Olfactory Cleft Polyps: REAH or Glandular Hyperplasia

Purpose of Review The purpose of this paper is to review anatomic and pathophysiologic contributions to the development of polyposis in the olfactory cleft (OC). Recent Findings The past decade has seen a growing body of literature demonstrating that ethmoid-derived mucosa in the central compartment (CC) and OC is preferentially involved in a type 2–mediated inflammatory response to aeroallergens. This mechanism appears to be heavily involved in the polypoid diseases which involve the OC, including respiratory epithelial adenomatoid hamartoma (REAH), aspirin-exacerbated respiratory disease (AERD), and central compartment atopic disease (CCAD). Summary Non-neoplastic polypoid lesions of the OC frequently present with olfactory dysfunction and are associated with high rates of allergic sensitization. Further research is needed to elucidate the contribution of the complex inflammatory microenvironment in the OC to development of polypoid disease in this anatomic region.