BackgroundAccidental displacement of a dental implant into the maxillary sinus is an infrequent although not uncommon complication encountered in dental clinical practice, with the main cause thought to be inadequate bone height in the posterior maxilla. We report a case of migration of a dental implant into the maxillary sinus, and discuss the benefits of its removal by a combination of endoscopically assisted and bone repositioning techniques.Case presentationA 35-year-old Japanese man with a partially edentulous maxilla underwent implant placement at a private clinic. Three months later, at the time of abutment connection, the implant at the site of his maxillary right first molar was accidentally pushed into the sinus. The hole on the alveolar ridge made for placement of the implant was small and far from the dislocated implant, thus access was achieved in a transoral manner via the frontal wall of his maxillary sinus with an endoscopic approach. Piezoelectric instruments were used to perform an osteotomy. The bone lid was removed, and the implant was identified using a rigid endoscope and removed with a surgical aspirator, followed by repositioning of the bony segment; the area was secured with an absorbable suture. Removal of migrated implants should be considered in order to prevent possible sinusal disease complications.ConclusionsIn the present case, removal of a dental implant displaced into the maxillary sinus by use of a combination of endoscopically assisted and bone repositioning techniques proved to be a safe and reliable procedure.

The present study was designed to investigate the biodegradation behavior of Mg alloy plates in the maxillofacial region. For in vitro analysis, the plates were immersed in saline solution and simulated body fluid. For in vivo, the plates were implanted into the tibia, head, back, abdominal cavity, and femur and assessed at 1, 2, and 4 weeks after implantation. After implantation, the plate volumes and the formed insoluble salt were measured via micro-computed tomography. SEM/EDX analysis of the insoluble salt and histological analysis of the surrounding tissues were performed. The volume loss of plates in the in vitro groups was higher than that in the in vivo groups. The volume loss was fastest in the abdomen, followed by the head, back, tibia, and femur. There were no statistically significant differences in the insoluble salt volume of the all implanted sites. The corrosion of the Mg alloy will be affected to the surrounding tissue responses. The material for the plate should be selected based on the characteristic that Mg alloys are decomposed relatively easily in the maxillofacial region.

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Idiopathic condylar resorption (ICR) is a major complication that can occur before or after orthognathic surgery, though the aetiology is unclear. ICR is defined as a change in condyle form, along with decreased condylar head volume and ramus height, and can lead to temporomandibular joint (TMJ) pain and dysfunction (Wolford & Cardenas, 1999). Essentially, excessive mechanical loading including compressive and tractional stress induces change to the form of the condylar head. Ichimiya et al. (2007) investigated the effects of compressive loading, while Gassner, Buckley, Studer, Evans, and Agarwal (2000) reported the effects

To characterize concentrated growth factors (CGFs) in vivo, we examined the degradation of implanted CGF in rabbits. Untreated CGF (U-CGF) and compressed CGF (C-CGF) were subcutaneously implanted into the dorsum. Histological analyses showed that the U-CGF and C-CGF induced very few inflammatory cells and that the U-CGF and C-CGF were subsequently degraded with dendritic invasion of granulation tissue. The C-CGF histopathologically remained for longer term than the U-CGF. Aggregated CD31+ and RAM11+ cells appeared in and around the implanted CGF. The number of macrophages and blood vessels in the CGF-implanted groups was greater than that in the sham group. There were more blood vessels in the U-CGF group than that in the C-CGF and sham group. We showed that CGF was degraded by macrophages in 4 weeks and enhanced angiogenesis with dendritically branching new capillaries. Therefore, the U-CGF and C-CGF can be clinically applied as a biomaterial inducing angiogenesis.