Craniosynostosis accounts for approximately 38% of cranial anomalies, and its clinical manifestations are mainly manifested by various different shapes of cranial deformities. The premature closure of the cranial suture restricts the growth of the skull and hinders the development of the brain, thus producing increased intracranial pressure. Patients may have protrusion of both eyes, downgaze, eye movement disorders, optic disc edema or secondary atrophy, visual impairment or blindness. Some patients may have mental retardation, and headache, nausea and vomiting may occur in the late stage. Some patients may develop seizures due to cortical atrophy. The clinical manifestations of sialocephaly can be divided into two categories: cranial deformities and secondary symptoms. So far, the etiology of the disease is unknown and there is no satisfactory explanation. Some scholars have found that the disease is familial, so it is thought to be genetically related. The lesions are mostly concentrated in the coronal suture or multiple sutures of ossification. Some scholars refer to cranial suture ossification of unknown origin, which is present at birth, as primary sarcopenia, while early ossification of the cranial sutures secondary to other diseases of the body, such as early cranial suture ossification in patients with cretinism accompanied by overuse of thyroid hormone replacement therapy, as secondary sarcopenia. The etiology of craniosynostosis was described in detail by Cohen in 1975 and Converse et al. in 1976. It is considered to be a congenital developmental malformation, but in general its etiology is unclear and may be related to impaired embryonic mesodermal development, to the presence of ectopic ossification centers in the membranous tissue of the sutures, or to the lack of certain embryonic substrates. In a few cases, there is a genetic component. Park and Power have suggested that the underlying cause is incomplete growth of the cranial mesenchymal bundle, resulting in cranial reduction and premature ossification of the suture tissue. The starting point of cranial suture ossification and how the ossification extends, the role of the corresponding cranial vault, cranial base suture and dura mater are not well understood. The development of the skull base plays a dominant role in the pathogenesis of craniosynostosis with facial dysmorphic changes.