High palatal arches are mostly seen in Marfan’s syndrome, mainly with elongated limbs, spider fingers (toes), arms extended flat with finger spacing greater than the length of the body, hands hanging down over the knees, upper body longer than the lower body. Long head deformity, narrow face, high palatal arch, large and low ears. Little subcutaneous fat, underdeveloped muscles, wrinkled skin on the chest, abdomen and arms. The muscle tone is low, with an inert body type. Ligaments, tendons and joint capsules are elongated and lax, and joints are hyperextended. Sometimes funnel chest, chicken chest, kyphosis, scoliosis, and spina bifida are seen. Cardiovascular lesions mainly invade the aorta, aortic valve and mitral valve and are the main cause of death. Since this disease is very characteristic, it can be described as a clear-cut disease. The disease can be demonstrated by a chain of genetic locus dominant inheritance in the family, as evidenced by increased urinary hydroxyproline excretion in the patient, which is an elastin fiber defect, also known as an abnormality of collagen metabolism. High palatal arch is the main manifestation of Marfan’s syndrome. The main danger of this disease is cardiovascular lesions, especially the combined aortic aneurysm, which should be detected early and treated early. The diagnosis can be made based on the clinical presentation of the three main signs of skeletal, ocular and cardiovascular changes and family history. There are two clinical types: those with all three main signs are called complete; those with only two are called incomplete. The simplest means of diagnosing Marfan’s syndrome is echocardiography, which can be performed in all cases of suspicion, and MRI (magnetic resonance imaging) is required for further confirmation. In younger, taller patients with pneumothorax, physical examination and family history should be noted to exclude the possibility of coexisting Marfan’s syndrome. Marfan’s syndrome is diagnosed if the patient has a family history and typical aortic root dilatation, aortic coarctation aneurysm, mitral valve lesion and lens prolapse with positive skeletal signs. The primary defect in the high palatal arch is unknown and has been suggested to be an impaired lateral association between elastin and collagen tissue peptide chains, i.e., a lysyl oxidase defect. It is also associated with acidic mucopolysaccharide deposition, increased sialic acid, hyaluronic acid accumulation, and poor or excessive destruction of chondroitin sulfate formation. In 1931, Weve summarized a large number of cases of the disease and officially named it Marfan’s syndrome, and considered it a dominantly inherited disease. Abnormal alterations in connective tissue extracellular matrix molecules, such as collagen, elastin and hyaluronic acid, have been considered as the cause in the past.