Prevalence of Egfr, Ki-67, Nf-Κb, Ma-1 marker in cleft affected tissue of soft palate


  • Jonas Tellermann Riga Stradiņš University, Riga
  • Sophie Charlotte Reiser Riga Stradiņš University, Riga
  • Mara Pilmane Riga Stradiņš University, Riga; Department of Morphology, Institute of Anatomy and Anthropology



cleft palate, growth factor, inflammation, proliferation


Introduction. Midline orofacial defects bear a high degree of morbidity for the affected individual, often associated with retardation in neonatal development and the need for surgical intervention. The etiology of the deformities, despite their high prevalence, remains, however, largely unknown. We report on the evaluation and quantification of proliferative and inflammatory markers in the cleft affected soft palate.

Material and methods. This study included soft palate samples of eight cleft lip and palate affected individuals and a control group of six soft tissue specimens obtained during correctional surgery of hyperdentia. All samples were processed via immunohistochemistry for marker EGFR, NF-κB, Ki-67, Ma-1. The results were evaluated semi-quantitatively and statistically analysed by IBM SPSS 25.0.

Results. Histopathological signs of inflammatory changes were continuous in cleft affected specimen. The quantitative distribution of the markers in the cleft affected group displayed a significant correlation between EGFR, Ki-67 and NF-κB (p< 0.05), along with a correlation among Ki-67 and NF-κB (p< 0.05). Immunoreactive structures in control group showed lower numbers in all evaluated specimen. A statistical significance between cleft affected and non-cleft tissue was observed in EGFR and Ma-1 (p< 0.05).

Conclusion. Results are suggestive of a tissue phenotype modification in cleft affected palate. Observation of distribution and statistical correlation hint towards the involvement of epithelial growth inducer EGFR and inflammatory/ proliferative marker in epithelial changes.


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