Imunoexpressão de Efrina-B2 e Eph-B4 em líquen plano oral

• Ano de defesa: 2025
• Autor(a) principal: Maynart, Lucas Lopes
• Orientador(a): Gordón-Núñez, Manuel Antonio
• Banca de defesa: Monteiro, Bárbara Vanessa de Brito , Nonaka, Cassiano Francisco Weege , Gordón-Núñez, Manuel Antonio
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso embargado
• Idioma: por
• Instituição de defesa: Universidade Estadual da Paraíba
• Programa de Pós-Graduação: Programa de Pós-Graduação em Odontologia - PPGO
• Departamento: Centro de Ciências Biológicas e da Saúde - CCBS; Pró-Reitoria de Pós-Graduação e Pesquisa - PRPGP
• País: BR
• Palavras-chave em Português: Líquen plano oral; Efrina-B2; Eph-B4; Inflamação
• Área do conhecimento CNPq: CIENCIAS DA SAUDE
• Link de acesso: https://repositorio.uepb.edu.br/handle/123456789/74306

The pathogenesis of oral lichen planus (OLP) is not yet fully understood and is classified as an immune-mediated disease. Ephrins and their receptors (Eph) can participate in bidirectional cell signaling events, modulating physiological and pathological processes, including the regulation of immunoinflammatory mechanisms. We analyzed the immunoexpression of Ephrin-B2 and Eph-B4 receptor in relation to clinico-histomorphological parameters of OLP samples, aiming to obtain information that may contribute to understanding the role of these proteins in its pathogenesis. Through immunohistochemistry, the membranous/cytoplasmic and nuclear expression of the proteins were analyzed in 20 OLP samples (10 reticular and 10 erosive). Percentages of cytoplasmic and nuclear immunoexpression were established in five fields of highest immunoreactivity (400x), both in the epithelium and in the connective tissue for Ephrin-B2 and Eph-B4. Data were statistically analyzed using Mann-Whitney and Spearman's correlation tests (p < 0.05). In the epithelium, there was high membranous/cytoplasmic immunoexpression of Ephrin-B2 (reticular OLP: Md = 83.61; erosive OLP: Md = 86.21), with no statistically significant difference (p = 0.850), and low nuclear immunoexpression of Ephrin-B2 (reticular OLP: Md = 8.95; erosive OLP: Md = 0.09), with a significant difference (p = 0.049). In the connective tissue, there was high membranous/cytoplasmic immunoexpression of Ephrin-B2 (reticular OLP: Md = 85.08; erosive OLP: Md = 95.05), with no significant difference (p = 0.579), and most samples exhibited low nuclear immunoexpression (reticular OLP: Md = 1.44; erosive OLP: Md = 0.74), with no significant difference (p = 0.597; p = 0.066). In the OLP epithelium, low percentages of membranous/cytoplasmic immunoexpression of Eph-B4 predominated (reticular OLP: Md = 8.95; erosive OLP: Md = 0.00), with no statistically significant difference (p = 0.066), and low percentages of nuclear immunoexpression (reticular OLP: Md = 0.07; erosive OLP: Md = 0.00), also with no significant difference (p = 0.709). In the connective tissue, low percentages of membranous/cytoplasmic immunoexpression of Eph-B4 were observed (reticular OLP: Md = 2.22; erosive OLP: Md = 0.02), with no significant difference (p = 0.052), and low percentages of nuclear immunoexpression (reticular OLP: Md = 0.04; erosive OLP: Md = 0.02), with no significant difference (p = 0.968). Positive correlations were observed between the membranous/cytoplasmic immunoexpressions of Eph-B4 in epithelial and connective tissue, with a statistically significant difference in erosive OLP (r = 0.932; p <0.001) and reticular OLP (r = 0.784; p = 0.007). In conclusion, the immunoexpression profile of Ephrin-B2 in the epithelium suggests its participation in modulating the chronic inflammatory response, aiming at events that offer protection to keratinocytes in OLP. The high membranous/cytoplasmic expression of Ephrin-B2 in the connective tissue, associated with reduced or absent membranous/cytoplasmic and nuclear immunoexpression of Eph-B4 in this tissue, suggests the promotion of a pro-inflammatory environment, characterized by the recruitment of an intense inflammatory infiltrate and the impairment of tissue repair mechanisms, common to OLP pathogenesis.