It has been 30 years since the first commercial three-dimensional (3D) printer was available on market. The technological advancement of 3D printing has far exceeded its implementation in medicine. The application of 3D printing technology has the potential of playing a major role within interventional pulmonology; specifically, in the management of complex airway disease. Tailoring management to the patient-specific anatomical malformation caused by benign or malignant disease is a major challenge faced by interventional pulmonologists. Such cases often require adjunctive therapeutic procedures with thermal therapies followed by dilation and airway stenting to maintain the patency of the airway. Airway-stent size matching is one key to reducing stent-related complications. A major barrier to matching is the expansion of the stent in two dimensions (fixed sizes in length and diameter) within the deformed airway. Additional challenges are created by the subjective oversizing of the stent to reduce the likelihood of migration. Improper sizing adversely affects the stability of the stent. The stent-airway mismatch can be complicated by airway erosion, perforation, or the formation of granulation tissue. Stents can migrate, fracture, obstruct, or become infected. The use of patient-specific 3D printed airway stents may be able to reduce the stent airway mismatch. These stents allow more precise stent-airway sizing and minimizes high-pressure points on distorted airway anatomy. In theory, this should reduce the incidence of the well-known complications of factory manufactured stents. In this article, the authors present the brief history of 3D printed stents, their consideration in select patients, processing steps for development, and future direction.
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http://dx.doi.org/10.21037/amj.2019.01.05 | DOI Listing |
Rhinology
January 2025
Kuopio, Finland.
Chronic rhinosinusitis with nasal polyps (CRSwNP), asthma, and non-steroidal anti-inflammatory drug-exacerbated respiratory disease (N-ERD) frequently coexist, forming a complex multimorbid condition often referred to as "global airway disease." This concept reflects shared pathophysiological mechanisms of eosinophilic inflammation and underscores the need for integrated treatment strategies targeting both upper and lower airway manifestations (1). The burden of severe CRSwNP, asthma, and N-ERD is substantial, particularly in terms of reduced quality of life, recurrent exacerbations, revision endoscopic sinus surgeries (ESS), and healthcare utilization (2).
View Article and Find Full Text PDFJ Thorac Dis
December 2024
Department of Thoracic Surgery and Oncology, the First Affiliated Hospital of Guangzhou Medical University, State Key Laboratory of Respiratory Disease & National Clinical Research Center for Respiratory Disease, Guangzhou, China.
J Asthma Allergy
January 2025
Amgen Inc., Thousand Oaks, CA, USA.
Airway inflammation, a hallmark feature of asthma, drives many canonical features of the disease, including airflow limitation, mucus plugging, airway remodeling, and hyperresponsiveness. The T2 inflammatory paradigm is firmly established as the dominant mechanism of asthma pathogenesis, largely due to the success of inhaled corticosteroids and biologic therapies targeting components of the T2 pathway, including IL-4, IL-5, IL-13, and thymic stromal lymphopoietin (TSLP). However, up to 30% of patients may lack signatures of meaningful T2 inflammation (ie, T2 low).
View Article and Find Full Text PDFFront Immunol
January 2025
Immunology Translational Research Programme, Yong Loo Lin School of Medicine, Department of Microbiology & Immunology, National University of Singapore, Singapore, Singapore.
Introduction: Collagen is essential for maintaining lung structure and function and its remodeling has been associated with respiratory diseases including chronic obstructive pulmonary disease (COPD). However, the cellular mechanisms driving collagen remodeling and the functional implications of this process in the pathophysiology of pulmonary diseases remain poorly understood.
Methods: To address this question, we employed ; mice with specific depletion of Lyve-1 macrophages and assessed the content, types and organization of collagen in lung compartments at steady state and after chronic exposure to cigarette smoke (CS).
JBMR Plus
February 2025
Radiology and Imaging Sciences, National Institutes of Health Clinical Center, National Institutes of Health, Bethesda, MD 20892, United States.
Jansen metaphyseal chondrodysplasia (JMC) is an ultra-rare disorder caused by constitutive activation of parathyroid hormone type 1 receptor (PTH1R). We sought to characterize the craniofacial phenotype of patients with the disease. Six patients with genetically confirmed JMC underwent comprehensive craniofacial phenotyping revealing a distinct facial appearance that prompted a cephalometric analysis demonstrating a pattern of mandibular retrognathia.
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