Normal embryonic development is regulated by different genes and related signaling pathways. In recent years, the association between different genes and genes, genes and signaling pathways in the same organization has been widely concerned by scholars at home and abroad. Sp and Wnt gene deletion or mutation can lead to abnormal embryonic development. The results of this review indicate that abnormal embryonic development is due to Sp gene deletion/mutation The zinc finger protein superfamily member Sp1-9 is involved in the development of various tissues and organs , such as the hematopoietic system, respiratory system and skeletal system, and its deletion or mutation can lead to developmental abnormalities in embryonic tissues. In addition, the Sp8 gene is associated with the occurrence of cleft palate. By summarizing the observations about the relationship between the Wnt gene and cleft lip and palate in recent years, we can understand the abnormal expression of Wnt3, Wnt3A, Wnt5A, Wnt9B, Wnt10A and Wnt11 in humans. The occurrence of cleft lip and palate is closely related; Sp5/8 is a key downstream effector of the Wnt signaling pathway during embryonic development and participates in the Wnt signaling pathway. Sp5/8 and the Wnt signaling pathway are involved in the regulation of normal neural crest development and the self-renewal of embryonic stem cells in embryonic mice. In summary, this paper proposes that the Sp and Wnt genes may be involved in the regulation of the formation and occurrence of embryonic cleft palate and provides a reference for further study of the associated mechanisms between the two genes in the cleft palate model.

Nonsyndromic cleft lip with/without cleft palate is a common congenital birth defect of the maxillofacial region. The pathogenic mechanism is related to the interaction of genes and environmental factors. At present, there are many studies on genes, and genome-wide association analysis has found that the new susceptibility gene v-maf musculoaponeurotic fibrosarcoma oncogene homolog B (MAFB) is associated with the development of nonsyndromic cleft lip with/without cleft palate. This paper reviews the research progress on the correlation between single nucletide polymorphism(SNPs) in MAFB and nonsyndromic cleft lip with/without cleft palate. The results of this review reveal how the MAFB gene is expressed and differentiated in various cell types and plays an important role in maintaining the development of various organs, such as the brain, pancreas, and parathyroid glands. The MAFB gene is significantly associated with the occurrence of nonsyndromic cleft lip with/without cleft palate in the Asian population. rs13041247, rs11696257, rs17820943 and other teratopoietic single nucleotide loci are the most commonly studied teratopoietic single nucleotide loci, and the research conclusions on the correlation between SNPs in MAFB genes are obviously different in different populations. The interaction between the MAFB gene and other susceptibility genes leads to the occurrence of nonsyndromic cleft lip with/without cleft palate; nevertheless, more in-depth research is needed on specific mechanisms and approaches based on the relationship between these two factors.

Congenital cleft lip and/or palate (CL/P) is a common malformation of maxillofacial development. At present, it is believed that the etiology of congenital cleft lip and palate mainly results from genetic factors and environmental factors. Epigenetic changes induced by environmental factors may be the key factor in the occurrence of fetal congenital malformations. As one of the important epigenetic modifications, DNA methylation has been widely and deeply studied in many fields, but as a link between the individual and the environment, its application in CL/P is limited. Existing studies have shown that DNA methylation is closely related to the occurrence of cleft lip and palate. Stimulation of folate deficiency, smoking, pollutant exposure and other environmental factors can induce changes in the state of DNA methylation, thus affecting gene expression in the development of lip and palate and leading to the occurrence of deformities.