Cytokines and Macrophages Type 1 in Cleft Lip Palate Affected Lip

Cleft lip palate (CLP) enrols one child from every 600-1000. However, there is very little known about the pro-inflammatory, regulatory, inflammatory cytokines and markers in cleft soft tissue. Thus, the aim of work was the detection of the distribution and appearance of different cytokines and inflammatory cells in lip of CLP affected children.

Materials and methods: The lip material was obtained from 16 children (10 boys, 6 girls) aged before primary dentition during plastic surgery of bilateral (2) and unilateral cases (14). Control was obtained from 7 non-CLP oral tissue. Tissues were stained routinely, and for IL1, IL4, IL6, IL8, IL10, Ma1 and TNFα immunohistochemically. Non-parametric and parametric statistic was used to evaluate results.

Results: Seborrheic keratosis was seen in epithelium. Infiltration with lymphocytes and macrophages was also detected. Up to numerous IL1, IL8 and IL10 positive cells were seen in epithelium, while controls showed this number from few to moderate; thus, there the statistically significant difference was observed of these factor positive structures between the patients and controls. Variable number of IL4 and IL6 cells was seen in epithelium, thus overlapping with a controls. Statistically significant difference was seen between patient epithelial IL1, IL10, IL8 cells and connective tissue IL10, IL4 cells, and controls. However, IL4 and IL10 moderate number of connective tissue cells in patients differed from only few positive cells in controls. Ma1 marked occasional cells in controls, but moderate number in patients. TNFα positive cells varied in inflamed patient tissue.

Conclusions: CLP affected epithelium is the main source for IL1, IL8 and IL10 proving the balanced regulation between pro- and anti-inflammatory cytokines, and induction for intraepithelial lymphocyte recruitment. The connective tissue show slightly changed profile of cytokine appearance (IL4 and IL10) and indicate still persisting anti-inflammatory response and induction of cellular proliferation maintained by inflammation.