The administration of ionizing radiation during CT scanning necessitates rigorous risk-benefit analysis before imaging pregnant individuals. While the radiation dose in a single nasal and sinus CT scan is typically below the level considered harmful to fetal development (50–100 mGy) (6), guidelines advise against performing the scan during the initial trimester of pregnancy and suggest cautious use in the second and third trimesters. However, terminating a pregnancy solely due to exposure to diagnostic-level radiation is not recommended. Adequate shielding for the abdomen is essential during the procedure. For instance, when necessary to detect bone damage, abnormal bone formation, or tumor changes, low-dose CT scans can be cautiously employed with proper abdominal shielding and the briefest scanning duration possible. Non-contrast CT has minimal impact on breast tissue and lactation, allowing immediate breastfeeding. Contrast-enhanced CT historically advised cessation of breastfeeding and discarding milk for 24 hours. However, less than 1% of water-soluble iodine contrast is excreted into breast milk, with infants receiving only 0.01% of the maternal dose. The American College of Radiology (ACR) and American College of Obstetricians and Gynecologists (ACOG) recommend continuing breastfeeding, suggesting increased water intake post-exam to enhance contrast agent elimination (7).

MRI is preferred during pregnancy and lactation due to its non-ionizing properties. However, gadolinium-based contrast agents (GBCAs) should be used cautiously as they cross the placental barrier. The ACR advises avoiding MRI in the first trimester unless clinically urgent, citing theoretical risks of fetal malformations, thermal injury, and hearing impairment (8). GBCAs are not recommended for pregnant women unless essential for diagnosis or prognosis, as they release toxic gadolinium ions in fetal circulation (9). For lactating women, non-contrast MRI is safe. GBCAs appear in breast milk at <0.04% of the maternal dose within 24 hours, with <1% absorbed by infants. The ACR states breastfeeding need not be interrupted, though a 24-hour pause may be considered (10). Informed consent is required before contrast-enhanced MRI.

A common benign tumor of sinus epithelial origin in the nasal cavity and paranasal sinuses, but it has a tendency for invasive growth, easy recurrence after surgery, and carcinogenesis (28). The onset of SNIP may be associated with HPV infection (29). The most common site of SNIP is the lateral wall of the unilateral nasal cavity near the middle meatus, and it spreads and fills the ipsilateral nasal cavity and paranasal sinuses, with the maxillary sinus being the most frequently affected. SNIP mainly affects men aged 40–70 years (30). The clinical manifestations lack specificity, and the common symptoms are mainly unilateral persistent and progressive nasal obstruction and anterior and/or posterior rhinorrhea. CT: Soft-tissue density, higher than that of the nasal concha and similar to muscle. Microcalcifications are present in 20% of cases (31). Large-sized SNIP causes compression and displacement of the middle and inferior nasal conchae and expansive changes of the maxillary sinus ostium bone with bone resorption. In some cases, a “bubble sign” can be seen during the process of the tumor filling the nasal cavity and paranasal sinuses, which represents the residual gas between the lesion and the intrinsic structures of the nasal cavity and paranasal sinuses. In some cases, bone hyperplasia and sclerosis occur at the base of the tumor, which is one of the signs suggesting SNIP. The reason is that the long-term inflammatory reaction at the origin site of SNIP stimulates osteogenesis. MRI: Iso-or slightly low signal on T1WI, heterogeneous slightly high signal on T2WI. The enhanced signal on T2WI and T1WI shows a striated structure with alternating high and low signals, often described as “convoluted cerebriform pattern, CCP”. CCP is one of the relatively characteristic imaging findings of SNIP. SNIP easily obstructs the ostiomeatal complex, thus leading to a large amount of mucus retention in the paranasal sinuses and obstructive sinusitis. MRI can easily distinguish the boundary between the tumor and inflammation. When necrosis occurs inside SNIP, the CCP signal is absent, and there is invasion of structures outside the nasal cavity and paranasal sinuses, the possibility of SNIP malignancy should be alerted (32) ( Figure 1 ).

A benign but invasive vascular tumor, accounting for 0.5% of all head and neck tumors (33). It mainly occurs in the sphenopalatine foramen or posterior nasal cavity. JNA is predominantly seen in adolescents and young males, rarely in females, with an average age of 17 years (34). The most common symptoms are unilateral nasal obstruction and recurrent epistaxis. It is prone to local invasion of the intracranial and orbital regions, which can cause headache and diplopia (35).CT: It is located in the sphenopalatine foramen area or centered in the pterygopalatine fossa, presenting as an expansively growing soft-tissue mass with a density similar to that of muscle. The adjacent sphenoid sinus and pterygoid process often show compression, reshaping, bone destruction, and enlargement of the sphenopalatine foramen. Recently, some scholars have proposed the Holman-Miller sign (36), which refers to the anterior bowing of the posterior wall of the maxillary sinus, resulting from bone remodeling and compression of the posterior wall of the maxillary sinus due to JNA growth. Since JNA is composed of blood vessels and a fibrocyte-rich extracellular matrix, it shows obvious and uniform enhancement on contrast-enhanced CT, with an enhancement degree almost equivalent to that of blood vessels. MRI: It shows isointense or hypointense signals on T1WI, similar to or slightly lower than the muscle signals. The signals on T2WI are heterogeneous, mainly because the vascular matrix shows hyperintense signals, while the fibrous components and vascular flow void effects show hypointense signals. Vascular flow void signals are seen inside and around JNA, which together with the hyperintense signals of the tumor parenchyma present the “salt-and-pepper sign”. The enhancement degree of JNA is significantly higher than that of the surrounding tissues. In addition, research reports that the ADC value of JNA is higher compared with other benign tumors (37).

A predominantly benign tumor originating from Schwann cells of peripheral nerves. Schwannomas occurring in the nasal cavity and paranasal sinuses account for 4% of those in the head and neck region (38). Most of them originate from the ophthalmic and maxillary branches of the trigeminal nerve or Schwann cells of the autonomic nerves, so they mainly occur in the sphenoid sinus, nasal septum, and the anterior part of the lateral nasal wall, followed by the maxillary sinus (39–41). Some schwannomas may be accompanied by intracranial extension. This disease is more common in middle-aged people aged 30–60 years, with no significant gender difference. The most common form is a unilateral tumor in the nasal cavity or paranasal sinuses, but bilateral tumors should raise a high suspicion of neurofibromatosis. The clinical manifestations are not characteristic. Larger tumors mainly present with nasal obstruction, decreased sense of smell, facial pain and numbness, and abnormalities in the eyeball and vision. CT shows a round-like, well-defined soft-tissue mass in one nasal cavity or paranasal sinus, with uniform density, and uneven density due to cystic degeneration and necrosis. Some tumors have punctate or strip-like calcifications. The tumor grows slowly. The bone in contact with the tumor shows bone resorption, thinning, and mild displacement, but bone destruction is rare. CT enhancement shows moderate to marked homogeneous enhancement, and the cystic area shows no enhancement. MRI: isointense or slightly hypointense on T1WI. T2WI shows heterogeneous hyperintensity, and the signal of the solid part is similar to that of the brainstem (41). Pathologically, schwannomas have an Antoni A area composed of solid parts and an Antoni B area composed of cystic parts. When the Antoni A area is located in the center of the lesion and the Antoni B area is located at the edge of the lesion, a characteristic “target sign” can be formed on T2WI, that is, slightly hypointense in the center of the lesion and hyperintense at the edge. The degree of MRI enhancement is the same as that of CT enhancement ( Figure 2 ).

EPAs are extremely rare tumors, and most of the statistical data are derived from case reports. EPAs are located outside the Sella turcica and originate from the anterior pituitary gland tissue. They are more common in middle-aged and elderly people aged 40-70, with no significant gender difference. Approximately 60% of the lesions are located in the sphenoid sinus and suprasellar region, followed by the clivus, nasal cavity, and cavernous sinus (42). This may be related to the migration path of the Rathke’s pouch during embryonic development (43). The clinical manifestations depend on the mass effect, invasive behavior, and hormone levels of the tumor. EPAs located in the cavernous sinus and clivus compress the cranial nerves, leading to visual impairment and facial paralysis (44). EPAs occurring in the sphenoid sinus can cause cerebrospinal fluid rhinorrhea (45). Since most tumors (75%) are functional, they can lead to Cushing’s syndrome, acromegaly, and hyperthyroidism (46). CT: The tumor appears as an isodense or slightly hyperdense mass. Expansive changes in the sphenoid sinus, bone resorption, or remodeling of the sphenoid sinus wall are common, but bone destruction is relatively rare. There is moderate to marked enhancement after contrast-enhanced CT. MRI: The tumor shows isointensity on T1WI, slightly hyperintensity on T2WI, and mild to moderate enhancement. Signal heterogeneity is caused by hemorrhage and cystic degeneration ( Figure 3 ).

A benign yet locally invasive tumor composed of osteoclast-like giant cells and osteoclast precursor cells. Less than 2% of GCTB occur in the head and neck. In cases involving the nasal cavity and paranasal sinuses, the lesions mainly occur in the sphenoid sinus (47, 48), followed by the maxillary sinus, and rarely in the nasal cavity. The affected population is mostly between 20 and 45 years old, with a median age of 25 years. The incidence in females is slightly higher than that in males (49). Since GCTB in the nasal cavity and paranasal sinuses mainly occurs in the sphenoid sinus, the clinical symptoms are mainly visual impairment, visual field defect, diplopia, hyposmia, and pituitary dysfunction. On CT, GCTB appears as a soft-tissue density mass with expansive bone destruction, but most of the bone cortex is intact, and periosteal reaction is basically invisible. It shows low or isointense signals on T2WI, and the low signal on the T2WI sequence is of great significance for the diagnosis of GCTB. T1WI shows a heterogeneous signal mainly with low signal. Of course, the “soap bubble” sign is also one of the important signs for the diagnosis of GCTB. The obvious circular T2WI low signal intensity around the tumor is an important feature of atypical GCTB, which is consistent with the feature of circular T2 low signal around the tumor of GCTB occurring in long bones reported in the literature (50) ( Figure 4 ).

The most common malignant tumor of the nasal cavity and paranasal sinus mucosal epithelium, accounting for 80% of nasal cavity and paranasal sinus malignancies (51). It is more common in men over 50 years old. The etiological factors for tumorigenesis include: smoking, chronic inflammation, nasal polyps, irritation from nickel, arsenic, chromium, leather, dust, isopropyl alcohol, etc., low immunity, malignant transformation of inverted papilloma, radiotherapy, and HPV infection (52). Moreover, the latest literature supports that HPV-positive SCC has a better prognosis than HPV-negative SCC (53–55). SCC occurs in the maxillary sinus (60%) and nasal cavity (25%), and less frequently in the ethmoid sinus, frontal sinus, and sphenoid sinus (56). CT: A unilateral irregular soft- tissue mass. Generally, the tumor is relatively large in size, with non-uniform density, unclear boundaries, disappearance of the maxillofacial fat space, involvement of adjacent sinuses and nasal cavity, and obvious bone destruction, resulting in the disappearance of the normal contour of the nasal cavity and paranasal sinuses. MRI: The SCC tumor itself shows low or equal signal on T1WI and slightly high signal on T2WI. Cystic changes and hemorrhage are commonly seen inside larger SCCs, and the signals of cystic changes are often located in the center of the tumor. MRI enhancement: Small-sized SCCs show uniform enhancement, while larger lesions show non-uniform enhancement, mostly moderate to severe non-uniform enhancement. The ADC value is usually higher than that of lymphoma but lower than that of ACC (57). Regional lymph node metastasis of SCC in the nasal cavity and paranasal sinuses is very common ( Figure 5 ).

A malignant tumor originating from salivary gland epithelium, it is the most common malignant tumor of minor salivary glands in the head and neck. ACC occurring in the nasal cavity and paranasal sinuses is generally considered to originate from ectopic minor salivary glands here, accounting for 10%-20% of head-and-neck ACC. In statistical cases of nasal cavity and paranasal sinus ACC, the maxillary sinus is the most commonly affected site, followed by the nasal cavity, ethmoid sinus, and sphenoid sinus. The disease occurs between the ages of 5 and 60, with a slight female predominance (58–60). The tumor grows slowly with insidious symptoms. Regional lymph node metastasis is rare, but hematogenous metastasis mainly to the lungs is common. ACC appears as a relatively large mass on CT or MRI. CT: It presents as a large, “ginger-shaped” soft-tissue mass. In the pathological classification, ACC of cribriform and tubular types shows cystic areas of varying sizes, while the solid-type ACC with the highest malignancy grade does not show cystic areas. The bone destruction of the paranasal sinuses by ACC often shows both expansile and erosive features, and the degree of bone destruction by ACC is lower than that by SCC. Nerve invasion is a characteristic manifestation of ACC. On CT, the enlargement and bone destruction of the pterygopalatine fossa and its adjacent foramina such as the foramen rotundum, foramen ovale, and foramen spinosum highly suggest ACC.

MRI: The signal on T1WI and T2WI is mainly isointense. The cribriform and tubular types of ACC show dense and uniformly-sized cystic areas. Due to different cystic components, T1WI may show high or low signal. The solid-type ACC shows no cystic areas, and the signal on T2WI is significantly reduced. Typical ACC show relatively low signal on DWI, and the ADC value is higher than that of other pathological types of malignant tumors. The nerve invasion of ACC on MRI is manifested as nerve thickening, enhancement, disappearance of normal nerve structure accompanied by a soft-tissue mass, disappearance of perineural fat signal, and atrophy of the muscles innervated by the nerve, etc. (14) ( Figure 6 ).

In 2022, the WHO defined SNUC as a high-grade epithelial tumor without any lineage differentiation (61). Currently, most literature supports that SNUC is a surface (Schneiderian) epithelial-derived malignancy (62). SNUC can occur across a wide age range (20–90 years), with a median age of 50–60 years, and it is slightly more prevalent in males than females. Nasal obstruction and epistaxis are common clinical symptoms. Proptosis, visual impairment, and cranial nerve palsy may be observed as the disease progresses (63). SNUC is difficult to cure completely and has a very poor prognosis. Recurrence, lymph node metastasis, and distant metastasis are more common than in other malignancies. Literature reports that approximately 10%-30% of SNUC patients have lymph node metastasis at the time of diagnosis (64). SNUC typically arises in the ethmoid sinuses and the roof of the nasal cavity, often involving multiple sinuses. It is difficult to determine the origin of large tumors, and they can easily cause bone destruction and involve the orbit, pterygopalatine fossa, cavernous sinus, parapharyngeal space, and the dura mater of the anterior/middle cranial fossa (65). On CT, it appears as an irregular soft tissue mass with a blurred border and uniform density, but shows heterogeneous enhancement after contrast administration. MR signals are not significantly specific ( Figure 7 ). Necrosis may occur in large tumors (>4 cm), with marked heterogeneous enhancement. The diagnosis of SNUC relies on pathology and requires the exclusion of other malignancies in the nasal cavity and paranasal sinuses. CT and MRI are mainly used for tumor localization and to determine the extent of the lesion for Tumor Node Metastasis (TNM) or Kadish staging (66).

Malignant tumors originating from the neural crest of the olfactory nerve epithelium are generally considered to be distributed in the olfactory region. Therefore, the tumors usually have a specific site of onset-the top of the nasal cavity or the lateral wall near the middle turbinate. The incidence accounts for approximately 3%-5% of malignant tumors in the nasal cavity and paranasal sinuses, with a slightly higher prevalence in males than females. According to the 5th edition of WHO, the age of onset ranges from 2 to 90 years, with a peak at 50–60 years (67). Recent studies have found that ONB in patients under 40 years old is not uncommon, and the grade is often higher (68).In the early stage, ONB is confined to the top of the nasal cavity. In the advanced stage, the tumor often involves multiple paranasal sinuses, the orbit, the optic nerve, and the frontal lobe brain parenchyma. The most common clinical symptom is nasal congestion. Other common symptoms include recurrent epistaxis and loss of smell. In the advanced stage, ONB may present with epiphora, diplopia, exophthalmos, and decreased visual acuity. When the frontal lobe is involved, headache and epilepsy may occur. Unilateral symptoms are more obvious than bilateral ones. CT findings show a “dumbbell-shaped” or “mushroom-shaped” mass located at the top of the nasal cavity and the anterior cranial fossa. When the mass is small, it has uniform density, similar to that of muscle. When the tumor is large, there are patchy necrosis and calcification. Most ONBs cause bone destruction in the ethmoid sinus, the orbital roof, and the frontoethmoidal complex. After enhancement, the solid part of ONB shows moderate to marked enhancement, and liquefactive necrosis leads to uneven enhancement of the tumor. MRI: Compared with muscle signals, ONB shows isointensity on T1WI and mainly slightly high-intensity on T2WI. Necrosis and calcification inside large tumors result in uneven tumor signals. The degree of enhancement on MRI is similar to that on CT. The latest research suggests that cystic changes at the edge of intracranial-involved tumors are indicative of ONB (69, 70) ( Figure 8 ).

Rarely, it is a highly invasive malignant tumor. Its incidence in the nasal cavity and paranasal sinuses is approximately 4% (71, 72). The nasal cavity and paranasal sinuses are the predilection sites for MSM (accounting for about 80%), with the nasal cavity being more commonly affected than the paranasal sinuses. In the nasal cavity, the anterior lower part of the nasal septum is a common site, and in the paranasal sinuses, the maxillary sinus is frequently involved (73, 74). MSM often occurs unilaterally in the nasal cavity and paranasal sinuses, so the common clinical manifestations are unilateral nasal obstruction and epistaxis (75). Essentially, most of these tumors contain melanin, but 10%-30% of the lesions are hypopigmented or amelanotic melanomas. The population distribution is mainly among those aged 50–80 years, with no significant gender difference. Due to the rich blood supply and lymphatic drainage in the head and neck region, MSM is highly invasive, has a high recurrence rate, and is prone to multiple recurrences. In the advanced stage, it is likely to metastasize to the lungs, brain, bones, and liver. The literature reports that 10%-20% of MSM cases in the nasal cavity and paranasal sinuses present with cervical lymph node metastasis at the time of onset (76).CT findings: MSM shows an isodense appearance. Larger MSMs can cause compression of the adjacent paranasal sinus accompanied by varying degrees of bone destruction.

MRI findings: Referring to the muscle signal, typical pigmented MSM appears hyperintense on T1WI and hypointense on T2WI. Hypopigmented or amelanotic melanomas show low, isointense, or slightly hyperintense signals on T1WI and slightly hyperintense or hyperintense signals on T2WI. MSM has a relatively high tendency to bleed (approximately 50%), but there is usually hemosiderin deposition around the bleeding area, which can be distinguished from melanin. Due to the relatively rich blood supply of MSM, it shows obvious enhancement on both CT and MRI. The contrast-enhanced scan sequence can also provide a reference for distinguishing melanin, high-protein secretions, and bleeding lesions. The literature reports that the ADC value of MSM is generally lower than that of SCC (77).

“A septate pattern” (a sign of alternating high and low signals on non-contrast T1WI) may also highly suggest MSM (78) ( Figure 9 ).

RMS is the most common malignant tumor in children and adolescents, mostly occurring in individuals under 20 years of age, and more prevalent in males than females (16, 79, 80). RMS originates from primitive mesenchymal cells that differentiate into skeletal muscle. 35%-40% of rhabdomyosarcomas occur in the head and neck region, and approximately 10-15% of head and neck rhabdomyosarcomas occur in the nasal cavity (81). Embryonal RMS (ERMS) is the most common subtype, followed by alveolar RMS (ARMS) (82), and the prognosis of ERMS is better than that of alveolar RMS.RMS is highly malignant and prone to invade adjacent tissues. Hematogenous metastasis is the main mode of metastasis for ERMS, which easily involves the bone marrow, lungs, cerebrospinal fluid, and abdominal organs, while lymph node metastasis is more common in ARMS.CT findings show a homogeneous soft-tissue density mass with obvious adjacent bone destruction. Larger tumors may have low-density liquefactive necrosis areas, and calcification is rare. ERMS is more likely to present with necrosis or mucoid degeneration than ARMS. After contrast-enhanced CT, the tumor shows moderate to marked heterogeneous enhancement, with a higher enhancement degree than that of muscle. MRI findings: On T1WI, the tumor shows isointense or slightly hypointense signals, and the hemorrhage within the tumor appears as hyperintense signals on T1WI. On T2WI, it shows heterogeneous hyperintense signals (presumably due to intratumoral hemorrhage, necrosis, and residual bone), but the overall signal is slightly higher than that of muscle. The enhancement pattern after contrast-enhanced MRI is similar to that of contrast-enhanced CT. Typical ERMS shows linear, circular, or grape-cluster-like enhancement, while ARMS mostly shows relatively homogeneous enhancement of solid components, and ARMS is more likely to invade the skull than ERMS (83) ( Figure 10 ). Literature reports indicate that ADC of RMS in the nasal cavity and paranasal sinuses is 0.992 ± 0.133×10–3 mm2/s, which is significantly lower than that of paranasal sinus carcinomas (84).

A rare aggressive tumor. Currently, the literature reporting this tumor mainly consists of case reports or small-sample studies. The SNTCS tumor has a complex composition, predominantly containing neuroepithelial components, mixed with stromal components and a small amount of epithelial components. It mostly occurs in the nasal cavity, followed by the ethmoid sinus and maxillary sinus. The incidence in males is 7 times that in females (85–88), with an average onset age of 60 years, and it is rare in children (89, 90). The clinical symptoms are not significantly specific. In the early stage, it is mainly characterized by unilateral nasal obstruction, epistaxis, and hyposmia. In the advanced stage, due to tumor invasion of the alveolus, orbit, and intracranial region, symptoms such as toothache, decreased vision, headache, and epilepsy may occur (87). CT shows an irregularly shaped soft tissue mass in the unilateral nasal cavity or sinus, with uniform density, and rare small cystic changes and calcification. There is obvious destruction of the sinus bone wall, nasal septum, pterygopalatine fossa, and skull base bone. MRI shows isointense or slightly hypointense signals on T1WI and slightly hyperintense signals on T2WI, with obvious heterogeneous enhancement on contrast-enhanced scanning ( Figure 11 ). The imaging diagnosis lacks characteristic features and is easily misdiagnosed as olfactory neuroblastoma, squamous cell carcinoma, and undifferentiated carcinoma of the nasal cavity and paranasal sinuses (91). The definitive diagnosis mainly relies on pathology. The latest pathological research suggests that most teratoid carcinosarcomas are associated with SMARCA4 gene defects (92).

Lymphoma is a common type of malignant tumors in the nasal cavity and paranasal sinuses, with diffuse large B-cell lymphoma (DLBCL) and NK/T-cell lymphoma (NKTCL) being the two most common subtypes (93). Both subtypes are more prevalent in males.

Metastatic tumors of the nasal cavity and paranasal sinuses are particularly rare, and the literature mainly focuses on case reports. The primary tumors reported in the literature mainly originate from the lungs, liver, kidneys, thyroid, prostate, breast, and colon (96–100), with renal cancer metastases being the most common. The most likely metastatic route is hematogenous metastasis (101). It is speculated that tumor cells reach the head and neck via the systemic circulation, pass through the pterygoid plexus and cavernous sinus, and move retrogradely to the nasal cavity and paranasal sinuses. Due to the slow blood flow here, tumor cells can easily detach from the circulation and implant, leading to the growth of metastatic tumors. The speculated metastatic routes of metastases from the liver and lungs may be related to the paravertebral venous plexus and thoracic duct (102). Metastatic tumors of the nasal cavity and paranasal sinuses are generally located in the maxillary sinus. The clinical symptoms lack specificity, typically presenting as facial pain, recurrent epistaxis, and nasal obstruction. The imaging findings also lack specificity, usually showing single or multiple lesions. On CT, they appear as soft-tissue masses with obvious bone destruction, and large-sized tumors may have necrosis, cystic changes, or hemorrhage. On MRI, the T2WI signal is mostly heterogeneous. Due to the rich blood supply of metastatic tumors, they show moderate to marked heterogeneous enhancement, and DCE- MRI indicates the characteristic of high tumor perfusion. Some researchers have summarized that for middle-aged and elderly patients presenting with nasal obstruction or epistaxis, if imaging reveals isolated or multifocal, hypervascular lesions centered on bone destruction in the nasal cavity and paranasal sinuses, combined with the clinical history, metastatic tumors should be included in the common diagnoses (103) ( Figure 14 ).

Osteosarcoma most commonly occurs in the metaphysis of long bones. Osteosarcoma located in the head and neck is rare, accounting for 15% of all osteosarcomas in the body. It mainly occurs in the mandible, followed by the maxilla, and is even rarer in the nasal cavity and paranasal sinuses (104). The median age of onset is 40 years (105). The clinical manifestations are non-specific and are often related to the site of onset. Since most lesions are located in the maxilla and mandible, the common symptoms are mostly facial masses, loose or fallen teeth. When the mass involves the nasal cavity and paranasal sinuses, epistaxis and nasal obstruction occur on this basis. There is an elevation of alkaline phosphatase in serology. The imaging manifestations are similar to those of long-bone osteosarcoma, showing both osteogenic and osteolytic features. CT shows an irregular soft-tissue mass with unclear boundaries, bone destruction accompanied by periosteal reaction. The typical ivory, cotton-wool and radial tumor bones inside the mass highly suggest the diagnosis of osteosarcoma. Due to the diverse internal components of osteosarcoma, the MRI signals are also mixed and variable. However, the tumor bone and periosteal reaction with low signals on both T1WI and T2WI can also suggest the diagnosis ( Figure 15 ).