Tympanic Membrane (Tympanum): The tympanic membrane, also known as the tympanum, is an extremely thin, three-layered, semitransparent membrane peripherally suspended from the tympanic ring by a fibrocartilaginous ring. The tympanic membrane is formed when the endoderm of the first pharyngeal pouch comes into close contact with the ectoderm of the first pharyngeal cleft or groove. Most of the tympanic membrane is held under tension so it can be deformed by and responsive to sound waves (Fig. 20-5). It covers the medial extremity of external acoustic meatus, demarcating the junction between the external ear and middle ear. Both surfaces of the tympanic membrane have an air interface.

In most species, the tympanum is an oval-to-round structure, whereas in ruminants, it is shaped more like a broad triangle (Fig. 20-6). Embedded in the tympanum is the manubrium of the malleus. The placement of the manubrium in the tympanic membrane is highly variable between species. It is more centrally located in horses versus a more rostromedial location in ruminants and pigs.

The tympanum is divided into two sections, the pars tensa and the pars flaccida. The majority of the tympanic membrane is made up of the pars tensa, which is a very thin, translucent, and taut membrane that bulges convexly into the tympanic cavity (Fig. 20-6, E). The pars tensa is made up of three layers: (1) outer layer of keratinizing squamous epithelium derived from ectoderm of the first pharyngeal groove; (2) middle layer of thin, variably vascularized fibrous connective tissue originating from the pharyngeal wall; and (3) inner layer of very low cuboidal to nonkeratinizing squamous epithelium, which is of pharyngeal pouch origin.

The dorsal most portion of the tympanic membrane is the pars flaccida, which is roughly triangular, thicker, more vascular, and flaccid when compared to the pars tensa (see Fig. 20-6, E). Overlain by keratinized epithelium, the underlying stroma of the pars flaccida in dogs is made of loosely arranged collagen, rare mast cells, and few elastin fibers. This latter feature is in direct contrast to humans in which there are abundant elastin fibers. Visualized from the external acoustic meatus, this portion of the tympanic membrane may bulge into or away from the middle ear.

The tympanic membrane is placed roughly at a 45-degree angle relative to the central axis of horizontal portion of the external acoustic meatus (Fig. 20-7, A). However, commonly, the actual placement of the tympanic membrane is more variable with the external, concave surface of the tympanic membrane angled more rostrally (Fig. 20-7, B and C). Cats have a similar orientation to their tympanum (Fig. 20-8). Interestingly, the surface area of the tympanic membrane from an approximately 550-kg horse is larger than the tympanic membrane of a Maltese dog but is approximately 15% smaller than the surface area of the tympanic membrane of a German shepherd dog. Additionally, the tympanum of the fetal goat is approximately 20% larger than that of large dog breeds.

Tympanic Cavity: The tympanic cavity is an air-filled compartment surrounded by bone that is separated from the external ear by a thin tympanic membrane (tympanum) and is in direct communication with the pharynx via the auditory tube (also known as the eustachian or pharyngotympanic tube). Both the tympanic cavity and the auditory tube are derived from the endoderm of the first pharyngeal pouch. The epitympanic recess is the dorsal extremity of the tympanic cavity within which lies the head of the malleus and short curs of the incus. Ligaments stabilize and anchor the incudomallearis joint and the short crus of the incus within this recess (Fig. 20-9).

In many species, there is a bulbous, ventral portion of the tympanic cavity called the tympanic bulla (see Fig. 20-3, B and C). Within the bulla of the dog and cat is a bony septum referred to as the septum bulla. In the cat, the septum bulla abuts the petrous portion of the temporal bone and separates the tympanic cavity into two compartments: the dorsolateral epitympanic cavity and the ventromedial tympanic cavity (see Fig. 20-8). This separation is incomplete, which allows communication between the two compartments through a narrow opening between the septum bulla and petrous portion of the temporal bone and a larger opening at its caudal edge. In the dog, this septum is a much smaller, incomplete bony ridge that only makes contact with the petrous portion of the temporal bone rostrally and often has tiny, elongate bony spicules with bulbous ends (see Fig. 20-7, B). The mucosal surfaces of the tympanic bullae of cats and dogs are lined by an epithelium that varies, depending on location. Dorsally, close to the auditory tube opening, the mucosa is composed mostly of ciliated columnar cells mixed with goblet cells and basal cells similar to the cells in the nasopharyngeal mucosae (Fig. 20-10 and see Fig. 20-20). Ventrally, the number of ciliated cells and goblet cells decreases and the number of cuboidal, less differentiated cells increases. The surfaces of the petrous portion of the temporal bone, auditory ossicles, and tympanic membrane are lined by cuboidal to noncornifying squamous epithelium. In ruminants, camelids, and pigs, the ventral portion of the tympanic cavity or bulla is made of more numerous bony compartments lined by noncornifying squamous epithelium (Fig. 20-11). In cattle and pigs, these compartments are air-filled with direct communication with the tympanic cavity. In camelids and small ruminants, the tympanic cavity does not appear to directly communicate with the bullae. Horses do not have readily identifiable tympanic bullae.

Auditory Ossicles: A chain of three bones or auditory ossicles forms the mechanical transduction system of hearing: the malleus, incus, and stapes (Figs. 20-12 and 20-13). The malleus and the incus, as well as the tensor tympani, are derived from the mesenchyme of the first branchial or pharyngeal arch. The stapes and the stapedius muscle originate from the mesenchyme of the second branchial or pharyngeal arch.

Cochlea: The cochlea is the most complex portion of the membranous labyrinth comprising two closed-end tubular structures that are highly coiled (see Fig. 20-21). The central core of bony labyrinth around which the cochlea spirals nearly three times is the modiolus. Sound waves vibrate the tympanic membrane and are converted by coordinated movements of the malleus, incus, and stapes to fluid waves within the perilymph by vibrations of the vestibular or oval window. Fluid waves travel through the scala vestibuli toward the cupula, reaching the helicotrema, and then returning within the scala tympani toward the round (also known as cochlear) window. Positioned between the scala vestibuli and the scala tympani is the second closed compartment known as the cochlear duct or scala media. The cochlear duct is separated from the scala vestibuli by the vestibular membrane (also known as Reissner’s membrane), which transmits fluid waves of perilymph in the scala vestibuli into fluid waves of endolymph in the cochlear duct. Within the cochlear duct is a ribbonlike strip of extracellular matrix called the tectorial membrane. It is composed of several genetically distinct types of collagen (collagen types II, IX, and XI) and three distinct noncollagenous glycoproteins (α-tectorin, β-tectorin, and otogelin). The tectorial membrane rests on and is affixed to tips of hair cells that make up the mechanosensory portion of the organ of Corti that lies on the basilar membrane (Fig. 20-22). There are a series of three rows of outer hair cells and a single row of inner hair cells (see Fig. 20-21). Fluid waves in the cochlear duct result in movement of the tectorial membrane, which distorts inner and outer hair cells (neural-like cells), resulting in their depolarization and afferent transmission of action potentials via the cochlear branch of the vestibulocochlear cranial nerve to the vestibular nucleus.

Vestibular System: The vestibular system is made of several endolymph-filled compartments located in the caudal third to half of the petrous portion of the temporal bone. It represents a major sensory system that (1) maintains balance in concert with general proprioception and visual systems, (2) coordinates body posture, and (3) helps maintain ocular position in relation to the position or motion of the head. Included in the vestibular system are the semicircular canals, utricle, saccule, vestibular ganglia, vestibular portion of cranial nerve VIII (vestibulocochlear nerve), vestibular nuclei, and vestibular lobules of the cerebellum.

There are three semicircular canals oriented at right angles relative to each other occupying three planes. Each canal has a terminal dilation or ampulla that contains a specialized surface sensory organ called the crista. In aggregate, the sensory portion is referred to as crista ampullaris. Each crista is lined by specialized sensory hair cells that send continuous tonic neural signals to the vestibular nucleus. Deflection of these sensory hair cells during acceleration, deceleration, or rotation results in variation of the tonic signals sent to the vestibular nucleus. However, the hair cells are not activated during constant velocity.

Maculae are receptors located within the membranous utricle and saccule of the vestibule. The saccular macula is oriented in the vertical plane, whereas the macula of the utriculus is oriented in the horizontal plane. Surface lining neuroepithelial hair cells of the macula project into an otolithic membrane. Movement of the otolithic membrane causes deflection of the hair cells and triggers action potential. As in the case of the crista ampullaris, macular receptors provide a continuous tonic nervous input, with a net effect of maintaining static head positioning relative to gravity.

On stimulation of sensory nerve endings, action potentials are transmitted through bipolar cells whose cell bodies are located in the vestibular ganglia of the vestibular branch of the vestibulocochlear nerve. Signals travel to the vestibular nuclei in the medulla. From the vestibular nuclei, connections are made with the oculomotor, trochlear, and abducent nuclei of the rostral brainstem via the medial longitudinal fasciculus, the vestibulocerebellum by the caudal cerebellar peduncle, and the spinal cord via the vestibulospinal tract located in the ventral funiculus.

Histologic Evaluation of the Internal Ear: See Web Appendix 20-1.

Extension from the External Environment: Extension from the external environment is a common portal of entry into the external ear. It is a specialized invagination of the skin that terminates medially at the tympanic membrane of the middle ear. As the external acoustic meatus gradually narrows, its funnel shape is conducive in directing foreign materials, fomites, parasites, and/or infectious microorganisms into the external ear and toward the tympanic membrane of the middle ear. Additionally, its moist environment favors colonization of skin and/or mucosa by pathogenic microorganisms (Table 20-1). Although dermatitides can affect any part of the dermis, including the external ear, occasionally, involvement of the ear is an important feature used to arrive at a definitive diagnosis.

Hematogenous Spread: Hematogenous spread is a portal of entry into the external ear. Septicemias and/or specific types of viremias are thought to contribute to the development of external ear disease. Otitis externa and possibly deafness have been attributed to canine distemper virus, but it is unclear if the virus is a primary cause or one of several factors leading to otic disease. In an animal with septicemia, circulating bacteria have the potential to adhere to the endothelium of the capillary beds of the external ear, colonize the endothelium, and spread into adjacent tissues (see Chapter 4).

Extension from the Middle Ear: Extension from the middle ear is another portal of entry into the external ear, especially in cavalier King Charles spaniels with primary secretory otitis media. In primary secretory otitis media, the external ear is typically unaffected unless the tympanic membrane is ruptured and mucoid debris is spread into the external acoustic meatus. However, it has been suggested that this breed may have underlying failure of mucosae of the middle ear predisposing these spaniels to auditory tube dysfunction and thus otitis media leading to rupture of the tympanic membrane.

Extension through Perforation of the Tympanic Membrane: Extension from the external ear through a perforated tympanic membrane is a portal of entry into the middle ear (Fig. 20-23). In dogs with chronic otitis externa, secondary otitis media may occur in as many as 80% of affected dogs. At the time of clinical diagnosis, the tympanic membrane is most often intact, although some studies report perforations in over 40% of cases with otitis externa and concurrent otitis media. Based on the results of bacteriologic studies, it has been shown that a majority of dogs with concurrent otitis externa and otitis media have different bacteria isolated from each compartment. Thus it is unclear if the portal of entry in otitis media involves perforation of the tympanic membrane and spread of otitis externa into the middle ear with subsequent healing of the tympanic membrane or if otitis media results from bacteria ascending a poorly functioning auditory tube. Multiple studies implicate the latter mechanism (see later).

Ascension of the Auditory Tube: Ascension up the auditory tube is a portal of entry into the middle ear. It appears that dysfunction of the auditory tube is a necessary precursor for development of otitis media and likely leads to impaired clearance of middle ear effusions and prolonged periods of negative pressure within the tympanic cavity. Dysfunction may be related to impairment of the opening of the auditory tube into the pharynx during swallowing when pressure equalization takes place or it could be related to alterations of mucociliary clearance facilitated by epithelial cells lining the tube. Via either mechanism, it appears that microorganisms can use this portal to reach the middle ear.

Extension Via Degeneration of the Temporohyoid Joint: Direct extension into the middle ear can occur from degeneration of the temporohyoid joint and release of microorganisms. See the discussion on temporohyoid osteoarthropathy in the section on Disorders of Horses.

Extension Via Erosion through the Tympanic Bulla: Erosion through the tympanic bullae is a rare portal of entry into the middle ear. Neoplastic processes, such as oral squamous cell carcinomas, regional lymphosarcoma, or local compression by an abscess, can lead to bone remodeling, as well as bone lysis, with subsequent spread into the middle ear.

Migration along Vascular or Neural Pathways: Branches of the caudal auricular artery and the facial nerve traverse within the middle ear and have the potential to serve as pathways for spread of microorganisms and neoplasms from the brain to the middle ear. This migratory process likely occurs via the extracellular matrix of arteries and nerves (see Chapters 3, 10, and 14) and via anterograde axonal transport in nerves (see Chapter 14). As an example, cranial nerve sheath tumors (see Chapter 14) in the brain have been reported to migrate along branches of the facial nerve and vestibulocochlear nerves and enter the ear via the internal acoustic meatus.

Extension from the Middle Ear: Extension from the middle ear is a portal of entry into the internal ear, thus otitis interna or labyrinthitis is most commonly thought of as occurring by direct extension from an infection of the middle ear. The most likely portal is the round or cochlear window. Based on studies in cats, the permeability of the round window is increased for elements (sodium) and macromolecules (tritiated albumin) during mild cases of experimentally induced otitis media. Penetration through the oval or vestibular window is less likely because of the annular syndesmosis that is formed between the petrous portion of the temporal bone and the stapes (Fig. 20-24). Although otitis media may be diagnosed in isolation, otitis interna is rarely diagnosed without concurrent otitis media.

Hematogenous Spread: Entry through hematogenous spread occurs in the internal ear (see the previous discussion on the middle ear in the section on Portals of Entry for details).

Migration along Vascular or Neural Pathways: Migration along vascular or neural pathways as a portal of entry occurs in the internal ear (see the previous discussion on the middle ear in the section on Portals of Entry for details).

Myringitis: Inflammation of the tympanic membrane is called myringitis and is most commonly caused by bacterial infection of the external or middle ear (see Fig. 20-39, B). Macroscopically, the tympanic membrane may be congested, hemorrhagic, or thickened, resulting in opacity. Microscopically, the tympanic membrane has all of the characteristics of acute inflammation and if the inciting cause is unresolved results in chronic inflammation (see Chapter 3). Prolonged and severe myringitis may lead to perforation of the tympanic membrane and prevent its healing.

Healing of the Tympanic Membrane: The tympanic membrane is a regionally well-vascularized membrane that has an air-interface along each surface. It can be perforated by traumatic injury, sudden exposures to high pressures, degradative enzymes and pressures from acute and chronic inflammation, chronic mite infestations, and neoplasms. Unique to the tympanic membrane, and likely related to its function, is its inherent ability to heal rapidly while maintaining its thin structure during healing through a process called epithelial migration. Unlike most other tissues, in which granulation tissue forms and bridges the defect followed by reepithelialization, the tympanic membrane closes the defect, first with migrating epithelial cells followed by a granulation tissue response that closes the mesenchymal portion of the tympanic membrane.

Within minutes to hours of the initial perforation, injured tissue at the edge of the perforation initiates an acute inflammatory response. Within hours, epithelial cells proliferate initially along the annulus and along the margin of the manubrium, corresponding to areas in which the blood supply is most prominent and epithelial stem cells of the tympanum are thought to reside. Proliferating epithelium advances toward the perforation using keratin as a scaffolding to initially bridge and reepithelialize the defect. As this epithelium is migrating across the defect, granulation tissue forms on the inner edge of the perforated membrane. Anchored to the epithelium that initially closes the perforation, the middle, mesenchymal layer of the tympanic membrane is repaired by this advancing granulation tissue. As granulation tissue remodels to its normal thin layer, the inner epithelial layer finally bridges the defect to complete the healing process. In an experimental animal model, 2.5-mm perforations were completely healed by 9 days after injury.

Goblet Cell Metaplasia and Impaired Mucociliary Clearance: An important defense mechanism of the middle ear is the mucociliary apparatus of the auditory tube and contiguous tympanic cavity. Chronic otitis media causes a decrease in the number of ciliated cells (ciliary atrophy) in the mucosa of the auditory tube. Studies in cats determined that neutrophil lysate (likely consisting of degradative enzymes) or lipopolysaccharide did not significantly reduce the number of ciliated cells in the auditory tube, but auditory tube obstruction and likely increased pressure in the middle ear resulted in a dramatic decrease in the number of ciliated epithelial cells. In the same study, there was a marked increase in the total number of goblet cells lining the tympanic cavity and bulla. It was hypothesized that obstruction of the auditory tube elevated partial pressure of carbon dioxide (pCO₂) in the mucus layer of the mucosa, triggering mucosal stem cells to differentiate toward goblet cells rather than ciliated cells. The viscoelasticity of the mucus produced by these goblet cells was greater than normal and resulted in a marked decrease of mucociliary clearance of the middle ear, probably further contributing to auditory tube obstruction, increased pressure in the middle era, and metaplasia of ciliated cells to goblet cells.

Osteosclerosis of the Tympanic Bulla: In infections of the middle ear caused by microorganisms, mediators of acute and chronic inflammation, such as cytokines and degradative enzymes, may lead to excessive periosteal proliferation of new bone and osteosclerosis (thickening) of the wall of the tympanic bulla (Fig. 20-26; see Chapter 16). The bulla may become grossly distorted, and the lumen volume typically decreases. Inflammation also can contribute to bone lysis.

Formation of Inflammatory Polyps: Inflammatory polyps are discussed later but are thought to represent both inflammatory and hyperplastic responses to injury induced by otitis media. Inflammation of the middle ear results in the formation of polypoid masses by an undetermined mechanism. These masses then result in clinical disease referable to where they exert their greatest effect. Polyps that involve the auditory tube and the nasopharynx can result in dysphagia and dyspnea, whereas those involving the tympanic membrane and external acoustic meatus lead to signs of otitis externa.

Horner’s Syndrome/Pourfour Du Petit Syndrome: Postganglionic sympathetic fibers that innervate the eye course through the middle ear with branches of the internal carotid artery via the tympano-occipital fissure. Smooth muscle that lifts the upper eye, retractor muscles of the third eyelid, smooth muscle that tonically pulls the eyes rostrally, and dilator muscles of the pupil are all innervated by these fibers. Thus, in otitis media, cells and mediators of inflammation can act on postganglionic sympathetic fibers that innervate the eye as they traverse through the middle ear, leading to primary demyelination and axonal injury.

Most commonly, injury resulting in partial paralysis of postganglionic sympathetic fibers causes Horner’s syndrome. This syndrome has the following clinical signs: miosis, enophthalmos, ptosis, a narrowed palpebral aperture, protrusion of the third eyelid, and peripheral vasodilation of the skin of the face. Resolution of signs typically follows clearance of the cause.

Injury to the postganglionic sympathetic fibers can much less commonly result in hyperexcitability or hyperirritability. This is most commonly reported in cats that have had their ears examined, sampled, and flushed while under anesthesia. Clinical signs include mydriasis, exophthalmos, widening of the palpebral aperture and cool skin over the face. In all cases reported, clinical signs resolved spontaneously. This hyperirritability syndrome is the opposite of Horner’s syndrome and is referred to by some as the Pourfour du Petit syndrome.

Sensory Cell Degeneration/Death: Within the organ of Corti are the outer and inner sensory hair cells, as well as spiral ganglion neurons. The sensory hair cells are the most vulnerable to injury. Damage to the sensory cells or ganglion cells results in impaired function that is often permanent. Whether the cause is labyrinthitis, noise-induced hearing loss (85 dB sound pressure level or higher), chemical ototoxins, or the poorly understood disorder called presbycusis (i.e., age-related hearing loss), sensory hair cells are targeted and undergo degeneration or death leading to hearing impairment or hearing loss. Bursts of intense noise are thought to result in disarrangement or breakage to the stereocilia, whereas continuous exposure to damaging noise leads to death of the hair cells.

Auditory Ossicular Chain Damage: Chronic otitis media can potentially lead to conductive hearing loss by damaging the auditory ossicles. Chronic exposure to infection, bacterial or fungal toxins, and degradative enzymes from inflammation can result in bony lysis. Excessively lytic bones may develop pathologic fractures. Additionally, chronic inflammation can result in fibrosis, which may restrict the movement of the ossicles. Finally, chronic inflammation can damage the articulations of the ossicles, thus impairing transmission of vibrations.

Integumentary Defenses: Defense mechanisms of the skin are discussed in Chapters 3 and 17.

Epithelial Migration: Migration of cornified epithelial cells to the periphery of the tympanic membrane and onto the external acoustic meatus continuously replaces the effete epidermal layer of the tympanic membrane. Epithelial migration is thus an important means of maintaining tympanic membrane thickness, clearance of debris and likely microorganisms and parasites from the tympanic membrane and external acoustic meatus, and retaining vibratory sensitivity. Alterations in this epithelial migratory pattern can lead to or may be the cause of disease of the external or middle ear. As discussed previously, epithelial migration is also the method by which perforations of the tympanic membrane are repaired.

Adnexa and Cerumen: Cerumen is an oily emulsion that coats and protects the integument of the external acoustic meatus. Its naturally hydrophobic properties make it an important barrier to the entry of excessive moisture into the epidermal cells or underlying dermis. In normal ears of dogs, cerumen is made of sloughed superficial squamous cells mixed with ceruminous and sebaceous gland secretions. There is a high lipid content in cerumen made up of neutral lipids. In otitic ears, the cerumen changes because ceruminous glands are typically more numerous and active during periods of inflammation and thus contribute more to the content of cerumen (see Fig. 20-25). One consequence is a decrease in the lipid content, a decrease in hydrophobicity, and impairment of a natural barrier.

Cerumen in otitic ears becomes more acidic than normal, which is believed to impair bacterial growth. This outcome is due to greater contribution by ceruminous glands during periods of external ear inflammation. The pH of the external acoustic meatus is variable in dogs, ranging from 4.6 to 7.2. During periods of inflammation, the mean pH in acute otitis externa may decrease, whereas the mean pH in chronic otitis externa tends to increase. The mechanistic consequences of these changes are poorly understood.

Immunoglobulins IgA, IgG, and IgM have been identified in canine cerumen; however, the predominant immunoglobulin is IgG. This high level of IgG is believed to be related to transudation of serum in the inflamed external ear. Lysozyme and interleukins have also been identified in cerumen and provide an antimicrobial function.

Commensal Organisms: A mixture of bacteria and yeast normally populates the external acoustic meatus. Various species of “potentially pathogenic” microorganisms have been cultured from external ears of dogs with no evidence of disease. They include Bacillus spp., Corynebacterium spp., Escherichia coli, Micrococcus spp., Staphylococcus spp., Streptococcus spp., and yeast organisms, most commonly Malassezia spp. Rarely, Pseudomonas spp. and Proteus spp. have been isolated. Based on a single study of horses, Corynebacterium spp. and Staphylococcus intermedius were isolated from normal ears. Presumably, these organisms live symbiotically and defense mechanisms limit or prevent proliferation of a monoculture. However, the spectrum of microorganisms cultured from diseased external ears closely mirrors this list.

Osseous External Acoustic Meatus: The length and diameter of the osseous portion of the external acoustic meatus are highly variable among species and provide a unique structural defense mechanism. Animals with longer and narrower osseous portions have tympanic cavities and tympanic membranes that are better protected than those with shorter osseous portions.

Mucociliary Apparatus: Various portions of the middle ear are lined by epithelium similar to that found in the nasopharynx. A combination of goblet cells and ciliated columnar epithelial cells extend through the auditory tube into the tympanic cavity. See Chapters 4 and 9 for discussion of the mucociliary apparatus.

Surfactant: Surfactant in the lung has long been recognized for its central role in reducing surface tension in alveoli, allowing them to expand and collapse normally during inspiration and expiration, respectively (see Chapter 9). However, recently, it has been shown that surfactant has other roles, especially in the function of the auditory tube. Surfactant is a complex mixture made up of 90% lipid and phospholipid and 10% surfactant proteins, designated surfactant protein-A (SP-A), SP-B, SP-C, and SP-D. Cuboidal epithelial cells lining the auditory tube are the source of surfactant and contain apical secretory granules analogous to what are seen in type II pneumocytes of the lung. One major difference between pulmonary surfactant and auditory tube surfactant is the ratio of phosphatidylcholine to sphingomyelin. Pulmonary surfactant has a ratio of 67 to 1, whereas auditory tube surfactant has a ratio of 2 to 1. This dramatic difference in auditory tube surfactant phospholipid content is reflected in a reduced ability to modify surface tension.

The most abundant surfactant protein in lung surfactant is SP-B, a strongly hydrophobic protein with high surface activity. However, auditory tube surfactant has a paucity of SP-B and relative abundance of SP-A and SP-D, two highly hydrophilic surfactant proteins. This difference may indicate a different function for auditory tube surfactant, namely, acting as a release agent and anti-adhesive rather than a surface tension modifying substance. Anti-adhesive properties would facilitate opening of the auditory tube.

Surfactant proteins are collectins that have two domains: (1) a lectin moiety that binds to the surface of foreign substances and organisms and (2) a collagenous domain that functions as a ligand for phagocytosis and complement activation (see Chapter 3). Finally, surfactant is believed to play a protective role against free radicals by early termination of free radical propagation, and protecting against oxidative injury. A lipid-binding pocket in surfactant proteins may prevent free radicals from propagating.