Search

Objectives/hypothesis: The aim of this study was to evaluate the nature and incidence of long-term maxillary sinus adverse events related to endosseous implant placement with protrusion into the maxillary sinus., Study Design: Retrospective cohort study., Methods: All patients who underwent placement of endosseous dental implants with clinical evidence of implant penetration into the maxillary sinus with membrane perforation were included in this study. Only patients with a minimum follow-up of 5 years after implant placement were included in this study. Maxillary sinus assessment was both clinical and radiological., Results: Eighty-three implants with sinus membrane perforation in 70 patients met the study's inclusion criteria. Mean age was 65.96 years ± 14.23. Twelve patients had more than one implant penetrating the maxillary sinus, and seven of them had bilateral sinus perforation. Estimated implant penetration was ≤ 3 mm in all cases. The average clinical and radiological follow-up was 9.98 years ± 3.74 (range 60-243 months). At the follow-up appointments, there were no clinical or radiological signs of sinusitis in any patient., Conclusion: This long-term study, spreading over a period of up to 20 years, indicates that no sinus complication was observed following implant penetration into the maxillary sinus. Furthermore, absence of occurrence of such complications is related to the maintenance of successful osseointegration. A contrario, and in the presence of an acute or chronic maxillary sinusitis, the differential diagnosis must always consider other potential odontogenic and nonodontogenic etiologies., (Copyright © 2013 The American Laryngological, Rhinological and Otological Society, Inc.)

In this study, we have found that dipeptidylpeptidase IV (DPPIV) plays in vivo an active role in the modulation of the inflammatory response of chronic rhinosinusitis. Human nasal mucosa expresses DPPIV-like immunoreactivity in submucosal seromucus glands, leukocytes, and endothelial cells of blood vessels. DPPIV enzymatic activity in nasal tissue biopsies taken from patients suffering from chronic rhinosinusitis was correlated inversely with the density of inflammatory cells in the nasal mucosa, and the DPPIV activity rose when chronic rhinosinusitis was treated. By using a pig animal model, we have shown that the intranasal administration of recombinant DPPIV decreased the vasodilatation induced by exogenous substance P (SP), a proinflammatory peptide released by sensory nerves. In contrast, an inhibitor of DPPIV enhanced the vasodilatatory effect at low doses of SP. SP5-11 was 100- to 1000-fold less potent than SP as a vasodilator of the nasal mucosa. The vasodilatatory effect of SP was abolished by a NK1 receptor antagonist. In conclusion, these results suggest a new pathophysiological pathway for rhinitis based on clinical observations in humans, indicating the involvement of an enzyme to modulate non-adrenergic and non-cholinergic substrate that occurred during nasal dysfunctions.