Temporal bone
The temporal bone is a paired, irregular bone that forms the lower lateral and posterior portions of the skull, contributing significantly to the base and sides while housing critical structures for hearing and balance.[1] It is situated bilaterally, articulating with the parietal, occipital, sphenoid, and zygomatic bones, and plays a vital role in protecting the middle and inner ear, as well as providing attachment points for muscles involved in mastication and head movement.[2] The bone's complex structure enables sound transmission through the external auditory canal to the tympanic membrane and ossicles, ultimately reaching the cochlea, while also enclosing the vestibular system for equilibrium.[3] Composed of four primary parts—the squamous, tympanic, petrous, and mastoid portions—the temporal bone develops from multiple ossification centers that fuse during growth.[1] The squamous part is a thin, flat plate forming the lateral wall of the cranium and including the zygomatic process that contributes to the zygomatic arch.[2] The tympanic part surrounds the external auditory meatus and forms the bony portion of the ear canal, while the petrous part is a dense, pyramid-shaped region containing the inner ear structures, including the cochlea and semicircular canals.[3] The mastoid part, located posteriorly, features the mastoid process for muscle attachments and houses mastoid air cells that help equalize pressure in the middle ear.[2] Additionally, the styloid process projects inferiorly from the base, serving as an attachment for ligaments and muscles of the neck and tongue.[1] The temporal bone contains several important foramina and canals that transmit cranial nerves and blood vessels, such as the internal acoustic meatus for the facial (VII) and vestibulocochlear (VIII) nerves, the jugular foramen for the glossopharyngeal (IX), vagus (X), and accessory (XI) nerves, and the carotid canal for the internal carotid artery.[3] It articulates with the mandible via the temporomandibular joint, facilitating jaw movement.[2] Sutures like the squamosal, occipitomastoid, and sphenopetrosal secure it to adjacent bones, forming stable connections that withstand mechanical stresses.[3] Clinically, the temporal bone's proximity to vital neurovascular structures makes it susceptible to fractures from trauma, which can lead to complications like hearing loss, facial nerve palsy, or cerebrospinal fluid leakage.[1] Infections such as mastoiditis can spread from the middle ear to the mastoid air cells, potentially causing intracranial abscesses if untreated.[2] Its role in auditory and vestibular function also implicates it in disorders like vertigo or conductive hearing impairment, underscoring its importance in otolaryngology and neurosurgery.[3]Anatomy
Parts and components
The temporal bone is composed of four primary parts: the squamous part (squama), the tympanic part, the petrous part, and the mastoid part. The styloid process is a slender projection arising from the inferior surface between the mastoid and tympanic parts.[2][3] The squamous part, also known as the squama temporalis, is a thin, flat, scale-like plate that forms the superior and lateral aspect of the temporal bone, contributing to the floor of the temporal fossa. Its outer surface is smooth and convex, while the inner surface is concave and bears impressions for the temporal lobe of the cerebrum. The average thickness of the squamous part measures approximately 2.11 mm, varying slightly with age and sex.[3][4] The petrous part is a dense, pyramid-shaped structure wedged between the sphenoid and occipital bones at the base of the skull, representing the most medial and robust component of the temporal bone. It points anteromedially with its apex near the foramen lacerum and base fusing with the squamous and mastoid parts. Extending inferiorly and posteriorly from the base of the petrous part is the mastoid part, which features the mastoid process, a conical projection posterior to the external auditory meatus that contains a system of interconnected air cells (mastoid air cell system) within its porous interior. The mastoid process typically measures up to 34 mm in anteroposterior thickness in adults.[5][6][7] The tympanic part consists of a curved, plate-like bone that forms the anterior and inferior walls of the external auditory canal, located inferior to the squamous part and anterior to the mastoid process. It features a C-shaped configuration with a posterior projection that partially encloses the canal opening.[2][3] The styloid process is a slender, pointed projection arising from the inferior surface of the temporal bone, between the mastoid and tympanic parts, serving as an attachment site for muscles and ligaments. It has an average length of 2.5 cm and is often enclosed proximally by a thin plate of the tympanic part known as the vaginal process.[3][8] In adults, these parts are interconnected through ossified sutures that fuse during postnatal growth, obliterating the embryonic boundaries. The petrosquamous suture marks the junction between the petrous and squamous parts, forming a thin bony septum (Körner's septum) that separates the mastoid air cells from the middle cranial fossa. The petrotympanic suture unites the petrous and tympanic parts, transmitting the anterior tympanic branch of the maxillary artery and chorda tympani nerve. These fusions create a unified, irregular structure essential to the temporal bone's integrity.[9][10]Surfaces and borders
The external surface of the temporal bone is divided into three primary regions: the squamous, mastoid, and tympanic. The squamous region consists of a thin, flat, and slightly convex plate that forms the lateral wall of the skull and contributes to the floor of the temporal fossa.[2][3] The mastoid region, located posteriorly, features the mastoid process as a prominent projection that houses mastoid air cells.[2][3] Anteriorly, the tympanic region forms the bony portion of the external acoustic meatus, providing structural support for the external ear canal.[2][3] The internal surface, facing the cranial cavity and known as the cerebral surface, is characterized by the petrous ridge—a sharp, pyramid-shaped elevation that separates the middle cranial fossa anteriorly from the posterior cranial fossa posteriorly.[3] This surface bears various impressions and grooves, including those for the dura mater of the temporal lobe and the sigmoid sinus, facilitating the accommodation of intracranial structures.[3][1] The temporal bone's borders define its articulations with adjacent cranial bones. The superior border, primarily along the squamous part, articulates with the parietal bone to form the squamous suture.[2][3] The anterior border connects with the greater wing of the sphenoid bone, establishing the sphenosquamous suture.[2][3] Posteriorly, the border articulates with the occipital bone via the lambdoid suture's extension, known as the occipitomastoid suture.[3] The inferior border, irregular and notched, includes the jugular notch where it meets the jugular process of the occipital bone to form the jugular foramen.[2][3] Notable features on the external surface include the zygomatic process, which extends anteriorly from the inferior aspect of the squamous part to articulate with the zygomatic bone, forming the zygomatic arch.[2][3] Adjacent to this, the mandibular fossa—a concave depression on the squama—serves as the site for articulation with the mandible in the temporomandibular joint.[2][3]Foramina, fissures, and canals
The temporal bone features numerous foramina, fissures, and canals that serve as passages for neurovascular structures, particularly those related to audition and cranial nerve transmission. These openings are distributed across its various parts, including the petrous, tympanic, and mastoid portions, facilitating connections between the cranial cavity, middle ear, and external regions. Key examples include the external acoustic meatus in the tympanic part, which forms the entrance to the external auditory canal for sound transmission to the eardrum.[11] Prominent foramina include the internal acoustic meatus, situated on the posterior surface of the petrous part, which transmits the facial nerve (CN VII), vestibulocochlear nerve (CN VIII), vestibular ganglion, and labyrinthine artery from the posterior cranial fossa to the inner ear.[12] The jugular foramen, formed at the junction of the petrous temporal bone and occipital bone, is divided into compartments that convey the glossopharyngeal nerve (CN IX), vagus nerve (CN X), accessory nerve (CN XI), inferior petrosal sinus, and the origin of the internal jugular vein from the sigmoid sinus.[13] The stylomastoid foramen, located between the styloid and mastoid processes in the petromastoid region, provides the exit for the extracranial facial nerve and stylomastoid artery.[3] Fissures in the temporal bone primarily represent developmental suture lines or communication pathways. The petrotympanic fissure (Glaserian fissure), between the petrous and tympanic parts, connects the middle ear cavity to the infratemporal fossa and transmits the chorda tympani nerve, a branch of the facial nerve.[11] The petrosquamous fissure, separating the petrous and squamous parts, marks the site of early ossification fusion and typically transmits no major structures in the adult bone, though it may contain minor venous connections during development.[14] Significant canals include the carotid canal in the petrous part, which enters the inferior surface of the temporal bone and courses superiorly and anteriorly, bifurcating into a vertical petrous segment and a horizontal tympanic segment before opening into the middle cranial fossa to transmit the internal carotid artery.[12] The facial canal, originating within the petrous part and extending through the tympanic and mastoid parts, encases the facial nerve along its labyrinthine, tympanic, and mastoid segments, terminating at the stylomastoid foramen.[3] Additionally, the vestibular aqueduct, a narrow bony channel in the petrous part, extends from the vestibule of the inner ear to the posterior surface of the temporal bone, draining endolymph via the endolymphatic duct.[15]Development and growth
Embryonic development
The temporal bone originates primarily from the first and second pharyngeal arches, with additional contributions from the otic capsule derived from periotic mesenchyme, including mesoderm and neural crest cells, surrounding the developing inner ear. Neural crest cells contribute to structures such as the superstructure of the stapes and parts of the otic capsule. The first pharyngeal arch gives rise to the tympanic ring and the handle of the malleus, while the second pharyngeal arch contributes to the stapes, styloid process, and lesser horn of the hyoid bone.[16][17][18] Embryonic development of the temporal bone begins around weeks 4 to 5 of gestation, when the otic placode induces the formation of petrous precursors from surrounding mesenchyme. The otic placode, appearing in week 4, invaginates to form the otic vesicle, which differentiates into the membranous labyrinth by week 8, establishing the foundational sensory structures encased by the future otic capsule.[16][19] Key early structures include Reichert's cartilage, which arises from the second pharyngeal arch and forms the styloid process, parts of the malleus and stapes, and the lesser horn of the hyoid; the tympanic ring develops separately from the first arch as a C-shaped cartilage that later ossifies.[17][18] Genetic regulation involves Hox genes, which specify pharyngeal arch identity and organogenesis, such as Hoxa3 in patterning the third arch derivatives, and BMP signaling pathways, including BMP2a and BMP5, which promote mesodermal specification and arch artery formation through the BMP/Smad cascade.[20][21][22]Ossification and postnatal development
The temporal bone forms through a complex process involving multiple ossification centers, with three primary ones contributing to its major components. The squamous part ossifies via intramembranous ossification, beginning at a single center around the 8th gestational week in the region of the future zygomatic process.[23] The petromastoid part, encompassing the petrous pyramid and mastoid process, undergoes endochondral ossification starting around the 16th gestational week from approximately 20 separate centers within the cartilaginous otic capsule.[24] The tympanic part develops from an intramembranous ossification center at the 12th gestational week, forming the tympanic ring around the external auditory meatus.[24] Fusion of these components occurs progressively during childhood. The petrosquamous suture, separating the petrous and squamous parts, typically obliterates in adulthood.[25] The petrotympanic fissure, connecting the tympanic cavity to the infratemporal fossa, undergoes partial ossification in adulthood, reducing its patency while allowing passage of structures like the chorda tympani nerve.[26] Postnatally, the temporal bone undergoes significant remodeling and expansion. The mastoid air cell system, which provides structural support and aids in pressure equalization, begins developing shortly after birth through mucosal invaginations from the epitympanum into the mastoid process; the antrum is present at birth, but cellular pneumatization accelerates between birth and 2-3 years, with cells forming via epithelial outgrowths.[27] This process continues, reaching near-adult volume by puberty around 15-18 years.[28] Concurrently, the squamous part expands laterally with overall calvarial growth, contributing to the broadening of the cranial vault.[23] Several factors influence mastoid pneumatization during postnatal development. Hormonal influences, including growth hormone, play a role in overall craniofacial bone remodeling and may support the expansion of air cell volume.[29] Mechanical stimuli from activities such as sucking in infancy and mastication during childhood provide functional loading that promotes bone apposition and pneumatization progression, as seen in comparative studies of masticatory function and temporal bone morphology.[30] Genetic predisposition and avoidance of early infections also contribute to optimal development, with chronic otitis media potentially arresting cell formation.[31]Functions
Role in audition
The temporal bone plays a central role in audition by providing structural support for the external, middle, and inner ear components essential for sound transmission. The tympanic part of the temporal bone forms the medial two-thirds of the external auditory canal, a bony conduit that channels sound waves from the outer environment to the tympanic membrane, initiating the vibratory process of hearing.[32] Within the middle ear cavity, the petrous part houses the auditory ossicles—malleus, incus, and stapes—which amplify and transmit mechanical vibrations from the tympanic membrane to the inner ear, optimizing sound conduction efficiency.[1][33] The petrous portion of the temporal bone encases the cochlea and associated structures of the inner ear, creating a protective bony labyrinth that facilitates the conversion of sound vibrations into neural signals. Specifically, the cochlea, embedded within this dense pyramid-shaped bone, receives vibrations via the oval window, where the stapes footplate connects the middle ear to the scala vestibuli filled with perilymph; these vibrations propagate as fluid waves through the cochlear duct to the round window, which allows pressure release and ensures efficient sound transduction.[32][33] The round window, covered by a thin membrane, completes the hydraulic system by permitting perilymph movement, thereby preventing energy dissipation and supporting frequency-specific hair cell stimulation in the organ of Corti.[1] Although the petrous bone also encloses the semicircular ducts, their primary involvement in audition is indirect through shared perilymphatic pathways.[32] The dense composition of the petrous temporal bone contributes to acoustic isolation by dampening extraneous vibrations and minimizing sound leakage to surrounding cranial structures, thus preserving the fidelity of auditory signals directed to the brain.[33] This protective density shields the delicate cochlear apparatus from external noise interference, enhancing overall hearing sensitivity.[1] Key anatomical features include the tegmen tympani, a thin bony roof overlying the middle ear cavity that separates it from the middle cranial fossa while supporting ossicular stability during vibration transmission, and the promontory, a rounded projection in the medial wall of the middle ear formed by the basal turn of the cochlea, which influences the acoustic resonance within the tympanic cavity.[32][1] The internal acoustic meatus, traversing the petrous bone, provides passage for the auditory nerve, linking peripheral sound processing to central neural pathways.[33]Role in balance and equilibrium
The petrous part of the temporal bone encases the vestibular apparatus, providing rigid protection for the structures responsible for detecting head movements and maintaining equilibrium. This bony housing includes the bony labyrinth, a series of interconnected cavities filled with perilymph that surround the membranous labyrinth containing endolymph. The vestibular apparatus comprises the three semicircular canals—superior, posterior, and lateral—along with the utricle and saccule. The semicircular canals, oriented approximately orthogonally due to the pyramid-shaped configuration of the petrous temporal bone, detect angular accelerations of the head in three-dimensional space by sensing the deflection of endolymph within their ampullae.[1][34][35] The utricle and saccule, located within the vestibule of the bony labyrinth, function as otolith organs that sense linear accelerations and gravitational forces. These structures feature maculae with hair cells embedded in a gelatinous matrix containing otoconia, which shift in response to linear motion, stimulating sensory transduction for static and dynamic balance. The endolymphatic system supports this sensory function by maintaining the ionic composition of endolymph, a potassium-rich fluid essential for hair cell depolarization. The vestibular aqueduct, a narrow bony canal in the petrous temporal bone, drains excess endolymph from the endolymphatic sac to regulate fluid volume and pressure, thereby preserving homeostasis within the vestibular apparatus.[34][35][1] Neural signals from the vestibular apparatus are transmitted via the vestibular division of the vestibulocochlear nerve (cranial nerve VIII), which originates from the vestibular ganglion (Scarpa's ganglion) located in the internal acoustic meatus of the temporal bone. This meatus serves as a conduit for the nerve fibers to exit the petrous part and reach the brainstem, where they integrate with other sensory inputs for reflexive control of posture and eye movements. The precise anatomical positioning of the internal acoustic meatus within the temporal bone ensures efficient and protected conveyance of these balance-related signals.[1][35][34]Articulations and muscular attachments
The temporal bone forms several key articulations with adjacent cranial bones, primarily through fibrous sutures and one notable synovial joint. The temporomandibular joint (TMJ) is a ginglymoarthrodial synovial joint located in the mandibular fossa, formed by the articulation between the condylar process of the mandible and the glenoid fossa of the squamous portion of the temporal bone.[36] This joint includes an articular disc that divides the joint cavity into superior and inferior compartments, along with a fibrous capsule reinforced by lateral and sphenomandibular ligaments.[36] Sutural articulations connect the temporal bone to surrounding skull elements via immovable fibrous joints. The squamosal suture joins the superior border of the squamous part of the temporal bone to the inferior border of the parietal bone.[37] The sphenosquamosal suture links the inferior border of the squamous part to the greater wing of the sphenoid bone.[37] Posteriorly, the parietomastoid suture unites the mastoid part of the temporal bone with the parietal bone, while the occipitomastoid suture connects the mastoid part to the occipital bone.[38] The temporal bone provides attachment sites for several muscles involved in head and neck movements. On the squamous part, the temporalis muscle originates from the temporal fossa and fascia covering the lateral surface.[39] The mastoid process serves as the insertion point for the sternocleidomastoid and posterior belly of the digastric muscles.[40] The styloid process, projecting from the temporal bone's base, gives origin to the stylohyoid and styloglossus muscles.[41] Ligamentous attachments further stabilize structures around the temporal bone. The stylohyoid ligament extends from the styloid process to the lesser horn of the hyoid bone and represents an ossified remnant of Reichert's cartilage from the second pharyngeal arch.[42] Additionally, extrinsic ligaments of the auricle, including the anterior and superior auricular ligaments, attach to the tympanic part of the temporal bone, anchoring the external ear to the skull.[43]Clinical significance
Trauma and fractures
Temporal bone fractures represent a significant component of skull base injuries, occurring in approximately 20-40% of such cases.[44] These fractures typically arise from high-energy blunt trauma, with motor vehicle accidents accounting for over 50% of adult cases and being the most common cause in children (47%), followed by falls (40%).[45][46] Assaults and other accidents contribute to the remainder, often resulting in unilateral involvement in about 83% of instances.[45] Notably, 70-80% of temporal bone fractures involve the petrous ridge, the dense portion of the bone housing critical auditory and vestibular structures.[45] Fractures are classified into two main types based on their orientation relative to the petrous axis: longitudinal and transverse. Longitudinal fractures, comprising 70-90% of cases, extend along the external auditory canal and petrous ridge, usually from lateral temporal impacts, and frequently spare the otic capsule while affecting the middle ear.[45][47] Transverse fractures, which are less common at 10-30%, propagate perpendicular to the petrous bone, often from occipital or frontal blows, and carry a higher risk of inner ear and cranial nerve damage due to their path through the otic capsule.[45][47] Associated injuries are common and can profoundly impact auditory and neurological function. Conductive hearing loss occurs in up to 66% of cases due to ossicular chain disruption from longitudinal fractures.[45] Sensorineural hearing loss affects about 5% overall but rises significantly with transverse fractures involving cochlear concussion.[45] Facial nerve palsy manifests in 7-12% of fractures, increasing to 48% when the otic capsule is involved, often due to breach of the facial canal.[45] Cerebrospinal fluid otorrhea is a frequent complication, particularly with fractures breaching the tegmen tympani or involving the internal acoustic meatus.[45]Infections and pathologies
The temporal bone is susceptible to various infectious and inflammatory pathologies, primarily arising from extensions of middle ear infections. Acute otitis media (AOM), a common bacterial infection in children, can progress to chronic suppurative otitis media if unresolved, leading to intratemporal complications such as mastoiditis and cholesteatoma.[48] Mastoiditis manifests as suppurative inflammation of the mastoid air cells within the temporal bone, often resulting in coalescent abscess formation due to pus accumulation and bone erosion in poorly pneumatized regions.[49] This condition disrupts the normal aeration of mastoid cells, which develop postnatally, exacerbating local spread.[49] Cholesteatoma represents another critical complication, characterized by the pathologic ingrowth of keratinizing squamous epithelium into the middle ear cleft, driven by tympanic membrane retraction or epithelial migration.[50] This leads to progressive bone resorption in the temporal bone through pressure necrosis and inflammatory mediators, potentially eroding structures like the ossicles or scutum.[51] Acquired cholesteatomas, the most prevalent type, often stem from repeated AOM episodes, while congenital variants arise from trapped epithelial rests during embryogenesis.[50] Osteomyelitis of the temporal bone, a more severe infectious process, involves bacterial invasion of the bone matrix, frequently complicating untreated otitis media or externa.[52] Petrous apicitis, an osteomyelitic focus at the petrous apex, can produce Gradenigo's syndrome, a classic triad of persistent otitis media, deep retro-orbital pain from trigeminal nerve irritation, and ipsilateral abducens nerve (CN VI) palsy due to inflammation in Dorello's canal.[53] This pathology arises from contiguous spread along vascular channels or air cell tracts, highlighting the temporal bone's interconnected anatomy.[54] Congenital anomalies of the temporal bone contribute to pathologic vulnerabilities by altering normal drainage and aeration pathways. External auditory canal atresia, a developmental malformation ranging from stenosis to complete absence, impairs sound conduction and predisposes to recurrent infections due to hypoplastic middle ear structures.[55] Similarly, persistence of the petrosquamous suture—manifesting as Körner's septum—divides the mastoid air cell system, potentially hindering pneumatization and facilitating infection trapping in superficial compartments.[56] Key risk factors for these temporal bone pathologies include eustachian tube dysfunction, which impairs middle ear ventilation and clearance, and immune compromise from conditions like diabetes or HIV.[48] Epidemiologically, AOM and its complications peak in pediatric populations aged 6-24 months, coinciding with immune maturation and exposure to respiratory pathogens in daycare settings.[48] Infection spread may occur via foramina such as the jugular, linking the temporal bone to deeper spaces.[57]Tumors and neoplasms
Tumors and neoplasms of the temporal bone encompass a range of benign and malignant growths that arise within or invade this complex structure, often presenting diagnostic challenges due to their proximity to critical neurovascular elements. These lesions are rare overall, with malignant tumors accounting for approximately 0.2% of all head and neck malignancies and an incidence of about 1 case per million population annually for cancers of the ear canal or middle ear. Benign neoplasms, while more common than their malignant counterparts, still represent a small fraction of intracranial tumors, with vestibular schwannomas alone having an estimated annual incidence of 1-2 per 100,000 individuals. Risk factors are limited but include prior ionizing radiation exposure to the head, which has been linked to an increased incidence of vestibular schwannomas. Benign tumors of the temporal bone include vestibular schwannoma, also known as acoustic neuroma, which originates from Schwann cells of the vestibulocochlear nerve (cranial nerve VIII) within the internal auditory meatus. This slow-growing, encapsulated lesion typically presents with gradual enlargement, leading to compression of adjacent neural structures. Glomus jugulare tumors, or jugular paragangliomas, are neuroendocrine neoplasms arising from paraganglionic tissue at the jugular foramen, often exhibiting vascularity and potential for local extension without distant metastasis. Another erosive benign growth is cholesteatoma, a non-neoplastic accumulation of keratinizing squamous epithelium in the middle ear or mastoid that expands destructively, eroding temporal bone and nearby ossicles through pressure and enzymatic activity. Malignant neoplasms primarily involve squamous cell carcinoma (SCC), the most common primary malignancy of the temporal bone, often originating from the external auditory canal, middle ear mucosa, or adjacent skin. This aggressive tumor accounts for 60-80% of temporal bone malignancies and tends to invade locally with a propensity for lymphatic spread to cervical nodes.[58] Temporal bone metastases are infrequent secondary lesions, typically from primaries such as breast, lung, or renal carcinomas, which seed hematogenously and cause osteolytic destruction within the bone. Staging of temporal bone tumors, particularly SCC, relies on systems like the modified University of Pittsburgh or Moody classification, which assess tumor extent based on involvement of the external auditory canal, middle ear, mastoid, petrous apex, and surrounding structures such as the facial nerve or dura. Tumors frequently spread via natural fissures and dehiscences, including the facial canal or petrotympanic fissure, allowing progression to the petrous apex and intracranial spaces. Common symptoms include progressive hearing loss, tinnitus, and facial nerve weakness due to compression or invasion, alongside otalgia and otorrhea in more advanced cases.| Tumor Type | Origin | Key Features | Common Symptoms |
|---|---|---|---|
| Vestibular Schwannoma (Benign) | Schwann cells of CN VIII in internal auditory meatus | Slow-growing, encapsulated; may erode canal walls | Unilateral hearing loss, tinnitus, balance issues |
| Glomus Jugulare (Benign) | Paraganglionic tissue at jugular foramen | Vascular, locally invasive but non-metastasizing | Pulsatile tinnitus, hearing loss, cranial nerve palsies |
| Cholesteatoma (Benign, erosive) | Keratinizing epithelium in middle ear/mastoid | Expansive cyst-like growth causing bone erosion | Recurrent infections, conductive hearing loss, vertigo |
| Squamous Cell Carcinoma (Malignant) | External/middle ear or skin | Aggressive local invasion, lymphatic spread | Otalgia, otorrhea, facial weakness |
| Temporal Bone Metastases (Malignant) | Hematogenous from distant primaries (e.g., breast, lung) | Osteolytic, multifocal possible | Hearing loss, pain, cranial neuropathies |