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Previous issue date: 2015-02-24 / A doen?a periodontal ? uma condi??o inflamat?ria cr?nica de car?ter infeccioso causada
primariamente por bact?rias presentes em um biofilme dent?rio que interagem com o
hospedeiro, determinando, assim, a natureza da doen?a resultante. Apesar de j? se conhecer
muito sobre a patog?nese destas patologias, ainda n?o se sabe a composi??o exata do perfil de
c?lulas T durante a fase ativa da doen?a (Th1, Th2 ou Th17). Este trabalho visou avaliar,
atrav?s da express?o imuno-histoqu?mica, a presen?a dos marcadores (IL-17, IL-23 e ROR?t),
envolvidos na resposta Th 17 em casos de gengiva clinicamente saud?veis (n=32), gengivite
induzida pelo biofilme dental (n=30), periodontite cr?nica (n=32) e periodontite agressiva
(n=25), objetivando analisar se a express?o e/ou distribui??o destas mol?culas em linf?citos e
macr?fagos, presentes no infiltrado inflamat?rio dos tecidos periodontais, influencia na
destrui??o tecidual observada nestas doen?as. Foi realizada a an?lise morfol?gica dos casos,
onde avaliou-se a intensidade do infiltrado inflamat?rio em leve, moderado e intenso. Para
cada caso, nas ?reas mais imunomarcadas, 5 campos foram escolhidos e analisados, tanto em
rela??o a intensidade do infiltrado inflamat?rio quanto a quantidade de c?lulas
imunomarcadas, baseando-se em escores predeterminados: escore 0 (aus?ncia de infiltrado
inflamat?rio/imunomarca??o), escore 1 (o infiltrado/imunomarca??o abrangia menos de 25%
da ?rea do campo), escore 2 (o infiltrado/imunomarca??o ocupava entre 25 e 50%) e escore 3
(infiltrado/imunomarca??o presente em mais de 50% da ?rea do campo). A partir disto, gerouse
uma mediana que representava cada caso. A intensidade do infiltrado inflamat?rio foi
correlacionada com a progress?o da doen?a, se mostrando crescente da gengiva clinicamente
saud?vel at? a periodontite agressiva (p<0,001). Detectou-se a presen?a da IL-17, IL-23 e do
ROR?t na maioria dos casos avaliados e a quantidade de c?lulas imunomarcadas foi
correlacionada tanto com a intensidade do infiltrado inflamat?rio (P<0,001) quanto com os
par?metros cl?nicos analisados (P<0,001), apresentando uma correla??o positiva,
predominantemente moderada. A periodontite agressiva apresentou um maior percentual de
imunomarca??o em rela??o ?s outras condi??es cl?nicas avaliadas, para todos os marcadores,
sugerindo uma poss?vel associa??o destes marcadores com a progress?o desta doen?a, onde
quanto maior a perda de suporte periodontal, maior a quantidade do infiltrado inflamat?rio e
maior n?mero de c?lulas imunomarcadas. / Periodontal disease is a chronic inflammatory condition primarily caused by bacteria
in dental biofilm, which interact with the host, thus determining the nature of the resulting
disease. Despite the wide knowledge about the pathogenesis of these diseases, the exact
composition of the T cell profile during the active phase of the disease (Th1, Th2 or Th17)
remains unknown. This study aimed to evaluate by immunohistochemical expression, the
presence of the markers (IL-17, IL-23 and ROR?t), involved in Th17 response in clinically
healthy gingiva cases (n = 32), biofilm-induced gingivitis (n = 30), chronic periodontitis (n =
32) and aggressive periodontitis (n = 25), in order to analyze if the expression and/or
distribution of these molecules in lymphocytes and macrophages, present in the inflammatory
infiltrate of periodontal tissue, influences the tissue destruction observed in these diseases.
The morphological analysis of cases was performed which assessed the intensity of the
inflammatory infiltrate in mild, moderate and intense. For each case, in the area with the most
representative immunostaining, 5 fields were chosen and analyzed, both for the intensity of
the inflammatory infiltrate as for the quantity of immunostained cells, based on predetermined
scores: score 0 (absence of inflammatory infiltrate/immunostaining), score 1 (the
infiltrate/immunostaining covered less than 25% of the field area), score 2 (the
infiltrate/immunostaining occupied between 25 and 50%) and score 3
(infiltrate/immunostaining present in over 50% of the field area). From this, a median was
generated representing each case. The intensity of the inflammatory infiltrate correlated with
the disease progression, in other words, it was crescent from clinically healthy gingiva to
aggressive periodontitis (P <0.001). It was detected the presence of IL-17, IL-23 and ROR?t
in most of the evaluated cases and the number of immunostained cells correlated with the
intensity of the inflammatory infiltrate (P <0.001) and with the clinical parameters analyzed
(P <0.001), showing a positive correlation, mainly moderate. Aggressive periodontitis
showed a higher percentage of immunostaining for all markers in relation to other clinical
conditions assessed, suggesting a possible association of these markers with the progression
of this disease, in which the higher the loss of periodontal support, the greater the amount of
inflammatory infiltrate and larger the number of immunostained cells.
| Identifer | oai:union.ndltd.org:IBICT/oai:repositorio.ufrn.br:123456789/19913 |
| Date | 24 February 2015 |
| Creators | Aguiar J?nior, Jos? Nazareno Moreira de |
| Contributors | 82134731400, http://lattes.cnpq.br/9634115210679435, Gurgel, Bruno C?sar de Vasconcelos, 02569549410, http://lattes.cnpq.br/4649601602612601, Silveira, ?ricka Janine Dantas da, 02869049420, http://lattes.cnpq.br/2186658404241838, N?brega, Fernando Jos? de Oliveira, 02692435427, http://lattes.cnpq.br/8597370276326959, Lemos, Janaina Cavalcante, 77846532472, http://lattes.cnpq.br/6756263467790240, Miguel, M?rcia Cristina da Costa |
| Publisher | Universidade Federal do Rio Grande do Norte, PROGRAMA DE P?S-GRADUA??O EM PATOLOGIA ORAL, UFRN, Brasil |
| Source Sets | IBICT Brazilian ETDs |
| Language | Portuguese |
| Detected Language | English |
| Type | info:eu-repo/semantics/publishedVersion, info:eu-repo/semantics/doctoralThesis |
| Source | reponame:Repositório Institucional da UFRN, instname:Universidade Federal do Rio Grande do Norte, instacron:UFRN |
| Rights | info:eu-repo/semantics/openAccess |
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