The human nasolacrimal ducts are a borderland of the disciplines ophthalmology and otorhinolaryngology, which work close together in the treatment of nasolacrimal disorders. However, little knowledge exists concerning the physiology of the nasolacrimal system and, therefore, its pathophysiology. The aim of the present investigations was to obtain a better understanding of tear flow physiology, microbial defence strategies and pathophysiological processes by analysing the nasolacrimal system, thus opening new perspectives against existing therapeutical concepts of diseases of the nasolacrimal ducts. The human nasolacrimal ducts consist of the upper and the lower lacrimal canaliculus, the lacrimal sac and the nasolacrimal duct. They drain the tear fluid from the ocular surface into the lower meatus of the nose. The lining epithelium of the lacrimal sac and the nasolacrimal duct is faced by microvilli, and animal experiments in rabbits support the hypothesis that tear fluid components are absorbed in the human nasolacrimal system. Evidence of seromucous glands, intraepithelial lipids and a specific mucus layer leads to the conclusion that the normal three-layering of the tear film is also present in the nasolacrimal ducts. Based on its composition, the mucus layer, which is mainly synthesised by goblet cells and intraepithelial mucus glands, functionally serves as a simplified drainage of tear fluid, and it is attributed similar properties to epithelia of the gastrointestinal tract. Further defence mechanisms are represented by antimicrobial peptides IgA and immunocompetent cells (lymphocytes and macrophages) which show intraepithelially and subepithelially a special distribution. Moreover, organised lymphoid tissue is present, which reveals the cytomorphologic and immunophenotypic characteristics of mucosa-associated lymphoid tissue. The wall of the lacrimal sac and the nasolacrimal duct are made up of a helical system of different connective tissue fibres. Wide luminal vascular plexus are embedded in this helical system, which is comparable to a cavernous body. Caudally, the vascular system is connected to the cavernous body of the inferior turbinate. With distension the system may be "wrung out" due to its medial attachment and helically arranged fibrillar structures. Thereby, tear fluid is drained distally. The embedded blood vessels underlie vegetative control. By means of this innervation, the specialised blood vessels permit regulation of blood flow by opening and closing the lumen of the lacrimal passage as effected by the engorgement and subsidence of the cavernous body, at the same time regulating tear outflow. Related functions, such as a role in the occurrence of epiphora related to emotional responses, are relevant. Moreover, malfunctions in the cavernous body and in its innervation may lead to disturbances in the tear outflow cycle, ocular congestion or total occlusion of the lacrimal passage. Thus, the pathophysiology of primary acquired dacryostenosis can be explained: Descending inflammation from the eye or ascending inflammation from the nose initiates swelling of the mucous membrane, remodelling of the helical arrangement of connective tissue fibres, malfunctions in the subepithelial cavernous body with reactive hyperaemia, and temporary occlusion of the lacrimal passage. In the follow-up, repeated isolated occurrence of dacryocystitis leads to structural epithelial and sub-epithelial changes, which may lead either to a total fibrous closure of the lumen of the efferent tear duct or to a non-functional segment in the lacrimal passage that is manifest on syringing. The normally constant absorption of tear fluid components into the blood vessels of the surrounding cavernous body that are connected to the blood vessels of the outer eye could be a feedback signal for tear fluid production, which comes to a halt if these tear components are not absorbed. Thus, dry eye could be initiated. Defective stimulation of tear duct-associated lymphoid tissue (TALT) could result in abnormal immune deviation at the ocular surface leading to an autoimmunologic response that could cause dry eye pathology.