlation between the markers themselves, and a negative correlation between lesion size and quantity of OPG positive MO cells (p=0,004) and total cells (p=0,009). Through these results, we suggest that the greatest CGCL resorptive potential compared to the PGCL, may have occurred to the high expression of RANKL. Furthermore differences in the biological behavior of aggressive and non-aggressive CGCL appear to be related to the expression of these bone resorption factors / As Les?es de C?lulas Gigantes, tanto as Les?es Centrais (LCCG) quanto as Perif?ricas (LPCG), correspondem a um grupo de les?es orais que apresentam-se histologicamente semelhantes, por?m demonstram um comportamento cl?nico vari?vel. O prop?sito deste estudo foi comparar a express?o imuno-histoqu?mica dos fatores de reabsor??o ?ssea RANK (Receptor Ativador do Fator Nuclear kappa B), RANKL (Ligante do Receptor Ativador do Fator Nuclear kappa B) e OPG (Osteoprotegerina) entre LCCG e LPCG. Adicionalmente, esses fatores foram analisados nas LCCG quanto ? agressividade destas. A amostra consistiu de 61 casos, sendo 30 casos de LPCG e 31 de LCCG (16 n?o-agressivos e 15 agressivos). A an?lise foi realizada por meio da quantifica??o das c?lulas mononucleadas (MO) e c?lulas gigantes multinucleadas (CG) imunopositivas aos anticorpos anti-RANK, anti-RANKL e anti-OPG, em 10 campos. Al?m disso, de acordo com a propor??o entre quantidade total de c?lulas positivas para RANKL e para OPG, os casos foram categorizados em: RANKL>OPG, OPG>RANKL e RANKL=OPG. As LCCG apresentaram maior quantidade de MO (p=0,002) e c?lulas totais (p=0,003) positivas para RANKL, em compara??o com as LPCG. As LCCG ainda revelaram uma associa??o significativa com a propor??o de RANKL>OPG (p=0,001). A an?lise dos fatores de reabsor??o ?ssea n?o revelou diferen?as significativas entre LCCG agressivas e n?o-agressivas (p>0,05). Foi constatada correla??o positiva dos marcadores entre si, bem como uma correla??o negativa entre o tamanho das les?es e a quantidade de MO (p=0,004) e c?lulas totais (p=0,009) positivas para OPG. Diante desses resultados, concluise que o maior potencial reabsortivo das LCCG frente ?s LPCG pode ser decorrente da elevada express?o de RANKL. Al?m disso, as diferen?as nos comportamentos biol?gicos de LCCG agressivas e n?o-agressivas parecem n?o estar relacionadas com a express?o desses fatores de reabsor??o ?ssea.

No description available.

CoordenaÃÃo de AperfeiÃoamento de Pessoal de NÃvel Superior / FundaÃÃo de Amparo à Pesquisa do Estado do Cearà / Conselho Nacional de Desenvolvimento CientÃfico e TecnolÃgico / A LesÃo Central de CÃlulas Gigantes dos maxilares (LCCG) à intra-Ãssea, nÃo tem predileÃÃo por sexo, classifica-se em agressivas e nÃo-agressivas, histologicamente consistem tecido fi-broso e celularizado fusiforme associado a cÃlulas gigantes multinucleadas (CGM), focos de hemorragia e neovascularizaÃÃo, tendo na cirurgia seu habitual tratamento. Novas abordagens terapÃuticas foram propostas, sendo a principal delas o uso de corticÃides intralesionais. Este trabalho analisa retrospectivamente 21 pacientes portadores de LCCG que foram tratados por hexacetonido de triancinolona intralesional, atravÃs do seguinte protocolo: injeÃÃo de hexace-tonido de triancinolona 20mg/ml diluÃdo na soluÃÃo anestÃsica de lidocaÃna 2%/epinefrina 1:200.000 numa proporÃÃo de 1:1; infiltrando 1ml de soluÃÃo para cada 1cm3 de lesÃo, totali-zando 06 aplicaÃÃes em intervalos quinzenais. Estabeleceu-se 04 critÃrios clÃnicos para classi-ficar a resposta ao tratamento: 1- estabilizaÃÃo ou regressÃo clÃnica da lesÃo 2- ausÃncia de sintomas 3- aumento da densidade nos controles radiogrÃficos 4- aumento da resistÃncia a infiltraÃÃo intralesional da droga, bem como, fez-se uma anÃlise imunohistoquÃmica quanto à expressÃo dos Receptores de corticÃides (GCR) e Calcitonina (CTR), Cox-2, proteÃna p16 e amplificaÃÃo gÃnica da Ciclina D1 por CISH, comparando quanto a agressividade e a resposta terapÃutica a corticoterapia intralesional. Dos 21 pacientes incluÃdos neste estudo, 11 eram homens e 10 mulheres, 09 tinham lesÃo em maxila, 12 em mandÃbula. Dez eram lesÃes agres-sivas e 11 nÃo-agressivas, 15 (71,4%) apresentaram uma boa resposta ao tratamento, 04(19%) moderada e 02(9,1%) negativa. Das 11 nÃo agressivas, 10(90,9%) apresentaram boa resposta e 01 (9,1%) resposta moderada, das 10 agressivas 05(50%), 03(30%) e 02(20%) apresentaram boa, moderada e negativa resposta respectivamente, nenhuma apresentou recidiva apÃs o tra-tamento, com preservaÃÃo que variou entre 04 a 08 anos. Os achados histopatolÃgicos mos-traram uma reduÃÃo da densidade e do tamanho das CG, e um estroma fibro-colagenoso das lesÃes. Dentre os marcadores pesquisados, apenas GCR em CG antes do tratamento mostrou significÃncia estatÃstica (p<0,004) com relaÃÃo a uma boa resposta terapÃutica. O CTR ex-pressou-se em cÃlulas gigantes e mononucleares de forma variada. A p16 apresentou-se ex-pressa em 30% da amostra, COX2 nÃo apresentou expressÃo na lesÃo e 33% da amostra apre-sentou amplificaÃÃo gÃnica da ciclina D1. NÃo mostraram significÃncia estatÃstica nem quanto à agressividade, nem quanto resposta ao tratamento, nenhum dos marcadores, exceto o GCR. O estudo mostrou que a corticoterapia intralesional à efetiva e segura para o tratamento das LCCG, com tendÃncia a melhor resposta nas lesÃes nÃo-agressivas do que nas agressivas. Mostrou ainda que a marcaÃÃo para GCR em CG demonstrou ser um parÃmetro confiÃvel para prever a resposta à terapÃutica com a corticoterapia intralesional e que 33% das LCCG tÃm comportamento neoplÃsico pela amplificaÃÃo gÃnica da ciclina D1. / Central Giant Cells Lesion (CGCL) of the jaws is an intra-bone lesion with no predilection for sex and clinically divided into aggressive and non-aggressive subtypes. Histological, it shows as fibrous tissue with fusiform cells, as well as multinucleated giant cells (GC) clusters, he-morrhagic foci and neovascularization. Surgery is the regular treatment option. As new the-rapeutic approaches have been proposed, intralesional glucocorticoid injection is the main option. This paper assesses retrospectively 21 patients presenting CGCL, treated with intrale-sional triamcinolone hexacetonide by using the following protocol: intralesional injection of triamcinolone hexacetonide 20mg/mL, diluted in a solution of lidocain 2% plus epinephrine 1:200000, at a 1:1 proportion; 1mL of this final solution for each 1cm3 of lesion volume was the injected, with a total of 06 injections, one in every 15 days. Four clinical criteria were sta-bilished to evaluate treatment outcome: 1- Clinical regression or stabilization of the lesion; 2- Absence of symptoms; 3- Raising in density on radiographic controls; 4-Increased resistence when injecting the drug intralesionally. It was also performed immunohistochemical assess-ment for glucocorticoid receptor (GCR) expression, calcitonin receptor (CTR) expression, COX-2 expression, p16 expression and Ciclin D1 gene amplification by CISH, making com-parisons related to aggressivity and to therapeutic outcome. Eleven out of 21 patients of this study were women, and 10 were men. Nine of the patients had lesion located in the maxilla, 12 in the mandible. Ten patients showed aggressive lesions and 11 non-aggressive lesions. Fifteen patients showed good treatment outcome, four patients showed moderate outcome, and two patients showed negative answer to the treatment. Among the 11 patients with non-aggressive lesions, ten showed good outcome and the other, moderate outcome. Among the ten aggressive lesions, five patients showed good outcome, three patients showed moderate outcome and the remaining two patients showed negative answer to the treatment. None of them showed reicidive in a four to eight years follow-up period. Morphologic analysis found positive correlation between volume density of GC/mm2 and lesion aggressiveness, as well as significant reduction in number of GC/mm2 after treatment. Among the markers, only GCR in GC showed statistical relevance associated to the treatment. CTR was espresse in GC and in mononuclear cells in a varying way; p16 was expressed in 30% of the sample; COX-2 was not expressed at all in lesion samples and 33% of the sample showed gene amplification in Ciclin D1. None of the markers showed any statistical significant difference related to aggres-siveness nor to treatment outcome, except for GCR. The study showed the feasibility of the adopted treatment, with tendency to better outcomes in non-aggressive lesion, if compared to the aggressive ones. It also showed evidence pointing to GCR expression in GC as a reliable parameter to predict therapeutic responsiveness to glucocorticoids; and it showed that 33% of CGCL have neoplastic behaviour by Ciclin D1 gene amplification.

No description available.