A Novel Method of Neo-osseous Flap Prefabrication: Induction of Free Calvarial Periosteum with Bioactive Glass.

BACKGROUND: Reconstruction of craniofacial bone defects is a primary focus of craniofacial surgery. Although autogenous bone grafts remain as the gold standard, alloplastic materials have also gained widespread popularity due to their off-the-shelf availability, ease of use, and durability. In addition to replacing the missing bone, some of these alloplastic materials have also been found to induce new bone formation. OBJECTIVES: In this study, the phenomenon of neo-osseous induction with bioactive glass was investigated for different implant-soft tissue configurations. MATERIALS AND METHODS: Thirty-two male, Wistar albino rats were divided into four equally numbered study groups. In group 1 (FP), adipofascial groin flaps were prefabricated with free periosteal grafts. In group 2 (FPB), adipofascial groin flaps were prefabricated with free periosteal grafts and bioactive glass. In group 3 (FB), adipofascial groin flaps were prefabricated with bioactive glass. In group 4 (control), adipofascial groin flaps were not prefabricated. Morphometric analyses of the prefabricated structures were performed using micro-CT. The histologic properties of the ectopic ossification were assessed by using a modified scoring system. RESULTS: Group 1 (FP) showed the greatest rate of mature lamellar bone formation. Group 2 (FBP) showed the greatest amount of bone density and volume. However, the addition of bioactive glass in group 2 (FBP) decreased the rate of mature lamellar bone formation when compared with group 1 (FP). Ectopic ossification was not observed in the control group. CONCLUSION: Bioactive glass can be successfully used in the prefabrication of vascularized compound structures for the reconstruction of complex bone defects. However, interference with the periosteal induction of mature lamellar bone formation should be taken into consideration, especially in pediatric bone defects, which primarily rely on spontaneous osteogenesis through periosteal induction.

Impact of high-fat diet and hypoxia on the serum levels of main vasoconstrictors in male rabbits.

Introduction: During atherosclerosis process, vasoconstriction phenomenon occurs which in turn leads to tissue hypoxia. A few studies have been performed on the combination of atherosclerosis and hypoxia as stressors that may accelerate secretion of constrictors. The aim of present study was to evaluate the effects of atherosclerosis and hypoxia on serum levels of main vasoconstrictors (epinephrine, norepinephrine and renin). Methods: In this interventional study, 32 New Zealand white rabbits were randomly divided into four groups (n = 8): normal diet (control group), normal diet exposed to hypoxia (11%, 10 days), high-fat diet (cholesterol-2%, 8 weeks), and high-fat diet with hypoxia. Later, serum levels of renin, epinephrine and norepinephrine were measured on second, 56th and 66th days. Results: High-fat diet and hypoxia caused significant increase in epinephrine and norepinephrine concentrations on days 56 and 66 compared to the control group (P < 0.05). Also, renin showed significance increase in high-fat diet and high-fat diet+ hypoxia groups compared to the control group (P < 0.05). Conclusion: Both high-fat diet and hypoxia increase renin levels in male rabbits. Furthermore, the combination of high-fat diet and hypoxia immensely increases renin levels. Both hypoxia and combined of high-fat diet and hypoxia increase norepinephrine levels. However epinephrine is only increased in the combination of high-fat diet and hypoxia. So the presence of hypoxia in combination with high-fat diet, cause accelerated and aggravated atherosclerosis.

Jejunum/DIEP Composite Flap: A Novel Rat Model of Viscerocutaneous Flap Prefabrication.

Background Reconstruction of complex pharyngoesophageal defects presents a major challenge, particularly in soft tissue deficient and previously scarred surgical sites. In recent years, the free jejunum flap method has emerged as a reliable means of esophageal reconstruction. However, it may require cutaneous coverage with an additional flap in extensively scarred, secondary reconstructions. Prefabrication of an intestinal/cutaneous composite flap can potentially solve this problem. Materials and Methods Total 28 Sprague Dawley rats were used in the study protocol. A vascularized jejunal segment was transposed beneath the deep inferior epigastric perforator (DIEP) flap. Contact with underlying abdominal fascia was prevented using a silicone sheet. Animals were distributed into five groups based on the timing of deep inferior epigastric vessel ligation to determine the time required for successful revascularization. The viability and the vascular anatomy of the prefabricated structures were analyzed using histology and microangiography. Results A jejunum/DIEP composite flap was successfully prefabricated based on mesenteric vessels. The skin component survived intact after 5 days of contact with serosal surface of the jejunal segment. Conclusion The clinical application of this technique can provide an alternative means of single-stage esophageal reconstruction, especially in patients with soft tissue deficiency and donor vessel unavailability.

Poly(L-Lactide)/Poly(ε-Caprolactone) and Collagen/ß-Tricalcium Phosphate Scaffolds for the Treatment of Critical-Sized Rat Alveolar Defects: A Microtomographic, Molecular-Biological, and Histological Study.

OBJECTIVE: To determine the efficacy of a newly developed scaffold (col/ß-TCP) in a preclinical rat model as compared with the gold standard treatment (autograft) and control scaffolds (PLLA/PCL). DESIGN: Fifty-six Sprague-Dawley rats were randomized into four experimental groups, and critical-sized alveolar defects (7 × 4 × 3 mm) were created in each animal. Group A was the blank defect group, group B received autograft, group C received col/ß-TCP scaffolds, and group D received PLLA/PCL blend scaffolds to fill the bone defects. New bone formation was assessed radiomorphometrically, histomorphometrically, and molecular-biologically at 1 and 4 months following surgery. RESULTS: Radiomorphometrically, the best new bone volume rate at 1 month (43.7%) and 4 months (45.4%) was observed in the autograft group, and the difference was significantly higher than in the other three groups (P < .005, P < .001, P < .001 for 1 month and P = .004, P < .001, P < .001 for 4 months). Even though the new bone volume rate in the col/ß-TCP group (21.5%) was higher than that of the PLLA/PCL group (18.2%), the difference was not significant (P = .08). Molecular-genetic analysis revealed significantly higher BSP and ALP gene expression levels in the autograft and col/ß-TCP groups than in the blank defect group (P = .002 and P = .004). CONCLUSION: The engineered tissue scaffolds described herein have great potential as an alternative treatment option when cost, donor region morbidity, and duration of hospitalization are considered.

Congenital maxillomandibular syngnathia: a new management technique using distraction techniques.

Complex zygomaticomandibular syngnathia is an extremely rare condition with an unknown etiology. The main goal of the surgery is to release the ankylosis, establish good functioning mandible, and prevent reankylosis, if possible. In our case, we offer a new solution to have an adequate oral opening and to prevent reankylosis. After the release of bony syngnathia, we placed a distractor between mandibular segment and maxillozygomatic complex. To our best knowledge, this is the only syngnathia case in the literature treated using distraction techniques. There is a major improvement in the patient's status. Distraction may broaden our horizons in this rare and difficult-to-treat deformity.

Mitochondria DNA deletions in atherosclerotic hypoperfused brain microvessels as a primary target for the development of Alzheimer's disease.

The pathogenesis, which is primarily responsible for Alzheimer's disease (AD) and cerebrovascular accidents (CVA), seems to involve chronic hypoperfusion. The role of hypoperfusion, as a key factor for vascular lesions that causes oxidative stress, appears to be widely accepted as an initiator of AD. Specifically, accumulated oxidative stress increases vascular endothelial permeability and promotes leukocyte adhesions, which is coupled with alterations in endothelial signal transduction and redox-regulated transcription factors. Based on these recent findings, we hypothesize that the cellular and molecular mechanisms by which hypoperfusion-induced reactive oxygen species (ROS) accumulation impairs endothelial barrier function and promotes leukocyte adhesion induces alterations in normal vascular function and results in the development of AD. We are theorizing that mitochondria play a key role in the generation of ROS, resulting in oxidative damage to neuronal cell bodies, as well as other cellular compartment in the AD brain. All of these changes have been found to accompany AD pathology. We have studied the ultrastructural features of vascular lesions and mitochondria in brain vascular wall cells from human AD, yeast artificial chromosome (YAC) and C57B6/SJL transgenic positive (Tg+) mice overexpressing amyloid beta precursor protein (AbetaPP). In situ hybridization using mitochondrial DNA (mtDNA) probes for human wild and 5 kb deleted types and mouse types was performed along with immunocytochemistry using antibodies against amyloid precursor protein (APP), 8-hydroxy-2'-guanosine (8-OHG) and cytochrome c oxidase (COX). There was a higher degree of amyloid deposition, overexpression of oxidative stress markers, mitochondria DNA deletion and mitochondrial structural abnormality in the vascular walls of the human AD, YAC and C57B6/SJL Tg (+) mice compared to age-matched controls. Therefore, selective pharmacological intervention, directed for abolishing the chronic hypoperfusion state, would possibly change the natural course of development of dementing neurodegeneration.

The role of nitric oxide in the pathogenesis of brain lesions during the development of Alzheimer's disease.

Nitric oxide (NO) is a key bioregulatory active molecule in the cardiovascular, immune and nervous systems, synthesized through converting L-arginine to L-citrulline by NO synthase (NOS). Research exploration supports the theory that this molecule appears to be one of the key factors for the disruption of normal brain homeostasis, which causes the development of brain lesions and pathology such as in Alzheimer's disease (AD). Especially the vascular content of NO activity appears to be a major contributor to this pathology before the overexpression of NOS activity in other brain cellullar compartments develop. We theorize that pharmacological intervention using NO donors and/or NO suppressors should delay or minimize brain lesion development and further progression of brain pathology and dementia.

Is nitric oxide a key target in the pathogenesis of brain lesions during the development of Alzheimer's disease?

Nitric oxide (NO) is a short-life key bioregulatory active molecule in the cardiovascular, immune and nervous systems. NO is synthesized by converting L-arginine to L-citrulline by enzymes called NO synthase (NOS). The growing body of evidence strongly supports the theory that this molecule appears to be one of the key targets for the disruption of normal brain homeostasis, which causes the development of brain lesions and pathology such as in Alzheimer's disease (AD) or other related dementia. The vascular content of NO activity appears especially to be a main contributor to this pathology before the over-expression of other NOS isoforms activity in a different brain cellular compartment. We speculate that pharmacological intervention using NO donors and/or NO suppressors will be able to delay or minimize the development of brain pathology and further progression of mental retardation.