Sinus mucosa thinning and perforation after sinus augmentation. A histological study in rabbits

Oral and Maxillofacial Surgery - To evaluate the modifications and possible perforations of the sinus mucosa lining graft particles and implant surfaces after sinus lifting. Twelve New Zealand...     

Melanocortins protect against progression of Alzheimer's disease in triple-transgenic mice by targeting multiple pathophysiological pathways

Besides specific triggering causes, Alzheimer's disease (AD) involves pathophysiological pathways that are common to acute and chronic neurodegenerative disorders. Melanocortins induce neuroprotection in experimental acute neurodegenerative conditions, and low melanocortin levels have been found in occasional studies performed in AD-type dementia patients. Here we investigated the possible neuroprotective role of melanocortins in a chronic neurodegenerative disorder, AD, by using 12-week-old (at the start of the study) triple-transgenic (3xTg-AD) mice harboring human transgenes APP_Swe, PS1_M146V, and tau_P301L. Treatment of 3xTg-AD mice, once daily until the end of the study (30 weeks of age), with the melanocortin analog [Nle⁴,D-Phe⁷]-α-melanocyte-stimulating hormone (NDP-α-MSH) reduced cerebral cortex/hippocampus phosphorylation/level of all AD-related biomarkers investigated (mediators of amyloid/tau cascade, oxidative/nitrosative stress, inflammation, apoptosis), decreased neuronal loss, induced over-expression of the synaptic activity–dependent gene Zif268, and improved cognitive functions, relative to saline-treated 3xTg-AD mice. Pharmacological blockade of melanocortin MC₄ receptors prevented all neuroprotective effects of NDP-α-MSH. Our study identifies, for the first time, a class of drugs, MC₄ receptor-stimulating melanocortins, that are able to counteract the progression of experimental AD by targeting pathophysiological mechanisms up- and down-stream of β-amyloid and tau. These data could have important clinical implications.     

Lack of influence of the Schneiderian membrane in forming new bone apical to implants simultaneously installed with sinus floor elevation: an experimental study in monkeys

Aim: To describe the early healing processes around the implants installed after elevation of the sinus mucosa applying the lateral access technique without the use of grafting material. Material and methods: Immediately after the elevation of the maxillary sinus Schneiderian membrane by the lateral approach in eight monkeys, implants were installed without the use of grafting material. The healing of the tissue around the implants was evaluated after 4, 10, 20 and 30 days. Ground sections were prepared and analyzed histologically. Results: After 4 days of healing, the formation of coagulum and provisional matrix was documented within the elevated area. At 10‐day interval, sprouts of woven bone were in continuity with the parent bone, and partly in contact with the implant surface at the base of the augmented area. While bone‐to‐implant contact increased after 20 and 30 days, the area underneath the Schneiderian membrane appeared reduced in volume and condensed toward the apex of the implants. The sinus mucosa was to some extent collapsed onto the implant surface and on the newly formed bone. Conclusions: The void initially occupied by the coagulum after sinus membrane elevation shrank substantially during the observation period. A lack of influence of the Schneiderian membrane in bone formation apical to implants was documented in the early phase of healing. To cite this article:
Scala A, Botticelli D, Faeda RS, Rangel IG Jr, de Oliveira, JA, Lang NP. Lack of influence of the Schneiderian membrane in forming new bone apical to implants simultaneously installed with sinus floor elevation: an experimental study in monkeys.
Clin. Oral Impl. Res. 23 , 2012; 175–181.
doi: 10.1111/j.1600‐0501.2011.02227.x     

Deproteinized bovine bone mineral in marginal defects at implants installed immediately into extraction sockets: an experimental study in dogs

Aim: To evaluate the influence of deproteinized bovine bone mineral (DBBM) particles concomitant with the placement of a collagen membrane on alveolar ridge preservation and on osseointegration of implants placed into alveolar sockets immediately after tooth extraction. Material and methods: The pulp tissue of the mesial roots of ₃P₃ was removed in six Labrador dogs and the root canals were filled. Flaps were elevated in the right side of the mandible, and the buccal and lingual alveolar bony plates were exposed. The third premolar was hemi‐sectioned and the distal root was removed. A recipient site was prepared and an implant was placed lingually. After implant installation, defects of about 0.6 mm wide and 3.1 mm depth resulted at the buccal aspects of the implant, both at the test and at the control sites. The same surgical procedures and measurements were performed on the left side of the mandible. However, DBBM particles with a size of 0.25–1 mm were placed into the remaining defect concomitant with the placement of a collagen membrane. Results: All implants were integrated into mature bone. No residual DBBM particles were detected at the test sites after 4 months of healing. Both the test and the control sites showed buccal alveolar bone resorption, 1.8±1.1 and 2.1±1 mm, respectively. The most coronal bone‐to‐implant contact at the buccal aspect was 2±1.1 an 2.8±1.3 mm, at the test and the control sites, respectively. This difference in the distance was statistically significant. Conclusion: The application of DBBM concomitant with a collagen membrane to fill the marginal defects around implants placed into the alveolus immediately after tooth extraction contributed to improved bone regeneration in the defects. However, with regard to buccal bony crest preservation, a limited contribution of DBBM particles was achieved. To cite this article:
Caneva M, Botticelli D, Pantani F, Baffone GM, Rangel IG Jr, Lang NP. Deproteinized bovine bone mineral in marginal defects at implants installed immediately into extraction sockets: an experimental study in dogs.
Clin. Oral Impl. Res. 23 , 2012; 106–112.
doi: 10.1111/j.1600‐0501.2011.02202.x     

Lessons from five states: public sector use of the Washington Circle performance measures

Five states (Connecticut, Massachusetts, New York, North Carolina, and Oklahoma) have incorporated the Washington Circle (WC) substance abuse performance measures in various ways into their quality improvement strategies. In this article, we focus on what other states and local providers might learn from these states' experiences as they consider using WC performance measures. Using a case study approach, we report that the use of WC measures differs across these five states, although there are important common themes required for adoption and sustainability of performance measures, which include leadership, evaluation of specification and use of measures over time, state-specific adaptation of the WC measure specifications, collaboration with consultants and partners, inclusion of WC measures in the context of other initiatives, reporting to providers and the public, and data and resource requirements. As additional states adopt some of the WC measures, or adopt other performance measurement approaches, these states' experiences could help them to develop implementations based on their particular needs.     

Functional recovery after delayed treatment of ischemic stroke with melanocortins is associated with overexpression of the activity-dependent gene Zif268

Melanocortin peptides afford strong neuroprotection and improve functional recovery in experimental ischemic stroke; they also have established neurotrophic actions. The expression of the immediate early gene Zif268 is dependent on synaptic activity and is involved in injury repair and memory formation. Here, we investigated the role of Zif268 in learning and memory recovery after delayed treatment of ischemic stroke with the melanocortin analog [Nle⁴, d-Phe⁷]α-MSH (NDP-α-MSH). A 10-min period of global cerebral ischemia was induced by occluding both common carotid arteries in gerbils. Treatment with a nanomolar dose of NDP-α-MSH (every 12 h for 11 days) was performed starting 3 h or 9 h after stroke induction; where indicated, gerbils were pretreated with the melanocortin MC₄ receptor antagonist HS024. Animals were subjected to the Morris water-maze test (four sessions from 4 to 50 days after the ischemic episode). Fifty days after stroke, histological damage and Zif268 expression were investigated in the hippocampus. Treatment with NDP-α-MSH significantly reduced hippocampal damage, including neuronal death, and improved learning and memory recovery. This protective effect was long-lasting (50 days, at least) and associated with Zif268 overexpression, with both schedules of NDP-α-MSH treatment. Pharmacological blockade of MC₄ receptors prevented these effects. Our data indicate that MC₄ receptor-mediated actions of melanocortins could trigger repair mechanisms able to improve neuronal functionality and synaptic plasticity, and to promote long-lasting functional recovery from ischemic stroke with Zif268 gene involvement.