Various buildings, churches, temples, palaces, etc., both in ancient and modern times, take “symmetry” as the basic element of beauty. The anatomical structure of the human body, the distribution and structure of the five facial features are also symmetrical and balanced. The human head, torso and limbs are symmetrical on both sides with the midline as the axis. The natural symmetry contains the beauty of the human body, and the natural symmetry determines the harmony and balance of the craniofacial structure, torso and limbs. Once this natural symmetry is destroyed, the beauty of appearance and body shape will be destroyed, and the corresponding dysfunction and disability will appear, leading to inconvenience in life, loss of learning and working ability, difficulties in work and social interaction, etc. Congenital craniofacial short deformity: Patients with congenital small or no ear deformity often have asymmetrical facial development, short facial features, and even some facial deformities are very serious. In addition to small ears, the developmental deformity of the mandible is also serious in patients with severe hemifacial shortening deformity. The mandibular branch on the affected side is often short, or even missing in severe cases, resulting in a skewed jaw deformity, facial asymmetry and coordination, and an unattractive appearance. This deformity of the mandible is not in the same plane, but is a change in three-dimensional space. Due to the imbalance between the growth of the healthy side and the affected side of the lower jaw, the facial asymmetry becomes more and more serious as the child develops, and the deformity is usually more severe in adulthood. At the same time, the growth of the maxilla is also hindered by the hypoplasia of the mandible. Craniomaxillofacial short deformity treatment and surgical techniques: For patients with craniofacial deformities, surgical treatment is generally performed according to their age and degree of deformity to restore normal function and shape. In the past, the commonly used methods such as osteotomy and bone grafting were complicated and the results were not very satisfactory. Traction osteogenesis, which has been developed in recent years, is a good method to treat craniofacial asymmetry deformity. By fixing two to three bone segments with blood supply with a bone traction device, the bone segments are gradually pulled apart at a certain speed and frequency, and new bone is created in the bone gap, thus achieving bone lengthening. This can be done simultaneously with ear reconstruction. Stage I: Simultaneous placement of traction device and skin expander for bone traction lengthening and skin expansion. Stage II: removal of the bone lengthening device and skin expander, and auricular reconstruction. Although the bone lengthening procedure takes a long time, it does not increase in time if it is performed simultaneously with the application of skin expansion to reconstruct the olecranon. As for the dysplasia of the maxilla and local soft tissues, after the mandibular lengthening in childhood, the normal length of the mandibular movement should be able to promote the development of the maxilla and the surrounding soft tissues, and the intermaxillary relationship will gradually be naturally corrected, so the surgery only lengthens the mandible but obtains the benefit of three-dimensional spatial changes. The traction osteogenesis established on the basis of Ilizarov’s traction osteogenesis theory has changed the traditional surgical treatment idea, making full use of the growth potential of the body’s biological tissues and dispensing with the traditional methods of bone grafting and intermaxillary fixation. Its treatment degree and surgical operation are greatly simplified, the surgical risk is significantly reduced, postoperative stability is improved, and the age of the recipient is greatly advanced. Detailed medical theoretical knowledge: Lecture 1 Classification of craniofacial asymmetries Craniofacial asymmetries occur in humans at a rate of one in every 8,000-10,000 births. Normal individuals can have mild craniomaxillofacial asymmetries. Cohen, a specialist in craniofacial surgery and pathology at Dalhousie University in Canada, has made a more detailed classification of craniofacial asymmetries, which is listed below for reference. I. Normal variation, developmental buffer, and lateral habit 1. normal facial mild asymmetry; 2. normal developmental asymmetry; 3. increased developmental buffer and variation; 4. lateral power habit (e.g., lateral chewing, etc.). II. Diseases with asymmetric traits 1. craniofacial malformations (malformations); 2. craniofacial deformations (deformations); 3. craniofacial ruptures (disruptions). Asymmetrical embryonic diseases 1.Eye asymmetry on both sides; 2.Nose asymmetry on both sides; 3.Oral ectopia; 4.Dental ectopia; 5.Tessier unilateral craniofacial cleft. 4.Hemihypoplasia (hemihypoplasia) 1.Involving bones; 2.Involving various tissues. V. Hemihyperplasia (hemihyperplasia) 1, involving bones; 2, involving a variety of tissues. Hemilateral craniofacial atrophy (hemiatrophy, Romberg’s disease) VII. Hemilateral craniofacial developmental abnormalities (hemidysplasia) VIII. Neuromuscular disorders 1. 5, unilateral masticatory hypertrophy. Tumors 1.Lymphangioleioma; 2.Hemangioma; 3.Chondromatosis; 4.Other tumors. Physical or traumatic causes 1, trauma; 2, misalignment healing; 3, unilateral temporomandibular joint ankylosis; 4, early surgical injury; 5, radiation injury. XI. Other pathological changes 1. poor bone fiber structure; 2. unilateral parotid hypertrophy. XII. Malformation or multiple tumors 1. Sturge-Webber hemangiomatosis; 2. Epidermal nevus syndrome; 3. Neurofibromatosis; 4. Proteus (deformation) syndrome. XIII. Premature closure of cranial suture 1. unilateral premature closure of coronal suture; 2. unilateral premature closure of herringbone suture; 3. Apert’s syndrome; 4. Saether-chotzen’s syndrome. Orbital asymmetry I. Etiology Unilateral premature closure of the cranial suture, congenital anophthalmia, microphthalmia, and asymmetric craniofacial cleft can cause asymmetry in the morphology, size, and position of the orbital skeleton on both sides. Meningeal-brain bulge, especially temporal, skull base and retro-orbital meningeal-brain bulge, can lead to structural and positional changes of orbital bones, presenting asymmetric deformity of both orbits, i.e., one orbit is asymmetrical with the healthy side in horizontal and vertical directions. Clinical manifestations: 1. Temporal meningoencephalic bulge: The meningoencephalic bulge is behind the lateral wall of the orbit and the temporal fossa, which becomes flat or even bulges outward. Bone defects at the connection of the frontoparietal temporal bone and the large wing of the butterfly bone may appear. Temporal meningoencephalic bulge can expand with age, so that the orbital skeleton is displaced forward, outward and downward, orbital zygomatic deformity, asymmetry of the orbital face on both sides, protrusion of the eyeball, can appear as optic nerve compression atrophy, decreased vision, the articulating nerve, the talocrural nerve, abducens nerve compression appears completely or partially paralyzed, resulting in limited or fixed eye movement, ptosis, etc. 2, skull base meningeal brain expansion: skull base brain expansion including pteriorbital type (or postorbital type), pteromandibular type and nasopharyngeal type (transseptal, pteroseptal and transseptal type), its incidence is low, less than 5% of the total number of patients with brain expansion. The main basis of its classification remains the site of the skull defect. Craniosynostosis may be associated with ocular malformations such as ocular protrusion, enlarged optic papillae, microphthalmia, and optic nerve atrophy. Concomitant malformations of the brain include agenesis of the corpus callosum. Concomitant pituitary insufficiency has been reported. Skull base brain bulge can have no external manifestations, mostly with a wider nasal bridge, occasionally showing a widened orbital spacing and slightly lowered both temporal regions. The pteriorbital type may have unilateral pulsating proptosis. The bulging sac in the nasal cavity or nasopharynx can cause obstruction of the airway and abnormal breathing sounds, often with respiratory infections and runny nose. Occasionally, nasal leakage of cerebrospinal fluid occurs and may lead to intracranial infection. Misdiagnosis of nasal polyps is not uncommon. Biopsy is an important cause of cerebrospinal fluid leakage. Cephalometric radiographs, including skull base radiographs and anterior cranial fossa tomograms, should be routinely performed to show the effect of the brain bulge on the orbit. Cranial defects are seen in the septum, pterygoid and pterygoid sinus regions. Masses are seen in the nose or pharynx. CT and MRI may show bony resorption defects in the lateral orbital wall and the large wing of the pterygoid bone, and displacement of the medial orbital wall to the opposite side. CT and MRI have definite diagnostic value for the contents of bulging masses and hydrocephalus with associated deformities. Hemifacial hypertrophy is divided into two categories: 1. Hemifacial hypertrophy is a hypertrophy of the skull, temporal bone, zygomatic bone, maxilla and mandible on one side, often accompanied by hypertrophy of soft tissues on the affected side, including skin, subcutaneous tissue and muscles, resulting in asymmetric deformity of the craniofacial surface on both sides, and often with disorders of dental relations. 2. 2, the deformity is limited to the mandible, manifesting as unilateral condyle, mandibular ascending branch and body hypertrophy, the lower edge of the mandible on the affected side is lower than that on the healthy side, and the plane of dentition is inclined to the affected side, and the dentition can be adaptively changed without obvious disorder; anterior open dentition and posterior anterior dentition can also appear. Unilateral mandibular hypertrophy is relatively common, and its correction sometimes requires multiple surgeries: 1) LeFort I osteotomy to correct the inclined plane of coaptation; 2) condylar resection to block the continued growth of the condyle; 3) bilateral osteotomy of the ascending area so that the function of the TMJ on the healthy side is not compromised during jaw movement; 4) pseudoarthroplasty on the affected side to reconstruct the function of the TMJ on the affected side; 5) mandibuloplasty to reconstruct the function of the TMJ on the affected side 5. mandibular osteotomy to restore facial symmetry; 6. chin osteotomy to align the midline of the chin with the midline of the face. The fourth lecture Hemimicrosomia (Hemimicrosomia) I. Definition of craniofacial short deformity is a broad general term for one side of the craniofacial dysplasia or hypoplastic deformity. As a class of congenital malformations, there have been many proper names to describe these malformations, such as ear-mandibular dysplasia, mouth-mandibular-ear syndrome, and more recently, hemimicrosomia. From the point of view of craniofacial surgery, clinically, most of the facial dysplasia on one side is more or less accompanied by some craniotemporal deformities, only the facial deformities are more obvious, while the craniotemporal deformities are often covered by hair. There is no obvious genetic factor for this type of malformation, and the cause of its development is unknown. Recently, some authors believe that it may be related to the obstruction of fetal development in utero, mainly involving the development of the first and second gill arches, which occurs during the first to seven months of fetal life. The causes of gill arch hypoplasia may be localized fetal poor blood supply, hematoma and certain drugs such as thalidomide. In terms of clinical features, some patients correspond to cleft anomalies of types 6, 7, 8 and 9 of Tessier’s craniofacial cleft classification. In terms of incidence gender, males are higher than females, and Grabb (1965) reported 63 males and 39 females out of 102 cases. The main symptoms are dysplasia of bones, muscles and other soft tissues centered on the ear, maxilla and mandible, and may involve the skull base, temporal bone, zygomatic bone and mastoid process upward. Skeletal deformities: Hypoplasia and shortening of the ascending branch of the mandible are the most common, and in severe cases, there may be defects of the ascending branch of the mandible and defects of the condyle of the temporomandibular joint. The chin part of the mandible is biased to the affected side, and the body part of the mandible is relatively normal. Pruzansky classifies mandibular deformities into three degrees according to the amount of loss of the mandibular ascending branches: mild with a small amount of shortening of the ascending branches, moderate with short and flattened ascending branches and condyles or with absence of the rostral process, and severe with minimal or no mandibular ascending branches. The maxilla on the affected side is shortened due to dysplasia, the vertical height is shortened, and the eruption of the molar is delayed. Due to the shortening of both maxilla and mandible on the affected side, the plane of dentition is elevated towards the affected side, while the maxillary sinus and the pear-shaped foramen on the affected side are elevated, but the orbital level is not changed. In severe cases, the temporal mastoid process and zygomatic arch of the affected side may be involved, showing a reduction of the mastoid air space, absence of the stem, loss of the zygomatic process and flattening of the affected canthus, and collapse of the affected canthus or orbital reduction. The orbital changes are mainly shortening of the longitudinal axis, and if the frontal bone is also dysplastic, small orbital deformity may occur. It has been reported (Grabb) that craniofacial shortening deformity can be accompanied by vertebral deformity. 2.Muscle deformity: The side of craniofacial dysplasia has poor muscle development, including expression muscle and masticatory muscle, but compared with hemifacial atrophy deformity (Romberg syndrome), the atrophy of the former muscle is not very obvious, sometimes only a local depression. 3. External ear deformity: Many congenital microtia are actually manifestations of various degrees of craniofacial shortening deformity, often synchronized with the degree of mandibular dysplasia. In mild cases, the outer ear is slightly smaller than the outer ear. In moderate cases, the deformity is hemi-ear deformity or residual ear deformity (residual earlobe and some cartilage). In severe cases, there is no ear deformity. In moderate and severe microtia, there is no external auditory canal, and the auditory chain is not developed and only bone conduction hearing is present. 4. Other soft tissue deformities: Most of the moderate and severe craniofacial microtia are accompanied by partial or complete facial nerve dysplasia, which may be the buccal branch or the mandibular rim branch, and may also involve the ophthalmic branch or the frontal branch. Generally there are few skin abnormalities, sometimes there may be orofacial cleft or corners of the mouth with transverse facial cleft, etc. Fourth, the treatment principle of surgical correction is firstly to correct the skeletal deformity, restore the craniofacial bone structure coordination, balance and symmetry on both sides. Then soft tissue deformities such as muscle dysplasia, soft tissue depression and external ear deformity are treated. 1.Pre-operative assessment and surgical planning: At present, a more effective and practical method of bone structure assessment is to study the amount of points, line segments, craniofacial angles and interrelationships of craniofacial bone structures through X-ray cephalometric measurements. This quantitative analysis can reveal the location of abnormal bone structures (e.g., cranial, maxillary, or mandibular), the direction and degree of skewness of the facial midline, and changes in occlusal relationships (Figure 18-9 removed). The surgeon can use the above analysis to decide the surgical plan: whether to perform bone grafting alone or both osteotomy and bone grafting; whether to perform osteotomy of the maxilla or mandible or combined osteotomy of both maxilla and mandible, etc. After the surgical plan is decided, the simulation of the surgery can be carried out, such as plaster model surgery, computer simulation surgery, etc. 2.Craniofacial bone graft surgery: For some mild craniofacial asymmetric deformities, bone graft filling can be performed, such as the body of the mandible on one side, the zygomatic area of the maxilla or the side of the pear-shaped foramen, the zygomatic arch and the temporal fossa. The incision may depend on the location, for example, the mandibular implant can be made through an intraoral lower lip gingival sulcus incision, the maxillary implant can be made through an intraoral upper lip gingival sulcus incision, the zygomatic arch implant can be made through an incision in front of the ear screen, and the temporal fossa implant can be made through a “T” shaped incision or coronal incision in the temporal area. The donor bone is mostly taken from the ribs, which can be fixed in the bone defect area after layering and binding. The bone graft is usually placed under the periosteum, and in some parts where the periosteum is tight, such as the body of the mandible and the zygomatic arch area, bone fixation may not be made. 3.Maxillary and mandibular osteotomy: Severe facial asymmetry, mostly accompanied by skewed facial midline and extreme inclination of the dental plane. In addition to the coordination of facial appearance, balance and midline restoration, the level of the dental plane and the coordination of the occlusal relationship should be taken into account in the surgical correction. To achieve these goals, simultaneous osteotomy of the maxilla and mandible is necessary. The LeFortI type osteotomy of the maxilla and the bilateral ascending sagittal osteotomy of the mandible can make the entire midface and lower part move horizontally, vertically and sagittally in three dimensions to achieve the coordination of facial appearance and occlusal function. In the process of rotation of the whole face in all directions, the gap after osteotomy can be embedded with autologous bone graft and fixed. Sometimes, chinplasty and maxillary and mandibular surface covering bone grafting can also be performed. In serious cases with one side of the mandibular ascending branch and temporomandibular joint defect, the mandibular ascending branch and temporomandibular joint can be reconstructed at the same time of osteotomy. 4.Other surgeries: The main purpose of soft tissue surgery is to improve facial appearance. According to the needs of the condition, the commonly used surgical methods include orofacial cleft repair, local soft tissue filling (dermis, fat, muscle), free tissue flap graft filling, external otoplasty and so on. For some mild cases, artificial composite materials can also be used for local filling. In 1973, Synder reported the first experimental study of successful lengthening of the mandible in dogs using the traction lengthening osteogenesis technique, and in 1990, Karp et al. reported the possibility of lengthening of the mandible. In 1992, McCarthy successfully corrected four cases of hemifacial microsomia in children using an extraoral approach. Since then, this technique has been gradually applied in clinical practice. There is no uniform understanding about the age of surgery, and the current clinical treatment age is from 1 year 6 months to 13 years 7 months. It is generally believed that the potential growth capacity of juvenile bone is strong, and early surgery can restore more normal function of the maxillofacial matrix bed and reduce the limitation of the mandibular deformity on the mid-facial development. The age at which mandibular lengthening is clinically advocated for application is 2 to 4 years old. Second, preoperative examination and preparation: 1. X-ray cephalometric film is taken and CT examination is done for measurement analysis and surgical simulation prediction. (1) The length of the mandible on both sides, Ar (condylar apex) – Gn (chin apex The midpoint of the line connecting the most anterior and the most inferior point of the chin), Go (mandibular angle point) – Gn. (2) The height of the mandibular ascending branch: Ar – Go. (3) The relationship between the skull and the maxilla and mandible The relationship of: SNA: the angle between the midpoint of the butterfly saddle – the point of the nasal root – the point of the upper alveolar seat. SNB: The angle between the midpoint of the butterfly saddle – the nasal root point – the seat point of the inferior alveolus. ANB: Upper alveolar seat point – nasal root point – lower alveolar seat point. If necessary, sagittal, coronal and cross-sectional tomographic images can be used to analyze and evaluate the jaw malocclusion by overlapping the bony anatomical landmarks and comparing them with the median sagittal line. It can also be used to understand the amount of bone loss in the mandible through three-dimensional measurement and surgical simulation, and to predict the amount of mandibular lengthening and the direction of traction. 2.Take a full-mouth dental and jaw model, record the occlusal relationship, and grind and modify the cusps and oblique surfaces of the teeth that may be dentally impaired, and make mating pads. 3.Do model surgery to further determine the osteotomy site and traction direction. 4.Prepare the mandibular extension. 3.Surgery method: Cut the skin, subcutaneous tissue, broad neck muscle, and sharp cut the occlusal muscle at 2cm below the lower edge of the affected mandible, and expose the mandibular angle in the superior plane of the periosteum. The osteotomy line is designed between the mandibular angle and the sigmoid incision. Osteotomy and protection of the inferior alveolar neurovascular bundle are performed, and holes are drilled in the osteotomy line for titanium nail fixation. A built-in mandibular retraction extender is placed. Care was taken to protect the periosteum and inferior alveolar neurovascular bundle as much as possible during the operation. The cervicalis muscle and skin are then sutured layer by layer. The fixation is maintained for one week. On day 7, the adjustment lever is turned to lengthen the bone. Once a day, 10-15 mm at a time, until the desired lengthening length was reached. After lengthening was completed, the mandible was maintained in traction on the lengthener for 3-6 months. After removal of the lengthener, orthodontic treatment is feasible to obtain a normal occlusal relationship. The sixth lecture on hemifacial atrophy Hemifacial atrophy (Romberg’s disease) is a slow-onset, progressive atrophic disease of the soft tissues or muscles and bones on one side. The cause of the disease is still unknown, but in 1846 Romberg described the typical features of the disease, so it is also known as Romberg’s syndrome. In 1964, Rogers observed 773 cases of hemifacial atrophy, the pathogenesis of which is still unclear. I. Pathogenesis: (a) Infection theory Mobius (1845) believes that this disease is due to the sympathetic nervous system to certain inflammatory processes produced by tissues such as certain infectious diseases such as scarlet fever, measles, dengue, tuberculosis, etc., oral lesions such as alveolar abscesses, periodontal inflammation, etc. (B) Sympathetic nerve theory Patients with this disease often have sympathetic hyperexcitation, which can lead to vasoconstriction disorders, neurokeratitis, iritis and migraine leading to tissue atrophy. (iii) Trigeminal nerve theory Mondel reported this disease in which tissue atrophy within the trigeminal nerve distribution area was found to be associated with trigeminal neuritis during autopsy. From what was seen on histological examination, Peskovo Stockar (1961). reported that the skin and subcutaneous tissues often show chronic inflammatory progressive necrotic lesions, eventually leading to scar formation, thinning of epidermal tissue in the form of keratosis, and loss of the dermal papillary layer, while the muscular layer still maintains a certain degree of elastic fiber tissue. (D) trauma theory many patients have facial, brain, neck trauma, or thyroid surgery caused by cervical sympathetic nerve stimulation induced hemifacial atrophy. Clinical symptoms: Hemifacial atrophy usually affects the subcutaneous tissues most severely, and then spreads to muscles, cartilage and bone, often limited to one side, and mostly the left side, there are very few cases of atrophy on one side of the whole body, such as the onset in early childhood (before the age of 10) facial bone, arthritis is not fully developed, it can affect the normal development of the affected side of the bone, resulting in serious deformities. If the onset of the disease is in adulthood, the facial bones have developed to a considerable extent; the deformity is not obvious, the initial onset of the disease often appears in certain areas of the face, such as the frontal area above the eyebrows or the lower part of the orbit, increased or reduced pigmentation, the skin becomes brown or white, and then gradually expand and present the depression of the subcutaneous tissue, until completely disappeared, and related to the distribution of the trigeminal nerve, some appear only in the distribution area of a branch, followed by skin, mucous membrane In some cases, the skin, mucosa, bones and muscles change, but the muscles can still maintain certain functions, and there is no clinical manifestation of facial nerve paralysis. Patients with longer disease can also see thinning and drying of the skin, showing scleroderma-like symptoms, and even adhesions with muscles and bones, forming obvious deformities and obvious depressions at the junction with the healthy side. In some patients, the affected side of the tongue, nasal cartilage, ear cartilage and mucosa of the hard palate, and the tissues of the mouth and lips can be affected. Hair thinning, loss of hair or white hair, sweat glands, salivary glands, and hair follicles can also be affected, and in severe cases, the ipsilateral side of the head can also be affected. Orbital contents, can make the eye sunken, vision loss or no vision, eyelid drooping. Treatment: The treatment of hemifacial atrophy should depend on the degree and extent of the deformity to select various surgical methods. The surgical treatment options are: autologous fat injection filling, temporal fascial-dermal fat flap grafting with blood vessels, anterolateral femoral fat fascial flap repair, and latissimus dorsi muscle flap repair.