A Multidisciplinary Approach to Malocclusion Caused by Facial Multiple Fracture.

In the case of multiple facial fractures, a simple open reduction occasionally causes various disorders during healing process after the surgery. Moreover, esthetic disturbance of a facial deformity might be induced. Therefore, the acquisition of facial symmetry and the recovery of occlusal and masticatory functions become increasingly important. This case report presents a successful treatment of facial multiple fracture induced by a car accident. A 20-year-old male was diagnosed with suffered multiple midface and mandibular fractures induced by a car accident. Midface fractures included the LeFort I and II type fractures, as well as sagittal fracture at midline and fractures from right maxillary sinus anterior wall to orbital wall. In the mandible, midline and left body fractures were detected. The patient underwent open reduction and rigid fixation of the fractured left zygoma, comminuted LeFort I and II fractures, and midline and left body of the mandible with intermaxillary fixation by multibracket appliance; maxillary osteotomy with iliac bone grafting; orthognathic two-jaw surgery with coronoid process grafts onto the depressed zygoma; and onlay graft of hydroxyapatite block on mandible. As the result, the multidisciplinary treatments successfully recover functions and esthetics to the satisfactory level of the patient with multiple facial fractures. As treatments for multiple facial fractures are required complexity due to the extent of trauma, multidisciplinary approach under the close cooperation between hospital departments is thought to be important.

Comprehensive treatment for severe periodontitis with pathologic tooth migration-related bimaxillary protrusion: A case report with 3-year follow-up.

BACKGROUND AND OVERVIEW: Patients with severe periodontitis often experience pathologic tooth migration (PTM), which impairs esthetics and leads to occlusal disharmony (for example, premature contacts and traumatic occlusion) that can further exacerbate periodontitis. The authors describe a patient who exhibited severe periodontitis with PTM-related bimaxillary protrusion. This report includes 3-year clinical outcomes after periodontal regenerative therapy, implant-anchored orthodontic therapy, and implant prosthodontics intended to achieve both functional and esthetic improvements. CASE DESCRIPTION: A 63-year-old woman sought treatment with the chief complaint of maxillary anterior tooth mobility. Clinical examination revealed excessive tooth mobility, deep periodontal pockets, and infrabony defects in all teeth. All teeth exhibited PTM; the mandibular anterior teeth exhibited marked protrusion caused by the progression of periodontitis. After initial periodontal therapy, periodontal regenerative therapy was performed in all molar regions. At 6 and 9 months postoperatively, comprehensive orthodontic treatment was initiated for the mandible and maxilla, respectively, using orthodontic anchorage devices to achieve acceptable functional occlusion. After orthodontic treatment, staged guided bone regeneration was performed and dental implants were placed in the severely resorbed maxillary anterior ridge. This comprehensive treatment yielded favorable periodontal conditions, stable occlusion, and good esthetic outcomes. CONCLUSIONS AND PRACTICAL IMPLICATIONS: Favorable esthetics, stable occlusion, and highly cleansable periodontal tissues were achieved with well-planned interdisciplinary and comprehensive treatment, although the patient had severe periodontitis and PTM-related bimaxillary protrusion.

The C-terminal region including the MH6 domain of Msx1 regulates skeletal development.

MSX1 is a causative gene for oligodontia in humans. Although conventional Msx1-deficient mice die neonatally, a mutant mouse lacking the C-terminus MH6 domain of MSX1 (Msx1ΔMH6/ΔMH6) showed two different phenotypes; newborn homozygotes with cleft palates died neonatally, whereas those with thin palates remained alive and had craniofacial dysplasia and growth retardation compared with wild-type mice, with most mice dying by the age of 4-5 weeks. In a previously reported case of human oligodontia caused by a heterozygous defect of the Msx1 MH6 domain, a small foramen was observed on the occipital bone. The aim of this study was to test the hypothesis that the Msx1 MH6 domain is involved in bone formation in vivo. In Msx1ΔMH6/ΔMH6 mice, cranial suture fusion was delayed at embryonic day 18.5, and the anteroposterior cranial diameter was smaller and long bone length was decreased at 3 weeks of age. The femoral epiphysis showed no change in the trabecular number, but decreased bone mass, bone density, and trabecular width in Msx1ΔMH6/ΔMH6 mice. In addition, cancellous bone mass was reduced and the cartilage layer in the growth plate was thinner in Msx1ΔMH6/ΔMH6 mice. The mRNA expression levels of major osteoblast and chondrocyte differentiation marker genes were decreased in Msx1ΔMH6/ΔMH6 mice compared with wild-type mice. These findings suggest that the C-terminal region including the MH6 domain of MSX1 plays important roles not only in tooth development and palatal fusion, but also in postnatal bone formation.