Tracheomalacia is a pathological condition characterized by increased flaccidity of the tracheal or bronchial walls due to underdevelopment or degeneration of the cartilaginous framework, resulting in dynamic airway collapse during respiration. It is classified into two main types: congenital and acquired. Congenital tracheomalacia arises due to developmental anomalies during fetal ontogenesis, while the acquired form may result from prolonged mechanical ventilation, chronic inflammation, or external compression, but importantly, can also originate from prenatal developmental disturbances. This ontogenetic link between congenital and acquired forms has been increasingly recognized in recent studies, particularly when the acquired variant emerges as a consequence of cartilaginous dysplasia during intrauterine development.

From a morphological perspective, tracheomalacia can manifest in various structural forms, including crescentic, bow-shaped, and concentric types. In all types, there is a common feature of anatomical underdevelopment of the tracheobronchial wall layers, especially affecting their cartilaginous and muscular components. In the crescentic and bow-shaped variants, the mucosal integrity is typically preserved, and the primary deficiency lies in the cartilaginous tissue. Histologically, this is expressed by a reduced number of chondrocytes, absence of continuous cartilaginous support along more than three-quarters of the airway circumference, and the presence of small, isolated cartilaginous islets. These anomalies lead to structural instability and dynamic collapse of the airways, exacerbated by contraction of the bronchial smooth muscle bundles.

Understanding the morphogenetic and structural characteristics of tracheomalacia is crucial for accurate diagnosis and appropriate therapeutic decision-making, particularly in neonates and infants presenting with airway obstruction symptoms.