Progressive hemifacial atrophy, also known as Romberg’s disease, is a relatively rare condition characterized by progressive atrophy of the skin, subcutaneous tissue or also bone and cartilage tissue confined to one side of the face. It was first reported by Parry in 1825, and then in 1846 Romberg described the typical features of the disease in detail, so it was named after Romberg. 1871 Enlenburg first introduced the name Progressive facial hemiatrophy (PFHA). The typical hemifacial atrophy mostly develops before the age of 20 years and progresses slowly. As the disease progresses, the atrophy starts from the hyperpigmented area and gradually extends to the hemifacial area, usually forming a clear demarcation with the healthy side at the midline of the face. In severe cases, it may even spread to the contralateral face, skull, neck and upper limbs. There is no significant difference between men and women, and the incidence is similar on the left and right sides. The peak of onset and activity is usually within 2.5 to 10 years of the initial onset of symptoms, and usually lasts for 2 to 3 years before becoming relatively quiescent. The cause of the disease is not known. The typical patient presents with varying degrees of soft tissue atrophy and bone dysplasia on the affected side, with the subcutaneous and connective tissues being more prominent. The skin on the affected side is dry and flaky, with localized hyperpigmentation, similar to scleroderma-like changes. The affected side of the nose and upper lip are poorly developed, and the corners of the mouth are tilted to the affected side. In juvenile onset, due to immature craniofacial skeleton, impaired skeletal development, delayed tooth eruption, and apical atrophy can lead to more severe deformities, manifested by severe depression of the affected zygomatic maxilla, longitudinal hypoplasia of the maxilla resulting in a tilted occlusal surface and openness on the affected side. Mandibular hypoplasia can produce a depression of the mandibular body on the affected side and a skewed chin on the affected side. If the onset of the disease is in adulthood, the facial skeleton has developed to a considerable extent and the skeletal deformity is not obvious, mainly manifesting as atrophy of soft tissues. It is not difficult to make the diagnosis by combining the medical history. The disease should be differentiated from limited scleroderma, first and second gill arch syndrome, and progressive lipodystrophy. Limited scleroderma is a punctate, patchy or band-like sclerotic lesion that rarely occurs on the face alone. The most reliable differential diagnosis is pathological examination, which shows microscopic atrophy of the skin adnexa and subcutaneous tissue, thickening and sclerosis of collagen fibers, and vascular occlusion. First and second gill arch syndrome is a congenital unilateral or bilateral facial tissue hypoplasia, often associated with facial cleft and auricular deformity as typical symptoms. Progressive lipodystrophy is a systemic disease without atrophy of the hard tissues and skin mucosa and is usually bilateral in distribution. The etiology of this disease is unknown, and there is no way to start the etiologic treatment. There is no specific method for conservative treatment, but the application of acupuncture, closure, physiotherapy, anti-inflammatory, immunotherapy and multivitamin treatment can make the disease relieved. At present, the treatment of PHFA at home and abroad is mainly surgical treatment. The aim of treatment is to design the corresponding surgical plan to reconstruct the shape and function of the affected side according to the deformity of the patient, and to strive for symmetry with the normal side. For patients with skeletal deformities that are not obvious but mainly soft tissue atrophy and depression, tissue transplantation can be used to fill in the repair; for patients with craniofacial skeletal dysplasia, the skeletal scaffold of the face should be reconstructed first, and on this basis, the soft tissue repair should be further completed. Most scholars believe that the best time for surgery is after the cessation of disease progression. Reconstruction of the skeletal scaffold of the face. In general, the facial shape can be significantly improved by reconstructing the facial skeleton. A better surgical result can be obtained by simultaneous or second-stage repair of soft tissues on this basis. Facial soft tissue filling: 1, autologous free fat particles injection filling; 2, autologous tissue transplantation with blood vessels or free skin flap transplantation; 3, lip repair.