Pure orbital blowout fracture first occurs at the weakest point of the orbital wall. Although the medial orbital wall theoretically should be involved more frequently than the orbital floor, the orbital floor has been reported as the most common site of pure orbital blowout fractures. A total of 82 orbits in 76 patients with pure orbital blowout fracture were evaluated with computed tomographic scans taken on all patients with any suspicious clinical evidence, including nasal fracture. Isolated medial wall fracture was most common (55 percent), followed by medial and inferior wall fracture (27 percent). The most common facial fracture associated with medial wall fracture was nasal fracture (51 percent), not inferior wall fracture (33 percent). This finding suggests that the force causing nasal fracture is an important causative factor of pure medial wall fracture as the buckling force from the medial orbital rim. Of patients with medial wall fractures, 25 percent had diplopia and 40 percent had enophthalmos. On plain radiographs, diagnostic signs were found in 79 percent of medial wall fractures and in 95 percent of inferior wall fractures. On computed tomographic scans, late enophthalmos was expected in 76 percent of medial wall fractures. Therefore, the medial orbital blowout fracture may be an important cause of late enophthalmos, because it has a high incidence of occurrence, a low diagnostic rate, and a high severity of defect. Among the causes of limitation of ocular motility, muscle traction of the connective septa and direct muscle injury were found frequently, but true incarceration of the muscle was extremely rare in all fractures. The medial and inferior orbital walls are clearly demarcated by the bony buttress, which is an important structure supporting these orbital walls. Its buttress was closely correlated with the fracture of these orbital walls. Most orbital blowout fractures without collapse of the bony buttress had a trapdoor fracture with or without small fragments of punched-out fracture.
The human gut microbiome performs prodigious physiological functions such as production of microbial metabolites, modulation of nutrient digestion and drug metabolism, control of immune system, and prevention of infection. Paradoxically, gut microbiome can also negatively orchestrate the host responses in diseases or chronic disorders, suggesting that the regulated and balanced host-gut microbiome crosstalk is a salient prerequisite in gastrointestinal physiology. To understand the pathophysiological role of host-microbiome crosstalk, it is critical to recreate in vivo relevant models of the host-gut microbiome ecosystem in human. However, controlling the multi-species microbial communities and their uncontrolled growth has remained a notable technical challenge. Furthermore, conventional two-dimensional (2D) or 3D culture systems do not recapitulate multicellular microarchitectures, mechanical dynamics, and tissue-specific functions. Here, we review recent advances and current pitfalls of in vitro and ex vivo models that display human GI functions. We also discuss how the disruptive technologies such as 3D organoids or a human organ-on-a-chip microphysiological system can contribute to better emulate host-gut microbiome crosstalks in health and disease. Finally, the medical and pharmaceutical significance of the gut microbiome-based personalized interventions is underlined as a future perspective.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.