Mycetoma / fungus ball

A sinus fungus ball (mycetoma) is a noninvasive accumulation of dense fungal hyphae within a paranasal sinus cavity, most characteristically the maxillary sinus.[1][2] It occurs in immunocompetent individuals and represents saprophytic colonization rather than tissue invasion.[1][3] The most common causative organism is Aspergillus fumigatus.[1][4] Pathogenesis is linked to impaired sinus ventilation and, in the maxillary sinus, frequently to odontogenic factors such as extruded endodontic materials or protruding dental implants that may serve as a nidus for fungal growth.[5][6] The signature imaging pattern is unilateral sinus opacification containing flocculent calcifications or metallic-density foci.[1][7] Management is surgical removal, which is usually curative without antifungal therapy.[2][3]

The term fungus ball is the currently preferred designation in otolaryngologic and radiologic literature, replacing the older term "mycetoma".[8][9] The 2025 AAO-HNS Clinical Practice Guideline explicitly notes that "fungus ball" was "previously termed 'mycetoma'".[8] The older term persists in some oral and maxillofacial radiology texts and should be recognized as synonymous. "Sinus mycetoma" and "sinonasal fungus ball" (SNFB) are accepted aliases.[10][11] The entity should not be confused with subcutaneous mycetoma (Madura foot), a chronic granulomatous soft-tissue infection caused by different fungi or actinomycetes that is endemic in tropical regions.[12] Within the classification of fungal rhinosinusitis, the fungus ball is categorized as a noninvasive form, distinct from allergic fungal rhinosinusitis (AFRS), chronic invasive, granulomatous invasive, and acute fulminant invasive fungal sinusitis.[2][11]

• Age and sex: Fungus balls predominantly affect middle-aged to older adults, with a mean age in the mid-to-late 50s and a female predominance (approximately 2:1 female-to-male ratio).[13][14]
• Sinus distribution: The maxillary sinus is involved in over 90% of cases. The sphenoid sinus is the next most common site; ethmoid and frontal sinus involvement is rare.[2][3][15]
• Laterality: Characteristically unilateral.[10]
• Odontogenic association: Odontogenic factors are identified in roughly half of maxillary sinus fungus balls, including extruded root canal treatment materials, protruding dental implants, periapical pathology, and oroantral communications. Fungus ball sides are significantly associated with sinus protrusion of endodontic filling materials and dental implants compared with the contralateral unaffected side.[5][14]
• Anatomic predisposition: Posterior nasal septal deviation toward the contralateral side and absence of concha bullosa or infraorbital (Haller) cells on the affected side have been identified as anatomic risk factors.[6]

Symptoms

A substantial proportion of patients are asymptomatic; the fungus ball may be discovered incidentally on dental or sinus imaging.[14] When symptomatic, common complaints include:

• Nasal obstruction and chronic unilateral nasal discharge
• Facial pain or pressure, typically over the affected maxillary sinus
• Cacosmia (fetid smell)[1]
• Postnasal drip

Examination findings

Nasal endoscopy is positive in roughly two-thirds of symptomatic patients, showing mucopurulent discharge at the middle meatus or polypoid mucosal changes.[14] Intraoral examination may reveal signs of odontogenic pathology in the posterior maxilla, including periapical radiolucency, failed endodontic treatment, or oroantral communication.

Tempo and complications

The clinical course is chronic and indolent. Bacterial superinfection with purulent sinusitis may coexist.[1] Apparent bony erosion on imaging reflects pressure-induced remodeling rather than fungal invasion.[1] Rare complications include extension toward the orbit or, in sphenoid sinus disease, proximity to the cavernous sinus.[3] Conversion to invasive fungal sinusitis is exceedingly rare in immunocompetent patients but is a recognized concern if immunosuppression develops.[10]

Red flags

Orbital symptoms (proptosis, diplopia), cranial neuropathy, or rapid clinical deterioration should prompt urgent evaluation for invasive fungal sinusitis, particularly in immunocompromised patients.[2][3]

Location and distribution

The maxillary sinus is the characteristic site, with the fungus ball typically occupying the dependent portion of the sinus.[3][7] Involvement is almost always unilateral. On panoramic radiography, the lesion appears as a radiopacity within the maxillary sinus, often partially or completely obscuring the normal sinus radiolucency. Because the maxillary sinus floor is intimately related to the posterior maxillary teeth, the finding is commonly encountered on routine dental imaging.

Periphery and shape

The fungus ball itself has an irregular, somewhat lobulated surface that is distinct from the smooth dome-shaped contour of a mucous retention cyst.[7][16] When the sinus is only partially opacified, the irregular surface of the intrasinus material is a characteristic discriminating feature.[7][17] Surrounding mucosal thickening is common, producing a peripheral rim of soft-tissue density that lines the sinus walls.

Internal architecture

• Calcifications: The hallmark internal feature is the presence of flocculent or punctate calcifications (intralesional hyperdensities) within the opacified sinus. These represent heavy metal deposition—primarily calcium and zinc—within fungal hyphae and are the most specific imaging characteristic. On panoramic radiographs, these appear as scattered radiopaque foci superimposed on the sinus opacification.[1][7][13][18]
• Metallic-density foci: Discrete spots of metallic density may be seen, sometimes related to extruded endodontic filling material (zinc oxide–based sealers, gutta-percha) that served as a nidus. Distinguishing intrinsic fungal calcification from iatrogenic foreign material can be challenging on conventional radiographs alone.[18][19]
• Fungus ball without intralesional hyperdensity: A minority of fungus balls lack visible calcification, making diagnosis more difficult. These cases are more commonly associated with male sex, diabetes mellitus, and adjacent odontogenic pathology.[13]

Effects on adjacent structures

• Sinus walls: Sclerosis of the lateral maxillary sinus wall is an occasional finding, reflecting chronic inflammation. Thinning or apparent erosion of the medial (inner) sinus wall is common and represents pressure remodeling rather than true invasion. The sinus floor may show remodeling adjacent to odontogenic pathology.[1][7][17]
• Teeth: The fungus ball itself does not directly affect teeth. However, the associated odontogenic source—periapical pathology, overextended endodontic filling, or a protruding implant—may be visible on dental radiographs and CBCT.[5][6]
• Ostiomeatal complex: Obstruction of the natural maxillary sinus ostium is common and contributes to retained secretions and secondary bacterial sinusitis.[17]

Extent and cortical involvement

The fungus ball is confined to the sinus lumen and does not invade bone. Apparent bony defects represent pressure-induced necrosis analogous to that seen in AFRS.[1] CBCT and medical CT can clarify whether bony thinning represents remodeling versus a true dehiscence, which is important for surgical planning and for excluding invasive disease.

Variants

• Complete versus partial opacification: Complete sinus opacification is seen in roughly half of cases; partial opacification with an irregular intraluminal surface is the next most common pattern.[7]
• Sphenoid sinus fungus ball: Rare but clinically significant because of proximity to the cavernous sinus and optic nerve; these cases may warrant postoperative antifungal therapy.[2][3]

CT (medical CT)

Contrast-enhanced CT demonstrates a centrally hyperattenuating fungal mass with peripheral mucosal enhancement in the majority of cases, even when calcifications are absent on non-contrast imaging.[15] This central hyperattenuation surrounded by enhancing inflamed mucosa is a useful diagnostic feature when intralesional calcification is not evident.[15][17] Sclerosis of the lateral sinus wall and erosion of the inner sinus wall are additional CT findings that help distinguish fungus ball from non-fungal chronic sinusitis, particularly in cases lacking calcification.[17]

MRI

On MRI, the fungal mass characteristically shows marked hypointensity (signal void) on T2-weighted images, surrounded by hyperintense inflamed mucosa—a pattern that can mimic an aerated sinus on cursory review.[15][20] On T1-weighted images, the fungal mass typically shows iso- to hyperintense signal, with high-signal foci present in the majority of cases; this T1 hyperintensity is attributed to paramagnetic metal accumulation within hyphae and is independent of calcification pattern.[20] MRI is most useful when CT findings are equivocal or when evaluating for possible extension beyond the sinus (orbital or intracranial involvement in sphenoid disease).[15]

The key diagnostic challenge is distinguishing a maxillary sinus fungus ball from other causes of unilateral sinus opacification, particularly when calcification is absent. The combination of unilateral opacification, intralesional calcification, irregular intraluminal surface, and an odontogenic association is highly suggestive.

The highest-risk diagnostic pitfall is failing to distinguish a noninvasive fungus ball from early invasive fungal sinusitis, particularly in patients with diabetes or immunosuppression. When bony erosion is present, sinus wall biopsy at the time of surgery should be considered to exclude mucosal invasion.[3]

Diagnostic microscopic findings

The fungus ball consists of a dense, matted conglomeration of fungal hyphae that is separate from but adjacent to the sinus respiratory mucosa.[1] The hyphae are septate and show dichotomous branching at approximately 45° angles, consistent with Aspergillus species.[4] Staining with Gomori methenamine silver (GMS) or periodic acid–Schiff (PAS) highlights the hyphal elements.[12] Calcium oxalate crystals may be identified within the fungal mass and are birefringent under polarized light.[19]

Key negative findings

• No allergic (eosinophilic) mucin, distinguishing the entity from AFRS[1]
• No fungal invasion of mucosa, blood vessels, or bone[1][3]
• The adjacent sinus mucosa shows a chronic, nongranulomatous inflammatory infiltrate of variable intensity[1]

Radiologic-pathologic correlation

The flocculent calcifications seen on imaging correspond to calcium and heavy metal (zinc, iron, manganese) deposition within fungal hyphae.[13][18] Fungal elements in the ball frequently have low viability, and cultures are often negative despite abundant hyphae on histology.[1] Molecular methods (PCR) on formalin-fixed tissue can identify the species when culture fails.[19]

Variants

Rare non-hyphal fungal structures such as cleistothecia, Hülle cells, and conidial heads have been reported within fungus balls, potentially complicating morphologic identification.[19] Aspergillus fumigatus is the most commonly identified species, followed by A. flavus and A. nidulans.[1][4]

Surgical treatment

Endoscopic sinus surgery (ESS) with removal of the fungus ball and wide maxillary antrostomy is the standard of care and is usually curative.[3][14] The Infectious Diseases Society of America (IDSA) 2016 guidelines recommend endoscopic removal for uncomplicated maxillary sinus fungus balls, noting that this approach achieves cure in the vast majority of cases.[3] The 2025 AAO-HNS guideline similarly identifies surgery as the primary treatment.[8]

Odontogenic source management