Abstract
Laryngotracheal stenosis (LTS) is a complex and heterogeneous disease whose pathogenesis remains unclear. LTS is considered to be the result of aberrant wound-healing process that leads to fibrotic scarring, originating from different aetiology. Although iatrogenic aetiology is the main cause of subglottic or tracheal stenosis, also autoimmune and infectious diseases may be involved in causing LTS. Furthermore, fibrotic obstruction in the anatomic region under the glottis can also be diagnosed without apparent aetiology after a comprehensive workup; in this case, the pathological process is called idiopathic subglottic stenosis (iSGS). So far, the laryngotracheal scar resulting from airway injury due to different diseases was considered as inert tissue requiring surgical removal to restore airway patency. However, this assumption has recently been revised by regarding the tracheal scarring process as a fibroinflammatory event due to immunological alteration, similar to other fibrotic diseases. Recent acquisitions suggest that different factors, such as growth factors, cytokines, altered fibroblast function and genetic susceptibility, can all interact in a complex way leading to aberrant and fibrotic wound healing after an insult that acts as a trigger. However, also physiological derangement due to LTS could play a role in promoting dysregulated response to laryngo-tracheal mucosal injury, through biomechanical stress and mechanotransduction activation. The aim of this narrative review is to present the state-of-the-art knowledge regarding molecular mechanisms, as well as mechanical and physio-pathological features behind LTS.
Highlights
Benign laryngotracheal stenosis (LTS) is an umbrella term for various pathological conditions resulting in a narrowing of the airways at the level of the glottis, the subglottic space, or the trachea
The results of this study described a synergistic action between IL-17A and TGF-B1 in supporting extracellular matrix (ECM) deposition and subglottic fibrosis
This study suggested that TGF-B1 single nucleotide polymorphism (SNPs) −509 C/C rs1800469 is associated with increased susceptibility for stenosis, while genotype −509 C/T rs1800469 may provide a protective function against Laryngotracheal stenosis (LTS) development
Summary
Benign laryngotracheal stenosis (LTS) is an umbrella term for various pathological conditions resulting in a narrowing of the airways at the level of the glottis, the subglottic space, or the trachea. Until recently the laryngotracheal scar resulting from airway injury was considered an inert tissue requiring surgical removal to restore airway patency. This assumption has been revised: tracheal scarring is seen as a fibroinflammatory event triggered by immunological alterations [1]. Studies in animal models helped clarifying molecular, immunological, and genetic aspects that may play a role in the development of airway stenosis and in the healing process of the laryngeal-tracheal area. The aim of this narrative review is to present and discuss the state-of-the-art regarding. LTS, focusing on its molecular mechanisms, mechanical and physio-pathological features, taking into consideration their clinical implications
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