Distribution of immunomodulation, protection and regeneration factors in cleft affected bone and cartilage

Objectives. Orofacial clefts can cause a significant defect in the underlying supportive tissue, which can disturb normal tissue homeostasis and remodeling processes. Multiple tissue factors can affect local immune response, provide protection and tissue growth regulation. Some of them have not been well studied in cleft affected supportive tissue like galectin-10 (Gal-10), nuclear factor kappalight- chain-enhancer of activated B cells protein 65 (NF-κB p65), heat shock protein 60 (HSP60) and 70 (HSP70), cathelicidin (LL-37) while regeneration factors like type I collagen (Col-I) and bone morphogenetic proteins 2 and 4 (BMP-2/4) have not been evaluated together with immunomodulation and protection factors. The information about the distribution and interactions between these factors could improve the understanding of cleft affected supportive tissue regeneration and healing potential after surgery.
Materials and methods. This study used immunohistochemistry with the semiquantitative counting method to detect and evaluate Gal-10, NF-κB p65, HSP60, HSP70, LL-37, Col-I, and BMP-2/4 containing cells in control tissue and cleft affected supportive tissue to determine the differences in factor distribution between healthy supportive tissue and cleft affected bone and cartilage. Patients and controls were subdivided into four groups with 5 individuals in each group (all mixed dentition age) – 2 control groups for bone tissue and cartilage, respectively and 2 cleft affected supportive tissue groups.
Results. Evaluated tissue factors were found in each study group. Multiple statistically significant correlations between factor positive cells were calculated.
Conclusions. The number of HSP70 positive cells was significantly increased in cleft affected cartilage which could indicate that HSP70 could provide protective action in cleft affected supportive tissue against stressors. The significant increase of Col-I positive osteocytes in cleft affected bone was also noted, which might indicate increased osteocyte activity and bone remodeling process. Correlations between factors indicate notable differences in molecular interactions between healthy and cleft affected supportive tissue.