The causes of subcutaneous emphysema of relevance to dental practitioners?

Data sources An electronic search was conducted using EMBASE, LILACS, PubMed, SciELO, Scopus, Web of Science, and two grey literature data sources. All issues of nine dentistry journals and relevant chapters in four endodontic textbooks were manually searched.Study selection Abstracts of all the studies that were identified during the electronic and manual searches were obtained and screened independently by two reviewers in order to select clinical studies, case series, or case reports describing subcutaneous emphysema that occurred in adult patients during or immediately after root canal treatment.Data extraction and synthesis Predetermined data were extracted from each study independently by two reviewers and organised into data tables. All disagreements were resolved through discussion with a third reviewer. The data obtained were combined through a narrative synthesis.Results Following full-text evaluation according to the inclusion criteria, 51 articles that described 65 cases of subcutaneous emphysema were included. There were 36 case reports and 15 case series. The condition was mainly reported in female patients and maxillary teeth. While the age of the patients ranged from 18 to 63 years, this demographic information was missing from a few studies. Details on the involved tooth and diagnosis were also missing from several articles. In most of the cases, subcutaneous emphysema developed during initial root canal treatment. The diagnosis was mainly based on intraoral, plain facial, neck, or chest radiographs, while computed tomography (CT) scans were obtained in fewer cases. The majority of the patients were referred to a different practice, a hospital or university clinic for the management of the condition by more specialised healthcare practitioners. In addition to drying root canals using air pressure, irrigation with hydrogen peroxide, and the air-water spray produced by handpieces, it was reported that laser-produced spray and ozone gas infiltration may also be the culprits of subcutaneous emphysema. The signs and symptoms resolve within 17 days. Its management mostly remains empirical and involves the use of antibiotics, analgesics, local application of cold or hot compresses, or administration of oxygen and hospitalisation, among other methods.Conclusions The systematic review showed that subcutaneous emphysema can occur during both surgical and nonsurgical endodontic treatment. Air streams or air-water sprays should not be directed toward the root canals or areas with mucosal discontinuity. None of the management approaches were clearly associated with a faster recovery. The review asked for developing guidelines in order to avoid unnecessary or potentially harmful interventions.

Degenerative and regenerative morphological aspects in peri-implantitis.

The purpose of this study was to describe the tissues surrounding two early failed dental implants morphologically and ultrastructurally. In the first case, the implant's surface was analyzed by scanning electron microscopy (SEM) using an environmental scanning electron microscope and the surrounding tissues were analyzed by light microscopy (LM) and transmission electron microscopy. In the second case we used only LM. By SEM analysis, very thin connective tissue was seen at the implant's apex; in the middle part, highly vascularized connective tissue and poorly mineralized areas were found, and there were fewer mineralized areas at the implant's base. Histologically and ultrastructurally, we identified a heterogeneous cellular population including fibroblast-like cells and osteoblasts with abundant amorphous extracellular matrix, as well as a number of inflammatory cells, predominantly neutrophils. In a small area around the implant, microorganisms classified as Actinomyces were identified. In this case, degenerative aspects were predominantly caused by infection. In the second case, our observations focused on recruitment of mesenchymal stem cells, their proliferation and differentiation into epithelial cells with keratinocyte phenotype, and formation of de novo capillaries from mesenchymal progenitors of endothelial cells. These regenerative events were accompanied by multiple areas of mineralization, culminating in bone formation around the implant. Correlative microscopic observations are necessary to conduct in future studies, in various clinical conditions and post-operative stages, to better define the cellular events involved in healing and osseointegration; our observations clearly depict significant regenerative aspects despite the degenerative ones.

Methamphetamine-induced neuronal necrosis: the role of electrographic seizure discharges.

We have evidence that methamphetamine (METH)-induced neuronal death is morphologically necrotic, not apoptotic, as is currently believed, and that electrographic seizures may be responsible. We administered 40mg/kg i.p. to 12 male C57BL/6 mice and monitored EEGs continuously and rectal temperatures every 15min, keeping rectal temperatures <41.0°C. Seven of the 12 mice had repetitive electrographic seizure discharges (RESDs) and 5 did not. The RESDs were often not accompanied by behavioral signs of seizures-i.e., they were often not accompanied by clonic forelimb movements. The 7 mice with RESDs had acidophilic neurons (the H&E light-microscopic equivalent of necrotic neurons by ultrastructural examination) in all of 7 brain regions (hippocampal CA1, CA2, CA3 and hilus, amygdala, piriform cortex and entorhinal cortex), the same brain regions damaged following generalized seizures, 24h after METH administration. The 5 mice without RESDs had a few acidophilic neurons in 4 of the 7 brain regions, but those with RESDs had significantly more in 6 of the 7 brain regions. Maximum rectal temperatures were comparable in mice with and without RESDs, so that cannot explain the difference between the two groups with respect to METH-induced neuronal death. Our data show that METH-induced neuronal death is morphologically necrotic, that EEGs must be recorded to detect electrographic seizure activity in rodents without behavioral evidence of seizures, and that RESDs may be responsible for METH-induced neuronal death.