Cancellous Bone Block Allografts for the Augmentation of the Anterior Atrophic Maxilla

Background: Pre‐implant augmentative surgery is a prerequisite in many cases in the anterior maxilla to achieve a stable, long‐term esthetic final result. Purpose: The aim of the present study was to evaluate the outcome of ridge augmentation with cancellous freeze‐dried block bone allografts in the anterior atrophic maxilla followed by placement of dental implants. Materials and Methods: Thirty‐one consecutive patients were included in the study. A bony deficiency of at least 3 mm horizontally and up to 3 mm vertically according to computerized tomography (CT) served as inclusion criteria. Sixty‐three implants were inserted after a healing period of 6 months. Nineteen of sixty‐three implants were immediately restored. Bone measurements were taken prior to bone augmentation, during implant placement, and at second‐stage surgery. Results: Forty‐six cancellous allogeneic bone blocks were used. The mean follow‐up was 34 ± 16 months. Mean bone gain was 5 ± 0.5 mm horizontally, and 2 ± 0.5 mm vertically. Mean buccal bone resorption was 0.5 ± 0.5 mm at implant placement, and 0.2 ± 0.2 mm at second‐stage surgery. Mean bone thickness buccal to the implant neck was 2.5 ± 0.5 mm at implant placement, and 2.3 ± 0.2 mm at second‐stage surgery. There was no evidence of vertical bone loss between implant placement and second‐stage surgery. Block and implant survival rates were 95.6 and 98%, respectively. All patients received a fixed implant‐supported prosthesis. Conclusion: Cancellous block allografts appear to hold promise for grafting the anterior atrophic maxilla.     

Efficacy of Cancellous Block Allograft Augmentation Prior to Implant Placement in the Posterior Atrophic Mandible

Background: The present study evaluated the outcome of ridge augmentation with cancellous freeze‐dried block bone allografts in the posterior atrophic mandible followed by placement of dental implants. Materials and Methods: A bony deficiency of at least 3 mm, horizontally, vertically, or both, according to computerized tomography (CT) para‐axial reconstruction served as inclusion criteria. Implants were inserted after a healing period of 6 months. Bone measurements were taken prior to bone augmentation, during implant placement, and at second‐stage surgery. Marginal bone loss and crown‐to‐implant ratio were also measured. Results: Twenty‐nine cancellous allogeneic bone blocks were placed in 21 patients. The mean follow‐up was 37 months. Bone block survival rate was 79.3%. Mean horizontal and vertical bone gains were 5.6 and 4.3 mm, respectively. Mean buccal bone resorption was 0.5 mm at implant placement and 0.2 mm at second‐stage surgery. A total of 85 implants were placed. Mean bone thickness buccal to the implant neck was 2.5 mm at implant placement and 2.3 mm at second‐stage surgery. There was no evidence of vertical bone loss between implant placement and second‐stage surgery. Implant survival rate was 95.3%. All patients received a fixed implant‐supported prosthesis. At the last follow‐up, the mean marginal bone loss was 0.5 mm. The mean crown‐to‐implant ratio was 0.96. Conclusion: Implant placement in the posterior atrophic mandible following augmentation with cancellous freeze‐dried bone block allografts may be regarded as a viable treatment alternative.     

Histomorphometric analysis following augmentation of the posterior mandible using cancellous bone-block allograft

The present study was conducted to histologically and histomorphometrically evaluate the application of cancellous bone-block allografts for the augmentation of the posterior atrophic mandible. Twenty-four consecutive patients underwent augmentation with cancellous bone-block allografts in the posterior mandible. A bony deficiency of at least 3 mm horizontally and/or vertically according to CT para-axial reconstruction served as inclusion criteria. Following 6 months, 85 implants were placed and a cylindrical sample core was collected. All specimens were prepared for histological and histomorphometrical examination. Implant survival rate was 95.3%. Follow-up ranged 12-66 months (mean 43 ± 19 months). The mean newly formed bone was 44 ± 28%, that of the residual cancellous bone-block allograft 29 ± 24%, and of the marrow and connective tissue 27 ± 21%. Statistically significant histomorphometric differences regarding newly formed bone (69% vs. 31%, p = 0.05) were found between younger (< 45 years) and older (> 45 years) patients, respectively. Histomorphometric differences regarding residual cancellous bone-block allograft (17% vs. 35%) and of the marrow and connective tissue (14% vs. 34%) were not statistically significant. Cancellous bone-block allograft is biocompatible and osteoconductive, permitting new bone formation following augmentation of extremely atrophic posterior mandible with a two-stage implant placement procedure. New bone formation was age-dependent.     

Repetitive nerve stimulation transiently opens the mitochondrial permeability transition pore in motor nerve terminals of symptomatic mutant SOD1 mice

Mitochondria in motor nerve terminals temporarily sequester large Ca(2+) loads during repetitive stimulation. In wild-type mice this Ca(2+) uptake produces a small (<5 mV), transient depolarization of the mitochondrial membrane potential (Ψ(m), motor nerve stimulated at 100 Hz for 5s). We demonstrate that this stimulation-induced Ψ(m) depolarization attains much higher amplitudes in motor terminals of symptomatic mice expressing the G93A or G85R mutation of human superoxide dismutase 1 (SOD1), models of familial amyotrophic lateral sclerosis (fALS). These large Ψ(m) depolarizations decayed slowly and incremented with successive stimulus trains. Additional Ψ(m) depolarizations occurred that were not synchronized with stimulation. These large Ψ(m) depolarizations were reduced (a) by cyclosporin A (CsA, 1-2 μM), which inhibits opening of the mitochondrial permeability transition pore (mPTP), or (b) by replacing bath Ca(2+) with Sr(2+), which enters motor terminals and mitochondria but does not support mPTP opening. These results are consistent with the hypothesis that the large Ψ(m) depolarizations evoked by repetitive stimulation in motor terminals of symptomatic fALS mice result from mitochondrial dysfunction that increases the likelihood of transient mPTP opening during Ca(2+) influx. Such mPTP openings, a sign of mitochondrial stress, would disrupt motor terminal handling of Ca(2+) loads and might thereby contribute to motor terminal degeneration in fALS mice. Ψ(m) depolarizations resembling those in symptomatic fALS mice could be elicited in wild-type mice following a 0.5-1h exposure to diamide (200 μM), which produces an oxidative stress, but these depolarizations were not reduced by CsA.     

Morphologic changes of the nasopalatine canal related to dental implantation: a radiologic study in different degrees of absorbed maxillae

Background: Implant rehabilitation of the edentulous anterior maxilla remains a complex restorative challenge. Intricate preexisting anatomy dictates meticulous and accurate osteotomy planning. With progressive bone loss, the alveolar crest may approach anatomic structures. The nasopalatine nerve and vessels may ultimately emerge from the ridge crest. The radiologic changes of the nasopalatine canal were evaluated in different resorption phases of the premaxilla alveolus with regard to dental implantation. Methods: The study consisted of 207 subjects who had maxillary computed tomography scans before dental implantation. The Lekholm and Zarb classification was used to divide images according to the residual bony ridge: Class A (control group) and classes B to E (study group). Anatomic mapping of the nasopalatine canal structure was carried out in both groups. Results: The canal diameter was wider along the degree of ridge resorption from classes A to E in all dimensions, mainly in the palatal opening (P <0.01), middle area (P <0.001), and nasal area. The mean diameter of the enlargement was 1.8 mm, which reached 5.5 +/- 1.08 mm (P <0.01) in type E bone. In the severely resorbed ridges (classes C through E), when the palatal opening was situated on the ridge, it occupied a mean of 35.6% (13% to 58%) of the area devoted to implant placement. Tooth loss was the main reason for ridge resorption (P <0.01). Conclusions: Canal diameter enlargement was greater anteriorly to the ridge and posteriorly to the palatal bone, mainly because of tooth extraction. The atrophy of disuse may influence surrounding structures, similar to the maxillary sinus tendency to expand into surrounding bone mainly after tooth loss.