<p>Olfactory dysfunction (OD) secondary to chronic rhinosinusitis (CRS) significantly impairs quality of life by hindering the detection of warning signals and reducing nutritional satisfaction. CRS, a prevalent inflammatory condition, commonly leads to diminished or complete loss of smell. A substantial component of CRS-associated OD is conductive, stemming from impaired odorant delivery to the olfactory neuroepithelium. The tools for assessing conductive OD range from clinical evaluations like endoscopy and CT scoring of the olfactory cleft to objective measures of nasal patency and advanced computational fluid dynamics modeling. The underlying conductive mechanisms are multifactorial, primarily involving two interrelated pathways: alterations in nasal airflow dynamics due to anatomical variations or obstructive lesions, and pathological changes in the physicochemical properties of olfactory cleft mucus. Obstructions from septal deviation, turbinate hypertrophy, nasal polyps, and mucosal edema within the olfactory cleft disrupt and redistribute inspiratory airflow, critically reducing odorant access. Concurrently, inflammation-driven changes in the olfactory mucus—including hypersecretion, ionic imbalance, and deficiencies in odorant-binding proteins and metabolizing enzymes—impair odorant transport, solubilization, and signal transduction. Current therapeutic strategies, such as endoscopic sinus surgery and corticosteroids, aim to relieve these conductive barriers but may offer only partial or temporary benefit, highlighting the need for precise phenotyping. A systematic, individualized assessment of both airflow patterns and mucus properties is crucial for understanding the conductive contribution and predicting outcomes. This review synthesizes current evidence on the conductive mechanisms of olfactory loss in CRS, evaluating the impact of nasal aerodynamics and mucus alterations, and discusses integrated management strategies for this debilitating condition.</p>