Abstract

To propose a new hypothesis that attempts to explain the pathogenesis of petrous apex cholesterol granuloma (PA CG). CLASSIC OBSTRUCTION-VACUUM HYPOTHESIS: PA CGs form when mucosal swelling blocks the circuitous pneumatic pathways to the apical air cells. Trapped gas resorption results in a vacuum that triggers bleeding, and CG forms through anaerobic breakdown of blood products. PROBLEMS WITH THE CLASSIC (OBSTRUCTION-VACUUM) HYPOTHESIS: Impaired ventilation of mucosa-lined pneumatic tracts in the middle ear, mastoid, paranasal sinuses, and lung are very common, but CG is rare. The extraordinary levels of temporal bone pneumatization typically observed in PA CG cases is indicative of excellent ventilation and freedom from inflammatory mucosal disease. Were under pressure due to gas absorption alone sufficient to trigger hemorrhage, CG ought to be frequent in otitis media with effusion.The opposite PA of 13 patients with PA CG compared with 31 highly pneumatic PAs in patients undergoing imagery for non-otologic reasons.The nature of the bony partition, as seen on computed tomography, between the PA air cell system and the adjacent marrow compartment.4 of 13 PAs with CGs on the opposite side showed deficient septation between air cells and marrow, whereas this was not observed in any of the 31 extensively pneumatized normal ears. NEW HYPOTHESIS (EXPOSED MARROW): As cellular tracts penetrate the apex during young adulthood, budding mucosa invades and replaces hematopoietic marrow. The bony interface becomes deficient, with coaptation of richly vascular marrow and the mucosal air cell lining. Hemorrhage from the exposed marrow coagulates within the mucosal cells and occludes outflow pathways. Sustained hemorrhage from exposed marrow elements provides the engine responsible for the progressive cyst expansion. As the cyst expands, bone erosion increases the surface area of exposed marrow along the cyst wall. This exposed marrow theory explains the unique proclivity of the healthy and well-pneumatized PA to form a CG.

View details for Web of Science ID 000180314500020

View details for PubMedID 12544037