Frontal Cholesterol Granuloma in a Pediatric Patient: A Case Report

Abstract

Cholesterol granuloma (CG) is a benign expansile lesion caused by the breakdown of blood products and subsequent granulomatous reaction, most often found in pneumatized bones. Frontal sinus involvement is exceedingly rare, especially in children, and may mimic mucoceles, abscesses, or fungal disease on imaging. We present a 16-year-old male with a painful, progressively enlarging frontal swelling and headache. MRI revealed a lobulated lesion hyperintense on both T1- and T2-weighted sequences with peripheral enhancement, initially suggesting an abscess-like process. CT showed an expansile lytic lesion with erosion of the frontal sinus tables. Due to significant bony destruction, a bicoronal open approach was performed, achieving complete excision and cranioplasty. Histopathology confirmed CG, demonstrating cholesterol clefts, hemosiderin-laden macrophages, and multinucleated giant cells. The postoperative course was uneventful, and no recurrence was observed. This case highlights the diagnostic challenge of frontal sinus CG, particularly in younger patients, and emphasizes the importance of recognizing its radiologic characteristics to avoid misdiagnosis. Early identification and surgical excision are essential to prevent orbital or intracranial complications and achieve favorable clinical outcomes.

Keywords

cholesterol granuloma - frontal sinus - pediatric - paranasal sinus - abscess

Introduction

Cholesterol granuloma (CG) is a benign lesion that occurs after the accumulated blood in a pneumatized area degrades into components such as cholesterol crystals and starts a granulomatous foreign body reaction, which results in osteolytic enlargement with a fibrous capsule.[1] [2] Although the petrous apex is the most frequent cranial site, involvement of the frontal sinus remains exceptional and often leads to diagnostic confusion with infectious or cystic lesions.[2] Only 91 cases were reported for the frontal location between 1970 and 2021.[3] Other possible locations of CGs are the peritoneum, lungs, breast, lymph nodes, kidney, and testis.[4] Additionally, the most common age for CG to occur is in the 5th decade, and it is extremely rare to be seen in children.[2] [5] The frontal location and the nature of the tumor might resemble mucoceles, mycetoma, or abscess-like lesions, which should be kept in mind for differential diagnosis.[1] [2] Possible rhinorrhea and orbital complications with bone destruction emphasize the importance of early diagnosis and surgical resection of CG.

The purpose of this case report is to highlight the specific characteristics of this rare lesion in a rare location, which can assist radiologists, neurosurgeons, and ENT surgeons in accurate diagnosis, as appropriate management depends on timely recognition. We present a 16-year-old male patient with a CG in the frontal sinus, which caused serious bony erosion.

Case Presentation

Clinical Findings

A 16-year-old male presented with a 2-month history of a painful, progressively enlarging swelling over the frontal region, accompanied by headache. There was no history of trauma, sinusitis, or prior infection. On physical examination, a firm, immobile, and tender mass measuring ∼5 × 3 × 3 cm was palpated over the frontal bone. The overlying skin was intact, and there were no neurological deficits or nasal symptoms.

Radiologic Findings

Magnetic resonance imaging (MRI) demonstrated a lobulated lesion occupying both frontal sinuses and extending slightly toward the right side of the midline, measuring 53 × 31 × 37 mm. The lesion appeared hyperintense on T2-weighted FLAIR sequences, consistent with a loculated fluid collection ([Fig. 1]). Following intravenous gadolinium administration, there was marked peripheral enhancement, suggestive of an abscess-like process such as Pott's puffy tumor ([Fig. 2]).

Fig. 1 On T2 FLAIR magnetic resonance images, a hyperintense lesion localized in the left frontal sinus without intracranial invasion is observed.

Fig. 2 On contrast-enhanced T1 magnetic resonance images, peripheral contrast enhancement with a hypointense center, which is similar to an abscess-like process, is observed.

The lesion caused bony remodeling of the frontal bone, with exophytic expansion involving both the internal and external tables. There was also mild mass effect on the frontal lobes with posterior displacement, but no evidence of intracranial abscess formation. The brain parenchyma, ventricular system, and posterior fossa structures were unremarkable ([Fig. 2]).

Computed tomography (CT) of the paranasal region and 3D facial reconstruction revealed a 52 × 34 mm expansile, predominantly lytic lesion in the frontal bone, leading to thinning and partial destruction of the bony walls ([Fig. 3]). These findings were suggestive of a CG or possibly an infectious or necrotizing lesion of the frontal bone.

Fig. 3 Extent and the size of the lesion are demonstrated on axial (A) and sagittal (B) computed tomography images. The lesion caused expansion of both the outer and inner walls of the frontal sinus without dural invasion. (C) On 3D reconstructed computed tomography images, the lytic nature of the lesion on the outer wall of the frontal has been shown.

Surgical and Histopathological Findings

Under general anesthesia, a bifrontal approach was performed with a skin incision extending across the hairline. Outer tables of the underlying frontal bone and frontal sinus were eroded. Following reflection of the scalp flap, destructed bone fragments were identified and meticulously removed using a high-speed drill until the healthy bone was reached. The frontal sinus was fully exposed, and the dura mater was found to be intact and not affected by the lesion. The frontal sinus was repaired with pericranial fascia, and a synthetic dural graft was placed over the base of the frontal sinus and sealed with fibrin glue to ensure watertight closure. Subsequently, cranioplasty with a mesh reconstruction was performed. The lesion was completely excised. On gross examination, the specimen measured ∼3 × 3 × 1.5 cm, appeared cystic, and contained brownish material. Microscopic examination revealed cholesterol clefts, hemosiderin deposition, and multinucleated giant cells, confirming a diagnosis of CG ([Fig. 4]).

Fig. 4 Numerous cholesterol clefts surrounded by multinucleated, hemosiderin-laden giant cells (hematoxylin and eosin, 4 × ) (A) and cholesterol clefts with adjacent multinucleated giant cells and areas of hemorrhage (hematoxylin and eosin, 20 × ) (B) are shown.

Postoperative Course

The postoperative period was uneventful. The patient recovered without neurological or infectious complications and was discharged in good condition. At follow-up, no recurrence or residual lesion was detected on control imaging ([Fig. 5]). No rhinorrhea was observed.

Fig. 5 (A, B) Postoperative computed tomography images show the total resection and the resolution of the compression on the frontal lobe.

Discussion

CG can be found in different parts of the body, with a predisposition to pneumatized air cells. Possible locations are the peritoneum, lungs, breast, lymph nodes, kidney, and testis.[4] In the head and neck region, the petrous apex and middle ear are more common than paranasal sinuses.[6] Fewer than 200 CG cases have been reported for paranasal sinuses, with around 100 in the frontal sinus.[2] [3] [6] They most commonly occur in middle-aged men and are very rare to be seen in the pediatric population.[2] [5]

The pathogenesis of CG is traditionally described as impaired drainage and poor ventilation of pneumatized cells, causing local tissue degradation and deposition of crystallized cholesterol, which results in a granulomatous reaction.[3] However, occurrence in nonpneumatized locations such as the orbit cannot be explained by the same mechanism. In such cases, hemorrhage after minor trauma is thought to be the pathogenesis of CG.[1]

Radiological findings can be misdiagnosed as mucoceles, mycetoma, or Pott's puffy tumor as in our case report.[1] [2] On CT images, it is seen as a well-circumscribed homogeneous either hypodense or isodense mass which may cause bony erosion and expansion.[7] MRI images show hyperintensity on both T1- and T2-weighted images and low signal intensity on diffusion-weighted images due to the cholesterol content of the lesion. A hypointense hemosiderin ring may be seen on T2-weighted images in cases with chronic hemorrhage.[6] Enhancement in contrast-enhanced images is either absent or a very faint peripheral enhancement can be observed.[1] [8]

Most common histopathological findings of CG are cholesterol clefts along with foreign-body giant cells, foam cells, and macrophages that are laden with hemosiderin. Also, pieces of bone, epithelial residue, and fibrin could be present in the lesion.[1] [3]

Even though CGs are benign lesions, an enlarged mass could erode the walls of the sinuses, extend through the orbit, and may cause serious symptoms such as rhinorrhea, proptosis, and diplopia, which can lead to serious morbidity and even mortality if not treated properly. The ultimate treatment of CG is removal through surgical means.[2] The surgical approach depends on the characteristics of the lesion, such as location, extension, and consistency. Possible approaches to the paranasal sinus CG are open craniotomy, lateral orbitotomy, endoscopic sinus surgery, and transglabelar approach in selected cases.[1] [2] [6] [9]

In this case report, we present a rare pediatric (16-year-old) male patient. Radiological images revealed a hyperintense lesion on both T1- and T2-weighted images with a rare peripheral contrast enhancement on contrast-enhanced images. The most important feature of the CT was bony erosion on both tables of the frontal bone. Due to this erosion, we preferred to perform resection through a bicoronal open craniotomy, which resulted in total removal of the lesion without postoperative rhinorrhea.

In conclusion, early recognition and complete surgical excision remain essential to prevent complications in this entity. This case highlights the importance of considering CG in the differential diagnosis of expansile frontal bone lesions, even in young patients. Timely surgical intervention is key to preserving function and avoiding irreversible orbital or intracranial involvement.

Conflict of Interest

None declared.

Authors' Contributions

D.İ. and A.İ.Ö. contributed to the conception and design of the work. Data acquisition was carried out by D.İ. and S.U., while data analysis was performed by D.İ. and A.İ.Ö. Manuscript preparation was undertaken by D.İ. and S.U., and manuscript editing and review were completed by S.U. and A.İ.Ö.

Ethical Approval

This report was approved by the legal guardians of the patient and was conducted in accordance with the Declaration of Helsinki.

• References

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Publication History

Article published online:
06 February 2026