Maxillary sinus

The maxillary sinus is the largest of the four paired paranasal sinuses, consisting of air-filled pyramidal cavities located bilaterally within the body of the maxilla bone in the cheek region adjacent to the nose.^[1] Its base forms the medial wall facing the lateral nasal cavity, while the apex points laterally toward the zygomatic process of the maxilla; the roof corresponds to the floor of the orbit, and the floor aligns with the alveolar process above the roots of the maxillary premolars and molars.^[2] In adults, each sinus measures approximately 3–4 cm in height, 3 cm in width, and 3 cm in anteroposterior length, with a volume of about 15 mL, and it drains into the middle meatus of the nasal cavity via a small ostium located high on the medial wall.^[3] The primary physiological functions of the maxillary sinus include humidifying and warming inspired air, producing mucus via ciliated epithelial cells and goblet cells to trap particles and maintain nasal moisture, and facilitating mucociliary clearance at a rate of about 6 mm per minute toward the ostiomeatal complex for drainage.^[4] Additionally, the sinuses reduce the weight of the skull, provide resonance to the voice, and offer a buffer against facial trauma while supporting immunological defenses through nitric oxide production in the paranasal sinuses.^[2][5] Innervation arises from branches of the maxillary nerve (V2), including the anterior, middle, and posterior superior alveolar nerves and the infraorbital nerve, while blood supply is derived from branches of the maxillary artery such as the infraorbital, posterior superior alveolar, and posterior lateral nasal arteries.^[3] Developmentally, the maxillary sinus originates as an evagination from the nasal epithelium around 17 weeks of gestation, forming a small rudimentary pouch of 60–80 mm³ at birth that expands laterally and inferiorly in phases: rapid growth by age 3 years, further extension into the zygomatic recess by age 9–12, and completion of pneumatization by late adolescence (around age 18 in males and 20 in females), reaching an average adult volume of 15 mL (range 10–25 mL).^[4] This postnatal expansion correlates with the eruption of permanent teeth and facial skeletal growth, with variations in size and septations (present in up to 50% of cases) influencing susceptibility to conditions like odontogenic sinusitis, which accounts for about 75% of unilateral cases.^[6][7] Anatomical variants, such as Haller cells (prevalence ~45%), can narrow the ostiomeatal complex and predispose to chronic rhinosinusitis.^[4]

Anatomy

Location and Morphology

The maxillary sinus is a pyramid-shaped, air-filled cavity situated within the body of the maxilla bone, constituting the largest of the four paranasal sinuses in adults.^[4] Its base faces medially toward the lateral wall of the nasal cavity, while the apex extends laterally toward the zygomatic process of the maxilla.^[8] In adults, the average volume ranges from 15 to 20 mL, with variations influenced by factors such as sex, ethnicity, and degree of pneumatization; males typically exhibit larger volumes than females.^[9] The typical dimensions include a height of approximately 3.5 cm (36–45 mm), a width of about 2.5 cm (25–35 mm), and an anteroposterior depth of roughly 3.8 cm (38–45 mm).^[4] Internally, the maxillary sinus features several distinct recesses that contribute to its irregular pyramidal morphology. The alveolar recess projects inferiorly over the roots of the maxillary teeth, with its depth varying from 3 to 5 mm below the nasal floor in most cases.^[4] The zygomatic recess extends laterally into the zygomatic bone, accommodating extensions of the sinus cavity.^[8] Additionally, the infraorbital recess forms superiorly along the orbital floor, following the course of the infraorbital canal.^[4] The extent of pneumatization in the maxillary sinus is closely tied to midface development, beginning in utero and progressively expanding postnatally to fill available space within the maxilla as the facial skeleton matures.^[4] This pneumatization process typically reaches its adult configuration by the late teens or early twenties, influencing the sinus's overall size and contour in relation to surrounding midfacial structures.^[8]

Walls and Adjacent Structures

The maxillary sinus is bounded by six walls, each formed primarily by the maxillary bone and exhibiting variable thickness that influences its relations to adjacent structures. These walls include the anterior, posterior, medial, lateral, superior (roof), and inferior (floor), with the medial wall being notably thin and contributing to the lateral boundary of the nasal cavity. The sinus's proximity to critical neurovascular elements, such as branches of the maxillary artery and the infraorbital nerve, underscores the importance of these boundaries in surgical and pathological contexts.^[3][4] The medial wall of the maxillary sinus, also known as the nasal wall, is a thin bony plate that forms the lateral wall of the nasal cavity and separates the sinus from the nasal airway. It lies adjacent to the middle meatus superiorly and the inferior turbinate inferiorly, with a smooth surface facing the sinus lumen. This wall measures approximately 0.5-1 mm in thickness in adults, rendering it susceptible to dehiscences or perforations.^[10][3] The posterior wall abuts the infratemporal fossa posteriorly and the pterygomaxillary fissure medially, providing a boundary to the deep facial spaces containing masticatory muscles and neurovascular structures. It is relatively thick, averaging 1-2 mm, and lies in close proximity to branches of the maxillary artery, such as the posterior superior alveolar artery, which may course along its lateral aspect. The wall's relation to the pterygopalatine fossa further positions it near the maxillary nerve (V2) divisions and the pterygopalatine ganglion.^[4][3] The floor of the maxillary sinus corresponds to the alveolar process of the maxilla and overlies the roots of the maxillary teeth, particularly the molars and premolars, which are often in close apposition or even protrude into the sinus cavity. The distance from the sinus floor to the tooth apices is minimal, typically 1-3 mm for second molars, facilitating potential pathways for odontogenic infections. This inferior boundary slopes downward from anterior to posterior, reflecting the alveolar ridge's contour.^[3][11] The roof, or superior wall, constitutes the orbital floor and is a thin bony lamina, approximately 0.5-1 mm thick, that separates the maxillary sinus from the orbital contents. It contains the infraorbital groove and canal, through which the infraorbital nerve and artery—a branch of the maxillary artery—traverse toward the face, occasionally forming a bony prominence into the sinus. This relation positions the sinus directly inferior to the eyeball and orbital fat.^[3][4] The anterior wall aligns with the facial surface of the maxilla, underlying the skin and the orbicularis oculi muscle of the cheek, and includes the canine fossa as a subtle depression above the canine tooth prominence. It is the thickest wall, measuring 1.5-3 mm, and features the infraorbital foramen inferiorly, through which the infraorbital neurovascular bundle emerges. This wall's external position makes it palpable and relevant for procedures like the Caldwell-Luc approach.^[11][3]

Drainage and Openings

The primary ostium of the maxillary sinus is situated in the medial wall of the sinus, opening into the hiatus semilunaris, a crescent-shaped cleft within the middle meatus of the nasal cavity.^[12] This opening, measuring approximately 2-4 mm in diameter, is positioned posteriorly and medially near the roof of the sinus.^[12] The hiatus semilunaris itself forms a groove bounded inferiorly and anteriorly by the uncinate process of the ethmoid bone and superiorly by the ethmoidal bulla, serving as the key aperture for sinus ventilation and drainage.^[13] The primary ostium typically drains into the posterior third of the hiatus semilunaris, facilitating the outflow of secretions from the sinus cavity.^[14] Accessory ostia, which provide additional drainage routes, occur in 10-30% of individuals and are most commonly found in the posterior fontanelle region of the ethmoidal bulla.^[15] These secondary openings, while beneficial for redundancy in mucus clearance, can sometimes lead to recirculation of secretions if not aligned properly with the primary pathway.^[15] In cases of chronic rhinosinusitis, the prevalence of accessory ostia may rise to around 30%, highlighting their anatomical variability.^[15] Mucus produced within the maxillary sinus drains through the primary or accessory ostia into the hiatus semilunaris, then flows into the middle meatus and ultimately to the nasopharynx, propelled by the coordinated action of cilia on the respiratory epithelium.^[16] This pathway ensures efficient ventilation and clearance of secretions, preventing stagnation.^[3] The paranasal sinuses as a whole generate approximately 1-2 liters of mucus daily, with the maxillary sinus— the largest paranasal sinus, averaging 15 mL in volume—contributing substantially to this output due to its extensive mucosal surface area.^[17][18]

Innervation and Blood Supply

The maxillary sinus receives sensory innervation primarily from branches of the maxillary nerve (CN V2), which is the second division of the trigeminal nerve. Specifically, the anterior superior alveolar nerve supplies the anterior and medial walls, the middle superior alveolar nerve innervates the anterolateral wall, and the posterior superior alveolar nerve provides sensation to the posterolateral wall and floor.^[2] These nerves enter the sinus through foramina in the bony walls, conveying general somatic afferent fibers for pain, temperature, and touch from the mucosa.^[19] Autonomic innervation of the maxillary sinus involves both parasympathetic and sympathetic components that regulate glandular secretion and vascular tone. Parasympathetic fibers originate from preganglionic neurons in the superior salivatory nucleus, traveling via the greater petrosal nerve (a branch of the facial nerve, CN VII) to synapse in the pterygopalatine ganglion; postganglionic fibers then distribute to the sinus mucosa via branches of the maxillary nerve, stimulating seromucinous gland secretion.^[20] Sympathetic innervation arises from postganglionic fibers of the superior cervical ganglion, conveyed through the carotid plexus and internal carotid artery branches, reaching the sinus to mediate vasoconstriction and inhibit secretion via noradrenergic effects on alpha-1 receptors.^[21] The arterial supply to the maxillary sinus derives mainly from branches of the maxillary artery, a terminal branch of the external carotid artery. Key contributors include the posterior superior alveolar artery, which supplies the posterior wall and floor; the infraorbital artery, providing blood to the anterior and superior walls; and the greater palatine artery, which vascularizes the inferior and medial aspects.^[18] Additional supply comes from the sphenopalatine artery for the medial wall, ensuring robust perfusion to support mucosal health and rapid response to inflammation.^[2] Venous drainage parallels the arterial supply, with veins from the sinus mucosa forming a plexus that drains anteriorly via the facial vein into the internal jugular vein and posteriorly via the pterygoid venous plexus, which communicates with the cavernous sinus through emissary veins.^[19] This network facilitates efficient clearance of deoxygenated blood and potential pathogens from the sinus cavity.^[20] Lymphatic drainage from the maxillary sinus follows vessels that accompany the venous plexuses, primarily directing lymph to the submandibular lymph nodes via channels through the infraorbital foramen and nasal cavity ostia, with additional pathways to the retropharyngeal nodes.^[22] This drainage supports immune surveillance and fluid balance in the paranasal region.^[20]

Histology

The maxillary sinus is lined by a specialized respiratory epithelium known as the Schneiderian membrane, which is a pseudostratified ciliated columnar epithelium interspersed with goblet cells.^[4] This epithelial layer, derived from the respiratory mucosa, facilitates mucociliary clearance by producing mucus via goblet cells and propelling it through coordinated ciliary action.^[23] The goblet cells, comprising approximately 5-15% of the epithelial cells, secrete mucins that form a protective gel-like layer over the epithelium.^[17] Beneath the epithelium lies the submucosa, a layer of loose connective tissue that includes seromucinous glands, elastic fibers, and transitions into the periosteum adjacent to the bony walls.^[24] These seromucinous glands, resembling minor salivary glands, contribute additional secretions to the mucus blanket, while the elastic fibers provide structural support and flexibility to the mucosal lining.^[25] The lamina propria within the submucosa harbors immune cells, including plasma cells, lymphocytes, and mast cells, which play roles in local immune surveillance and response.^[26] Ciliated cells in the epithelium each possess 200-300 cilia, typically 5-10 μm in length, that exhibit a metachronal rhythm with a beat frequency of 10-20 Hz, directed toward the sinus ostium to aid in particle removal.^[27][28] In healthy states, the overall mucosal thickness ranges from 0.5-1 mm, but it can thicken to up to 5 mm in response to inflammatory stimuli, reflecting hyperplasia of the epithelial and submucosal components.^[29][30][4]

Development and Variations

Embryology

The maxillary sinus originates from an evagination of the nasal epithelium lining the middle meatus into the developing maxillary prominence during the 10th to 12th weeks of gestation.^[3] This initial outgrowth, known as the recessus maxillaris or ethmoido-maxillary recess, forms as a small diverticulum from the primordial ethmoidal infundibulum, marking the first stage of paranasal sinus development.^[31] The process begins with the invagination of the mucous membrane into the mesenchymal tissue of the maxilla, establishing the foundational cavity that will later expand.^[32] The development of the maxillary sinus occurs in close relation to the nasolacrimal duct, which forms earlier during the fusion of the frontonasal and maxillary processes around the sixth week of gestation.^[33] As the epithelial evagination progresses, it surrounds the future nasolacrimal canal, positioning the sinus posterior and lateral to this structure within the maxillary bone.^[34] This spatial relationship arises from the maxillary prominence's growth, which encases the canalizing nasolacrimal groove derived from the merged facial prominences.^[35] Pneumatization of the maxillary sinus commences around 3 to 4 months of gestation, with the small ethmoido-maxillary recess expanding into the maxillary bone through progressive epithelial proliferation and bone resorption.^[4] By this stage, the recess measures approximately 1-2 mm and begins to aerate the surrounding mesenchyme, setting the course for further cavity enlargement.^[31] The formation of the maxillary sinus is influenced by the fusion of the maxillary and frontonasal prominences, which occurs between the 6th and 10th weeks and shapes the midfacial skeleton.^[35] This merger integrates neural crest-derived mesenchyme, providing the structural framework for the sinus anlage within the maxilla. Genetic regulation of midface patterning plays a key role, with genes such as SHH (Sonic Hedgehog) and FGF (Fibroblast Growth Factor) family members directing epithelial-mesenchymal interactions essential for proper prominence fusion and outgrowth.^[36] SHH expression in the medial nasal and anteromedial maxillary ectoderm promotes proliferation and patterning, while FGF8 modulates growth in the maxillo-nasal region to ensure balanced development.^[37]

Postnatal Development

At birth, the maxillary sinus is present but minimally developed, with a volume ranging from 60 to 80 mm³ and dimensions approximately 7 × 4 × 3 mm.^[4] During infancy, it undergoes rapid pneumatization, expanding primarily downward and laterally in conjunction with facial growth; by age 2 years, the volume reaches about 2 mL, and this acceleration continues such that significant enlargement occurs by ages 3 to 5 years, marking the first phase of biphasic growth.^[38][39] In childhood, maxillary sinus development correlates closely with the eruption of deciduous and permanent teeth as well as overall cranial and midfacial expansion, driving further pneumatization that increases the sinus floor toward the alveolar process.^[40][41] By age 9 years, the volume approximates 10 mL, and the sinus attains roughly 80% of its adult size by age 12 years, with notable increases in width and depth during ages 6 to 12.^[38][42] Recent computed tomography (CT) studies in children up to 2024 confirm a statistically significant positive correlation between maxillary sinus dimensions and cranial base growth, underscoring the influence of skeletal maturation on sinus expansion.^[43] During puberty, the final phase of pneumatization coincides with the eruption of permanent dentition, leading to the adult pyramidal configuration and a volume increase to 15-20 mL by late adolescence.^[18][44] Post-puberty, gender dimorphism becomes evident, with male maxillary sinuses exhibiting volumes 10-20% larger than those in females, attributable to differences in overall craniofacial growth.^[45][46]

Anatomical Variations

The maxillary sinus exhibits several anatomical variations that can influence its size, shape, internal structure, and relationships with adjacent structures. These deviations occur across populations and may arise during development, though their exact etiologies often remain multifactorial. Common variations include differences in pneumatization extent, presence of internal partitions, additional drainage pathways, and proximity to dental elements, with prevalence rates derived from computed tomography (CT) and cone-beam CT (CBCT) studies. Hypoplasia of the maxillary sinus, characterized by a small or absent cavity, affects approximately 5-6% of individuals and is frequently unilateral. This condition can be classified into types based on the degree of underdevelopment, with type I (minimal pneumatization) being the most common subtype in about 70% of cases. Hypoplasia is often incidental on imaging but may complicate endodontic or surgical procedures due to altered sinus volume and positioning relative to the orbit and nasal cavity.^[47][48] Hyperpneumatization represents the opposite extreme, where the sinus expands excessively beyond typical boundaries, such as into the alveolar process, zygomatic bone, or hard palate. This variation, also termed extensive pneumatization, occurs in association with tooth loss or aging-related bone resorption, potentially leading to thinning of the sinus floor. While precise prevalence is lower than other variations (estimated around 8% in some cohorts), it is more commonly observed in edentulous patients and can extend the sinus inferiorly by several millimeters, altering the alveolar ridge morphology.^[49][50] Bony septa within the maxillary sinus, which are incomplete partitions dividing the cavity into compartments, are present in 20-50% of cases, with a meta-analysis reporting an overall prevalence of 33.2%. These septa often originate from the sinus walls or floor and vary in height (typically 5-10 mm) and orientation (anterior-posterior or transverse). They are most frequently located above the roots of the first and second molars (in 40-60% of instances), where they may mimic root apices on radiographs and increase risks during dental implant placement.^[6][51][52] Accessory ostia, additional drainage openings in the sinus membrane, occur in 10-30% of maxillary sinuses, with higher rates (up to 30%) noted in individuals with chronic sinusitis compared to 10-20% in asymptomatic populations. These ostia, usually located posteriorly in the hiatus semilunaris, can promote mucus recirculation and impair clearance, thereby elevating infection susceptibility. Their presence is bilateral in about half of affected cases and is best visualized on coronal CT slices.^[15][53] The relationship between the maxillary sinus floor and posterior teeth roots shows significant variability, with 30-60% of maxillary molars demonstrating close proximity or protrusion into the sinus on CT imaging. The palatal root of the first molar exhibits the highest involvement (up to 46% protrusion rate), while second molar roots are less frequently affected (around 20-30%). This anatomical closeness, often under 1 mm, arises from pneumatization encroaching on the alveolar bone and can facilitate odontogenic sinusitis if periapical pathology develops. Septa overlying molar roots further complicate this interface in 20-40% of proximity cases.^[54][55][56] Ethnic differences in maxillary sinus morphology include variations in volume and dimensions, with individuals of East Asian ancestry typically exhibiting larger and taller sinuses compared to those of European (Caucasian) descent. For instance, East Asian maxillary sinus volumes average 15-20% greater than in Caucasians, potentially influencing airflow dynamics and disease susceptibility. These disparities are attributed to broader craniofacial skeletal patterns and have been quantified through volumetric CT analyses across diverse cohorts.^[57][58]

Physiology

Primary Functions

The maxillary sinus plays a key role in conditioning inspired air as part of the paranasal sinus system, humidifying it to nearly 100% relative humidity and warming it to approximately 37°C through its mucosal lining and vascular supply, thereby protecting the lower respiratory tract from desiccation and cold stress.^[59] This process enhances overall respiratory efficiency by maintaining optimal air quality for gas exchange in the lungs.^[4] Pneumatization of the maxillary sinus significantly reduces the weight of the skull, lightening the maxilla and facilitating easier head and neck movements while preserving structural integrity.^[59] Additionally, the sinus contributes to voice resonance by acting as an acoustic chamber that modifies nasal timbre during speech, influencing sound quality through its volume and shape.^[59][60] Recent research highlights its role in producing nitric oxide within the sinus mucosa, which serves as an antimicrobial agent to bolster local immune defense against pathogens in the upper airways.^[61][62]

Mucociliary Clearance

Mucociliary clearance in the maxillary sinus relies on the coordinated beating of cilia on the epithelial surface, which propels mucus toward the ostium. Cilia exhibit a metachronal rhythm, generating waves that beat at a frequency of 8-12 Hz in healthy respiratory epithelium, facilitating the directional transport of the mucus gel layer.^[63] This ciliary motion is essential for moving trapped particles and secretions out of the sinus cavity, preventing accumulation and maintaining sinus health.^[4] The mucus in the maxillary sinus consists of approximately 95% water, along with mucins (2-3%), electrolytes, and other proteins, forming a biphasic structure with a low-viscosity sol layer underlying a higher-viscosity gel layer. The sol layer allows free ciliary movement, while the gel layer captures particulates and pathogens for transport. In healthy conditions, the clearance rate of this mucus is typically 5-10 mm/min, though it can vary based on factors such as mucus viscosity; increased viscosity impairs transport efficiency.^[64][65] Regulation of mucociliary clearance involves autonomic neural inputs and hormonal influences. Sympathetic and parasympathetic nerves modulate ciliary beat frequency and mucus secretion rates, with parasympathetic stimulation generally enhancing clearance. Hormones like estrogen can slow clearance; during pregnancy, elevated estrogen levels reduce ciliary beat frequency and mucociliary transport, contributing to nasal congestion.^[66][67] Dysfunction in mucociliary clearance can be assessed using the saccharin test, where a small saccharin particle is placed on the anterior nasal septum, and the time until the subject tastes sweetness is measured. Normal clearance time is under 30 minutes; times exceeding 30 minutes indicate impaired function, often due to ciliary or mucus abnormalities.^[17] This simple, non-invasive method provides a practical evaluation of transport efficiency in the nasal and sinus regions.^[68]

Clinical Significance

Inflammatory Conditions

Inflammatory conditions of the maxillary sinus primarily involve sinusitis, characterized by inflammation of the sinus mucosa due to infectious or noninfectious etiologies. This inflammation disrupts normal mucociliary clearance and can lead to fluid accumulation within the sinus cavity. While viral infections predominate in acute cases, bacterial involvement occurs in a subset, with common pathogens including Streptococcus pneumoniae and Haemophilus influenzae.^[69][70] Acute maxillary sinusitis is defined as symptomatic inflammation lasting less than 4 weeks, often arising as a complication of a viral upper respiratory infection that impairs sinus drainage. Typical symptoms include facial pain or pressure over the maxillary region, purulent nasal discharge, and fever, which may be accompanied by maxillary dental pain or hyposmia. Bacterial superinfection is suspected when symptoms persist beyond 10 days, worsen after initial improvement, or present with severe features such as high fever and intense facial pain.^[69][70] Chronic maxillary sinusitis persists for more than 12 weeks and is frequently associated with persistent mucosal inflammation rather than acute infection. Symptoms mirror those of the acute form but are more protracted, including nasal congestion, purulent discharge, and facial fullness, often without fever. Contributing factors include allergic rhinitis, which promotes eosinophilic inflammation, and anatomical obstructions such as a deviated nasal septum that hinders ostiomeatal complex drainage. On computed tomography (CT) imaging, chronic cases typically show mucosal thickening exceeding 4 mm, indicating sustained edema and potential polypoid changes.^[71][72] Complications of maxillary sinusitis arise from contiguous spread of infection or chronic obstruction. Orbital cellulitis may develop through the thin orbital floor, presenting with periorbital swelling, proptosis, and restricted eye movement, potentially progressing to vision-threatening abscesses if untreated. Mucocele formation occurs when prolonged obstruction leads to mucus retention and cystic expansion, eroding surrounding bone and exerting mass effect on adjacent structures like the orbit.^[73][71]

Oroantral Fistula

An oroantral fistula (OAF) is defined as a pathological, epithelialized communication between the oral cavity and the maxillary sinus, typically arising when an initial oroantral communication (OAC) persists beyond 48-72 hours without intervention.^[74][75] This condition disrupts the normal barrier provided by the thin maxillary sinus floor, which is in close proximity to the roots of upper molars and premolars.^[74] The primary etiology of OAF is iatrogenic, with upper molar or premolar extractions accounting for approximately 48% of cases due to the anatomical projection of tooth roots into or near the sinus floor.^[75] Other causes include dental trauma (about 7.5%), such as tuberosity fractures during procedures, and infections leading to osteomyelitis or abscesses that erode the sinus floor.^[74] Less commonly, cysts, tumors, or implant surgeries contribute, with overall incidence following posterior maxillary extractions ranging from 0.3% to 4.7%.^[74] Symptoms of OAF often manifest as escape of air or fluids through the nose during oral activities, producing a whistling sound or nasal regurgitation, accompanied by a foul taste from purulent drainage and recurrent episodes of sinusitis.^[74] Patients may also experience malar pain, postnasal drip, altered voice resonance, or cheek swelling if infection spreads.^[75] OAFs are classified as acute if the communication develops within 72 hours and remains non-epithelialized, or chronic if it persists longer and becomes lined with epithelium, increasing the risk of persistent infection.^[74] By size, defects smaller than 2-3 mm often heal spontaneously via blood clot formation, while larger ones (>3-4 mm) require surgical intervention to prevent chronicity.^[74][75] Primary closure of acute OACs aims to seal the defect promptly to achieve high success rates of 90-95%, using techniques such as the buccal advancement flap for small to medium defects (<1 cm), where a trapezoidal mucosal flap is mobilized and sutured over the site.^[74][75] For larger defects, the buccal fat pad (BFP) graft is preferred, involving pedicled transposition of the fat pad, which promotes rapid epithelialization within 4-6 weeks and yields success rates up to 100% in some studies, outperforming other flaps.^[75] Secondary closure for established OAFs has lower success, around 67%, often necessitating combined approaches with sinus debridement.^[74]

Neoplastic Conditions

Neoplastic conditions of the maxillary sinus involve both benign and malignant growths that arise from the sinonasal epithelium or extend into the sinus from nearby sites, often presenting with nonspecific symptoms like nasal obstruction or facial swelling that delay diagnosis until advanced stages. Benign tumors, though non-life-threatening, can exhibit locally aggressive behavior leading to bone erosion or recurrence, while malignant tumors dominate, accounting for the majority of cases and posing significant therapeutic challenges due to the sinus's proximity to vital structures.^[76] Among benign neoplasms, inverted papilloma stands out as a key entity, representing 0.5% to 4% of all sinonasal tumors and frequently originating or extending into the maxillary sinus from the lateral nasal wall. This endophytic, epithelial proliferation is characterized by a high recurrence rate of up to 18% and a potential for malignant transformation in 5% to 15% of cases, necessitating complete surgical excision with clear margins. Retention cysts, benign cystic accumulations of mucus due to glandular obstruction, are another common finding, present in up to 13% of adults on imaging; while typically incidental and asymptomatic, larger cysts may cause pressure effects or mimic more serious pathology.^{[77][78][79][80]} Malignant tumors of the maxillary sinus are predominantly squamous cell carcinomas, comprising approximately 80% of cases and arising from the mucosal lining with a propensity for local invasion. Adenocarcinomas, though less prevalent, are notably linked to chronic wood dust exposure in occupational settings, with affected individuals showing odds ratios as high as 58.6 for developing this subtype. Staging employs the TNM classification system per the American Joint Committee on Cancer (AJCC), where T1 denotes tumors confined to the sinus mucosa without bone erosion, and T4 indicates invasion of adjacent structures such as the orbital contents, skull base, or pterygoid plates, which correlates with worse outcomes.^[81][82] Key risk factors for these malignancies include tobacco smoking, which elevates squamous cell carcinoma risk by two- to threefold through chronic mucosal irritation, and human papillomavirus (HPV) infection, implicated in up to 20-30% of squamous cell cases via oncogenic mechanisms. Industrial exposures further contribute, with wood dust strongly predisposing to adenocarcinoma and agents like nickel or chromium compounds increasing overall sinonasal cancer incidence. Prognosis remains guarded, particularly for advanced disease, with 5-year survival rates of 30% to 50% reflecting challenges in achieving local control and preventing distant metastasis.^{[83][84][85][86]}

Epidemiology

The maxillary sinus is commonly affected by sinusitis, with acute forms impacting 10-15% of adults annually in the United States, corresponding to approximately 30-35 million cases per year.^[69] Chronic rhinosinusitis involving the maxillary sinus has a lower prevalence, affecting 2-5% of adults globally, though diagnosed rates in some populations reach up to 5.1%.^[72][87] Oroantral fistulas, pathological communications between the oral cavity and maxillary sinus, occur in 0.3-4% of cases following maxillary posterior tooth extractions, with higher rates associated with third molar removals due to anatomical proximity.^[88][89] Neoplasms of the maxillary sinus are rare, with an annual incidence of 0.5-1 per 100,000 individuals worldwide; these tumors are more prevalent in males and typically diagnosed between ages 50 and 70.^[90][91] Anatomical variations such as maxillary sinus hypoplasia occur in 1-5% of the population, with studies reporting rates up to 5.65% on computed tomography.^[47][92] Recent trends indicate an increasing prevalence of chronic maxillary sinusitis, attributed to rising allergic burdens and climate change effects, such as prolonged pollen seasons and heightened aeroallergen exposure; from 2020 to 2025, studies have documented elevated morbidity in chronic rhinosinusitis correlating with environmental shifts.^[93][94]

Diagnostic Imaging

Plain radiography, particularly the Waters view, remains a simple and inexpensive initial imaging modality for evaluating the maxillary sinus, primarily detecting air-fluid levels and overall opacity indicative of acute sinusitis.^[95] In this occipitomental projection, the X-ray beam is angled to profile the maxillary sinuses against the facial bones, allowing visualization of mucosal thickening or complete opacification, though it has limitations in assessing posterior structures or subtle pathologies.^[96] While debated for standalone use in bacterial sinusitis, it is often reserved for persistent symptoms after initial treatment, with studies showing moderate sensitivity for gross abnormalities.^[97] Computed tomography (CT) serves as the gold standard for maxillary sinus imaging due to its high-resolution depiction of bony and soft tissue structures, enabling detailed assessment of mucosal thickening, ostium patency, and bone erosion in conditions like chronic rhinosinusitis.^[98] Non-contrast CT protocols provide multiplanar reconstructions, particularly coronal views, to evaluate sinus ventilation and potential complications such as orbital or intracranial extension.^[99] Since the 2020s, low-dose CT protocols have become prevalent, reducing effective radiation doses to below 2 mSv while maintaining diagnostic quality through iterative reconstruction techniques, making it suitable for routine clinical use.^[100][101] Magnetic resonance imaging (MRI) excels in providing superior soft tissue contrast for maxillary sinus evaluation, particularly in neoplastic conditions, where it differentiates tumors from inflammatory mucosa or secretions without ionizing radiation exposure.^[102] T2-weighted sequences highlight fluid-filled sinuses or cystic components, while contrast-enhanced T1 images delineate tumor margins and perineural spread, aiding preoperative planning for malignancies.^[103] Though less effective for bony details compared to CT, MRI's multiplanar capability and lack of radiation make it preferable for pediatric patients or follow-up imaging in tumor surveillance.^[97] Cone-beam computed tomography (CBCT) is widely applied in dental and maxillofacial contexts for maxillary sinus imaging, offering high spatial resolution for implant planning and assessment of sinus septa or floor integrity with substantially lower radiation doses than conventional CT, typically under 0.2 mSv.^[104] Its conical X-ray beam captures a volumetric dataset in a single rotation, ideal for evaluating odontogenic influences on the sinus, such as root apices or cysts, though it provides limited soft tissue contrast.^[105] CBCT's accessibility and cost-effectiveness have made it a standard in preoperative dental evaluations involving the posterior maxilla.^[106] Recent advances in AI-enhanced CT have improved maxillary sinus volume measurement through automated segmentation algorithms, achieving accuracies exceeding 95% compared to manual methods, as demonstrated in 2024 studies using deep learning on paranasal CT datasets.^[107] These models facilitate precise quantification of sinus volume for assessing hypoplasia or post-surgical changes, enhancing diagnostic efficiency and reducing inter-observer variability in clinical workflows.^[108]

Surgical and Therapeutic Interventions

Medical management of acute maxillary sinusitis typically involves antibiotics such as amoxicillin-clavulanate as first-line empiric therapy for adults, administered for 5 to 10 days to target bacterial pathogens like Streptococcus pneumoniae and Haemophilus influenzae.^[109] Intranasal corticosteroids, such as mometasone or fluticasone, are recommended to reduce inflammation and promote sinus drainage, particularly in cases with allergic components or persistent symptoms.^[69] Saline nasal irrigation serves as an adjunctive measure to clear mucus and allergens, improving mucociliary function and alleviating congestion without significant side effects.^[110] Functional endoscopic sinus surgery (FESS) represents the primary surgical intervention for chronic maxillary sinusitis refractory to medical therapy, focusing on widening the ostiomeatal complex to restore natural drainage and ventilation while removing polyps or mucosal obstructions.^[111] This minimally invasive approach, performed via nasal endoscopes, achieves symptomatic improvement in 85-90% of patients, with low complication rates including minor bleeding or adhesions.^[112] The Caldwell-Luc procedure, an open transoral approach historically used for radical debridement of the maxillary sinus, is now rarely employed due to its higher morbidity, including facial swelling and dental injury, and has been largely supplanted by endoscopic techniques.^[113] Modern alternatives like balloon sinuplasty offer a less invasive option for ostial dilation in select cases, dilating the maxillary sinus ostium with a balloon catheter to enhance patency without tissue removal.^[114] For neoplastic conditions involving the maxillary sinus, such as squamous cell carcinoma, treatment often entails partial or total maxillectomy to achieve oncologic resection, followed by adjuvant radiotherapy and chemotherapy to address microscopic disease and improve locoregional control.^[115] Reconstruction typically utilizes microvascular free flaps, such as the radial forearm or anterolateral thigh flap, to restore oral-nasal separation, support orbital contents, and enable prosthetic rehabilitation, achieving functional outcomes in over 80% of cases.^[116] Recent advances include the use of biologics like dupilumab, an interleukin-4 and interleukin-13 inhibitor, for severe chronic rhinosinusitis with nasal polyps affecting the maxillary sinus, demonstrating sustained reduction in polyp size and symptom scores in up to 60% of patients after 52 weeks.^[117] In orthognathic surgery, maxillomandibular advancement procedures have been associated with a 20-30% postoperative increase in maxillary sinus volume, as measured by cone-beam computed tomography, potentially alleviating sinus obstruction in patients with sleep apnea.^[118]

History

Early Anatomical Descriptions

The earliest references to facial cavities, including those later identified as paranasal sinuses, appear in ancient Egyptian medical texts dating from approximately 3700 to 1500 BCE, where physicians demonstrated familiarity with the structure of the maxillary bones through descriptions of head and facial anatomy.^[119] These writings, such as the Edwin Smith Papyrus around 1500 BCE, reflect an awareness of hollow spaces within the skull, though without detailed anatomical dissection or specific nomenclature for the maxillary sinus.^[119] During the Renaissance, Leonardo da Vinci provided the first known illustrations of the maxillary sinus in the late 15th century, around 1489–1490, through meticulous dissections and sketches of the human skull.^[119] In these drawings, now housed in collections like the Royal Library at Windsor Castle, da Vinci depicted the sinus as a cavity within the maxilla and noted its close proximity to the roots of the upper teeth, speculating that it might contain a fluid to nourish them.^[119] His work marked a shift toward empirical observation in anatomy, emphasizing the sinus's pyramidal shape and its extension toward the dental structures.^[120] The 17th century saw the first comprehensive textual description of the maxillary sinus in Nathaniel Highmore's 1651 treatise Corporis Humani Disquisitio Anatomica, where he detailed its location, size, and communications with the nasal cavity.^[119] Highmore, an English anatomist, illustrated the sinus—subsequently named the antrum of Highmore—and highlighted its anatomical relations, observing that the roots of the upper molar teeth often protrude into its floor, potentially influencing dental pathology.^[119] This publication established the maxillary sinus as a distinct entity in anatomical literature, building on da Vinci's visuals with precise verbal accounts derived from cadaveric studies.^[121] In the 18th century, Giovanni Battista Morgagni contributed to the understanding of the maxillary sinus's variability in his seminal 1761 work De Sedibus et Causis Morborum per Anatomen Indagatis, noting cases where the sinus was absent or underdeveloped, which underscored its non-universal presence in human anatomy.^[122] Although primarily focused on pathological correlations, Morgagni's observations reinforced earlier descriptions of the sinus's relations to adjacent structures, including the maxillary teeth, by integrating anatomical findings with clinical dissections.^[122] Early radiographic imaging of the paranasal sinuses, including the maxillary, emerged in 1896 shortly after Wilhelm Röntgen's discovery of X-rays, with German physician Max Scheier among the first to apply the technique clinically for visualizing sinus opacification and disease.^[123] Scheier's work demonstrated the utility of X-rays in non-invasively depicting the maxillary sinus's contours and contents, revolutionizing diagnostic access beyond dissection.^[123]

Etymology and Nomenclature

The term "maxillary" originates from the Latin maxilla, denoting the upper jawbone and derived as a diminutive form of mala, meaning "jaw" or "cheekbone." This nomenclature was formalized in modern anatomical usage by Andreas Vesalius in his seminal 1543 publication De humani corporis fabrica, where he distinguished the maxilla as the paired bone forming the upper jaw.^[124] The component "sinus" stems from the Latin sinus, signifying a "bay," "curve," "fold," or "hollow," which by the early 15th century had been adapted in medical contexts to describe bodily cavities or recesses. Ancient physicians, including Galen in the 2nd century CE, employed the concept of such hollows to refer to natural voids within the body, laying groundwork for its application to paranasal structures.^[125][126] An alternative historical designation for the maxillary sinus is the "antrum of Highmore," honoring the English anatomist and surgeon Nathaniel Highmore (1613–1685), who first provided a detailed anatomical description of the structure in his 1651 treatise Corporis humani disquisitio anatomica. This eponymous term, often rendered as "Highmore's antrum," persisted in older medical literature to emphasize its cavernous nature, with "antrum" itself derived from Greek antron meaning "cave."^[19][4] In contemporary anatomical terminology, the maxillary sinus's drainage pathway is termed the ostium maxillare, a Latin phrase where ostium denotes an "opening" or "doorway," reflecting its role as the primary exit into the nasal cavity. This ostium communicates via the hiatus semilunaris, a crescent-shaped fissure whose name combines Latin hiatus ("gap" or "yawn," from hiare meaning "to gape") with semilunaris ("half-moon-like," from semi- "half" and luna "moon"), evoking its curved, semicircular form in the middle meatus. Such Latin-based terms maintain consistency in international medical nomenclature, as standardized by bodies like the Federative International Programme on Anatomical Terminologies.^[127]