Frontal sinus obliteration with iliac crest bone grafts: review of 8 cases

This study evaluated postoperative results of 8 cases of frontal sinus fractures treated by frontal sinus obliteration with autogenous bone from the anterior iliac crest. Patients and methods: The medical charts of patients sequentially treated for frontal sinus fractures by obliteration with autogenous cancellous iliac crest bone in the Oral and Maxillofacial Surgery Division of this institution were reviewed. From those, eight had complete records and adequately described long-term follow-up. All were operated by the same surgical team. Those patients were recalled and independently evaluated by 2 examiners. Radiographs and/or CT scans were available for this evaluation. Associated fractures and complications were noted. The average postoperative follow-up was 7 years, ranging from 3 to 16 years. The main complication was infection. Four patients (50%) had uneventful long-term follow-ups and four (50%) experienced complications requiring reoperation. Based on the studied sample studied the authors conclude that the obliteration with autogenous bone presented a high percentage of complications in this series.

Frontal sinus obliteration with iliac crest bone grafts

This study evaluated postoperative results of 8 cases of frontal sinus fractures treated by frontal sinus obliteration with autogenous bone from the anterior iliac crest.

Sub-crestal positioning of implants results in higher bony crest resorption: an experimental study in dogs

To compare peri-implant soft- and hard-tissue integration at implants installed juxta- or sub-crestally. Furthermore, differences in the hard and soft peri-implant tissue dimensions at sites prepared with drills or sonic instruments were to be evaluated. Three months after tooth extraction in six dogs, recipient sites were prepared in both sides of the mandible using conventional drills or a sonic device (Sonosurgery(®) ). Two implants with a 1.7-mm high-polished neck were installed, one with the rough/smooth surface interface placed at the level of the buccal bony crest (control) and the second placed 1.3 mm deeper (test). After 8 weeks of non-submerged healing, biopsies were harvested and ground sections prepared for histological evaluation. The buccal distances between the abutment/fixture junction (AF) and the most coronal level of osseointegration (B) were 1.6 ± 0.6 and 2.4 ± 0.4 mm; between AF and the top of the bony crest (C), they were 1.4 ± 0.4 and 2.2 ± 0.2 mm at the test and control sites, respectively. The top of the peri-implant mucosa (PM) was located more coronally at the test (1.2 ± 0.6 mm) compared to the control sites (0.6 ± 0.5 mm). However, when the original position of the bony crest was taken into account, a higher bone loss and a more apical position of the peri-implant mucosa resulted at the test sites. The placement of implants into a sub-crestal location resulted in a higher vertical buccal bone resorption and a more apical position of the peri-implant mucosa in relation to the level of the bony crest at implant installation. Moreover, peri-implant hard-tissue dimensions were similar at sites prepared with either drills or Sonosurgery(®) .

Cone Beam Computed Tomographic Evaluation of a Maxillary Alveolar Ridge Reconstruction With Iliac Crest Graft and Implants

The present article discusses an atrophic maxilla reconstruction with iliac crest bone block and particulate grafts and dental implants. Onlay block grafts were used to restore bone volume of the anterior maxilla, whereas bilateral sinus floor augmentation was performed using a particulate graft. Ten months after the grafting surgery, 9 dental implants were placed to rehabilitate the case. Results of a 7-year follow-up were obtained clinically and by cone beam computed tomographic images.

Effetti dell'acido urico sulle cellule glomerulari mesangiali: meccanismi intracellulari di trasduzione del segnale e possibili implicazioni nella progressione del danno renale e nella sindrome infiammatoria in corso di nefropatie croniche

Uric acid is a major inducer of inflammation in renal interstitium and may play a role in the progression of renal damage in hyperuricemic subjects with primary nephropathies, renal vascular disease, and essential hypertension. At the same time, UA also acts as a water-soluble scavenger of reactive oxygen species. We evaluated the cellular effects of UA on cultured HMC as a potential interstitial target for abnormally elevated levels in acute and chronic renal disease. Intracellular free Ca2+ ([Ca2+]i) was monitored by microfluorometry of fura 2-loaded cells, while oxidation of intracellularly trapped non-fluorescent 2’,7’-dichlorofluorescein diacetate (DCFHDA, 20 uM) was employed to assess the generation of reactive oxygen species during 12-hr incubations with various concentrations of UA or monosodium urate. Fluorescent metabolites of DCFH-DA in the culture media of HMC were detected at 485/530 nm excitation/emission wavelengths, respectively. UA dose-dependently lowered resting [Ca2+]i (from 102±9 nM to 95±3, 57±2, 48±6 nM at 1-100 uM UA, respectively, p <0.05), leaving responses to vasoconstrictors such as angiotensin II unaffected. The effect was not due to Ca2+/H+ exchange upon acidification of the bathing media, as acetate, glutamate, lactate and other organic acids rather increased [Ca2+]i (to max. levels of 497±42 nM with 0.1 mM acetate). The decrease of [Ca2+]i was abolished by raising extracellular Ca2+ and not due to effects on Ca2+ channels or activation of Ca2+-ATPases, since unaffected by thapsigargin. The process rather appeared sensitive to removal of extracellular Na+ in combination with blockers of Na+/Ca2+ exchange, such as 2’,4’-dichlorobenzamil, pointing to a countertransport mechanism. UA dose-dependently prompted the extracellular release of oxidised DCFH (control 37±2 relative fluorescence units (RFU)/ml, 0.1uM 47±2, 1 uM 48±2, 10 uM 51±4, 0.1 mM 53±4; positive control, 10 uM sodium nitroprusside 92±5 RFU/ml, p<0.01). In summary, UA interferes with Ca2+ transport in cultured HMC, triggering oxidative stress which may initiate a sequence of events leading to interstitial injury and possibly amplifying renal vascular damage and/or the progression of chronic disease.