The elastic fibre network of the respiratory tract provides critical structural support and mechanical resilience to airways during cyclical breathing, coughing, and forced expiratory maneuvers. Composed of elastin protein embedded within a scaffold of fibrillin microfibrils, these fibres enable tissue recoil and maintain luminal patency against compressive forces. In the trachea and main bronchi, elastic fibres form dense lamellae within the submucosa and around cartilaginous plates, contributing to the biomechanical properties essential for efficient airflow [1,2].

Aging universally affects extracellular matrix components throughout the body. Elastic fibres undergo progressive structural deterioration characterized by fragmentation, thinning, reduced density, and disorganization of the fibrillar architecture. These changes reflect cumulative mechanical fatigue, enzymatic degradation, oxidative damage, and impaired synthesis of new elastin, which ceases after adolescence in humans. While age-related elastic fibre changes have been extensively documented in vascular tissues and pulmonary parenchyma, the conducting airways have received comparatively limited systematic investigation [3,4].

Clinical observations suggest functional consequences of airway aging. Healthy elderly individuals demonstrate altered respiratory mechanics including increased airway compliance, reduced peak expiratory flow rates, and modified cough effectiveness compared to younger adults, even without diagnosed pulmonary disease. Whether structural deterioration of elastic fibres underlies these physiological changes remains incompletely established through direct anatomical evidence [5,6].

Previous histological studies examining airway elastic fibres have been limited by small sample sizes, lack of age stratification, qualitative rather than quantitative assessments, or focus on diseased rather than normal aging. Precise morphometric quantification across standardized anatomical regions and well-defined age groups is needed to establish baseline patterns of structural senescence [7].

This study aimed to comprehensively evaluate age-related changes in elastic fibres of the human trachea and main bronchi using rigorous histological methods and quantitative morphometry. We hypothesized that elastic fibre density and integrity decline progressively with advancing age while fragmentation increases. By examining multiple anatomical regions across a broad age range with blinded semi-quantitative validation, we sought to provide robust evidence characterizing the structural basis for age-related alterations in large airway mechanics.

Forty-one cadavers were included in the final analysis after excluding 3 specimens due to tissue processing artifacts (n=2) or incomplete data collection (n=1). The study cohort comprised 28 males (68.3%) and 13 females (31.7%) with ages ranging from 21 to 93 years (mean 62.7 ± 20.6 years). Specimens were stratified into four age groups: 18-39 years (n=6, mean age 27.3 ± 3.6 years), 40-59 years (n=10, mean age 48.1 ± 3.7 years), 60-79 years (n=15, mean age 70.1 ± 2.8 years), and >=80 years (n=10, mean age 87.5 ± 3.5 years). All specimens were obtained from routine dissection cadavers donated through institutional body donation programs. Fixation parameters were standardized across all age groups (mean fixation duration 37.1 ± 6.1 hours, range 30-50 hours) with no significant differences between age strata (p=0.961). A total of 880 microscopic fields (20x magnification) were captured from four anatomical regions per cadaver: tracheal anterior wall, tracheal posterior wall, right main bronchus, and left main bronchus. Of these, 775 fields (88.1%) passed quality control criteria and were included in morphometric analysis.

Elastic area fraction showed highly significant progressive decline with age across all four anatomical regions (all p<0.001). In the tracheal anterior wall, elastic area fraction decreased from 17.97 ± 0.82% in the youngest group to 11.33 ± 1.88% in the oldest group (37% reduction). Similar patterns were observed in the tracheal posterior wall (22.42 ± 0.97% to 16.00 ± 1.94%, 29% reduction), right main bronchus (16.23 ± 1.06% to 10.05 ± 1.88%, 38% reduction), and left main bronchus (14.96 ± 0.90% to 8.77 ± 1.78%, 41% reduction). Fibre density decreased from 517.04 ± 47.73 to 348.98 ± 34.13 per mm2 in tracheal anterior wall (32% reduction) and ~29-30% in main bronchi (all p<0.001). The fragmentation index increased more than three-fold across all regions (tracheal anterior wall: 48.10 ± 11.00 to 149.93 ± 25.90 per mm2, p<0.001; right bronchus: 57.62 ± 11.33 to 172.32 ± 20.62 per mm2, p<0.001). Mean fibre thickness showed modest reductions (p<0.05 in anterior trachea, posterior trachea, and left bronchus).

This comprehensive histomorphometric study provides robust anatomical evidence for progressive age-related deterioration of elastic fibres in the human trachea and main bronchi. Analysis of 775 quality-controlled microscopic fields from 41 cadavers spanning seven decades revealed significant quantitative changes across all measured parameters. Elastic area fraction declined by 29-41% from young adulthood to advanced age, while fragmentation increased more than three-fold. These findings align with established concepts of extracellular matrix senescence but extend previous work by providing precise quantification across standardized anatomical regions with rigorous quality control [12,13].

The strong negative correlations between continuous age and elastic fibre integrity (r = -0.79 to -0.85) demonstrate that chronological aging dominates as the primary determinant of structural changes. This relationship persisted after controlling for sex and anatomical region in multivariate models, which explained over 84% of variance in elastic parameters [14,15]. The exponential increase in fragmentation compromises coordinated recoil properties and uniform force distribution. In large airways, this structural failure may contribute to increased compliance and reduced peak expiratory flows in elderly individuals [18,19].

Regional anatomical differences persisted across the lifespan, with the tracheal posterior membranous wall maintaining 20-25% higher elastic area fraction than the anterior cartilaginous wall, reflecting dynamic functional demands during cough and respiration. Paired main bronchi showed symmetric age-related changes without significant laterality in fragmentation (p = 0.291), supporting systemic ECM aging [20].

This histomorphometric study demonstrates significant age-related deterioration of elastic fibres in the human trachea and main bronchi, with elastic area fraction declining 29-41% and fragmentation increasing three-fold from young adulthood to advanced age. Strong correlations confirm age as the dominant determinant, explaining over 84% of structural variance. Regional anatomical hierarchy persists throughout life, with the tracheal posterior wall maintaining superior preservation. These anatomical changes provide mechanistic insight into age-related alterations in airway compliance and respiratory mechanics, with implications for clinical assessment and surgical planning in elderly populations.