Characterization of Immunomodulators and Cellular Signaling Molecules in Cleft Lip and Palate Tissues According to Cleft Laterality

Introduction: Cleft lip and/or palate (CLP) is a defect caused by the failure of palatal shelf fusion and growth, which is heavily influenced by many environmental and biological factors. Transcription, growth, inflammation and antimicrobial factors modulate molecular events in clefted tissue and are, therefore, vital in the morphopathogenic assessment of CLP. The aim of this study is to determine the expression of immunomodulators and cellular signaling molecules (bone morphogenetic proteins (BMP), nuclear factor kappa beta (NF-κB), interleukin 10 (IL-10), galectin 10 (Gal-10), heat shock protein 70, Caspase 3, cathelicidin 37 (LL-37)) between sinistral (left), dextral (right) and bilateral cleft-affected tissue. Materials and Methods: Tissue samples were obtained from 19 patients—5 with CLP of the right side, 6 on the left side, and 8 bilateral. Five controls were used for comparison. Due to cohort size, this study was conducted as a preliminary pilot investigation. Data were evaluated with immunohistochemistry, semi-quantitative evaluation and the Mann–Whitney U test. Results: Epithelium of CLP presented with significant changes in Gal-10 (U = 3, p = 0.030); IL-10 (U = 3.0, p = 0.030), (U = 1.0, p = 0.002), (U = 2.0, p = 0.032); NF-kB p105 (U = 2.0, p = 0.017), (U = 14.5, p = 0.017). Connective tissue presented with significant differences in Gal-10 (U = 2.5, p = 0.032), (U = 5, p = 0.019), and HSP70 (U = 1.5, p = 0.016). Caspase 3, LL-37 and BMP2/4 showed no significant differences. Conclusions: CLP on the right side presented with a larger number of statistically significant differences than any other type of CLP. An increase in factor expression in the epithelium illustrates the conditions of chronic inflammation. An increase in factor expression in connective tissue suggests protective actions. Factors that showed no change in their distribution suggest unaffected osteogenesis and antimicrobial activity in CLP.