Abstract
Cleft lip with or without cleft palate (CL/P) and isolated cleft palate (CPI) are two of the most common congenital craniofacial birth defects in humans. These orofacial clefts (OFC) cause profound psychosocial distress as well as an enormous economic burden to the affected individual, their families, and the community. While genetic and environmental factors contribute to the complex etiology of OFC. Affected infants have an increased risk of death due to associated conditions, such as prematurity, respiratory and infectious diseases, and central nervous system disorders, while affected adults have been shown to have increased risk of cardiac disease, suicide, epilepsy, and various cancers. [1] Thus, it is considered a pressing public health problem. Thirteen loci (genomic positions) on various chromosomal regions and 20 genes associated with CL/P have been reported by linkage and association analysis. Nevertheless, the etiology of this disorder is still poorly defined. Recent studies indicate that disruption on microRNAs (miRNAs) activity may also play a role on the onset of these deformities. [2‑4] miRNAs are approximately 22 nucleotide
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