Cleft Lip and Palate Midfacial Hypoplasia: Criteria to Choose the Treatment.

A series of skeletal and dentoalveolar/occlusal criteria were proposed for choosing the treatment modality for the management of midface hypoplasia in cleft lip/palate patients, focusing on functional improvement, aesthetics, and minimizing the risk of recurrence and secondary alterations. For which, 42 patients with nonsyndromic cleft lip/palate, all with previous primary lip/palate surgeries and without previous osteotomies, were analyzed. Orthognathic surgery (OS) (n = 24) and maxillary distraction osteogenesis (n = 18) with anterior segmental osteotomies (segmental distraction osteogenesis [SD]), alveolar transport disc (TD), and midface total distraction osteogenesis (TDO) by modified Le Fort III osteotomy was done.

Modified Le Fort III osteotomy: A simple solution to severe midfacial hypoplasia.

Purpose: There are multiple conditions that may affect the development of the middle third of the face and with varying degrees of severity. The surgical treatment alternatives for major midfacial sagittal deficiencies consist in Le Fort I, II, or III with conventional osteotomies or with distraction osteogenesis (DO). Both techniques have advantages and disadvantages that should be evaluated specifically in each case.

Orthognathic surgery in craniofacial microsomia: treatment algorithm.

Craniofacial microsomia is a broad term that covers a variety of craniofacial malformation conditions that are caused by alterations in the derivatives of the first and second pharyngeal arches. In general terms, diverse therapeutic alternatives are proposed according to the growth stage and the severity of the alteration. When craniofacial growth has concluded, conventional orthognathic surgery (Le Fort I osteotomy, bilateral sagittal split osteotomy, and genioplasty) provides good alternatives for MI and MIIA type cases.

Life-threatening complications following orthognathic surgery in a patient with undiagnosed hereditary angioedema.

As described in the literature, hereditary angioedema (HAE) is an autosomal dominant disease that presents with recurrent events of angioedema caused by a) deficiency or b) functional alteration of the plasma protein C1 inhibitor (C1-inh); this enzyme is involved in the regulation of the complement, kallikrein-kinin, fibrinolytic, and coagulation systems. HAE is characterized by episodes of edema in the larynx, facial structures and tissues, gastrointestinal tract, or extremities. Laryngeal edema has been reported to occur predominantly after oral surgery.