Micrognathia with temporomandibular joint ankylosis and obstructive sleep apnea treated with mandibular distraction osteogenesis using skeletal anchorage: a case report.

Background: We describe the case of a 16-year-old female patient with micrognathia, temporomandibular joint (TMJ) ankylosis, and obstructive sleep apnea, who was treated with mandibular distraction osteogenesis (DO) combined with sliding genioplasty, using skeletal anchorage.

Case Presentation: We first performed interpositional arthroplasty, in which an interposition of fascia temporalis and surrounding fat tissue was inserted into the defect after bilateral condylectomy, increasing the maximum mouth opening from 5.0 to 32.

Clinical significance of magnetization transfer contrast imaging for edematous changes in masticatory muscle.

Objective: To evaluate inflammatory changes in masticatory muscles by magnetization transfer contrast (MTC) imaging.

Methods: Gradient-recalled echo (GRE) and MTC-GRE images of relaxed masticatory muscles in 28 healthy volunteers were obtained before and after exercise. At the same time, muscle stiffness and pain in the masseter muscles were also measured.

Gastroesophageal reflux symptoms in adults with skeletal Class III malocclusion examined by questionnaires.

Introduction: Patients with masticatory dysfunction have a higher incidence of gastrointestinal disorders including gastroesophageal reflux disease (GERD). Masticatory function is significantly lower in patients with skeletal Class III malocclusion than in those with normal occlusion. However, GERD symptoms in patients with skeletal Class III malocclusion are still unknown.

NSAIDs suppress the expression of claudin-2 to promote invasion activity of cancer cells.

Non-steroidal anti-inflammatory drugs (NSAIDs) show chemopreventive effects; however, the precise molecular mechanism of these effects is still unclear. On the other hand, the expression of proteins that form tight junctions (TJs) (such as claudins) in clinically isolated tumors is frequently altered relative to normal tissue. We previously reported that NSAIDs upregulate the expression of claudin-4 and that this upregulation contributes to NSAID-dependent inhibition of both migration activity and anchorage-independent growth of cancer cells.