Institutional members access full text with Ovid®

Share this article on:

Atrophic rhinosinusitis: progress toward explanation of an unsolved medical mystery

deShazo, Richard D; Stringer, Scott P

Current Opinion in Allergy and Clinical Immunology: February 2011 - Volume 11 - Issue 1 - p 1–7
doi: 10.1097/ACI.0b013e328342333e
Rhinitis, sinusitis and upper airway disease: Edited by Ruby Pawankar and David P. Skoner

Purpose of review Atrophic rhinosinusitis is a chronic condition associated with considerable morbidity and decreased quality of life. This review describes progress in the characterization of primary and secondary atrophic rhinosinusitis and the development of diagnostic criteria for both syndromes.

Recent findings Primary atrophic rhinitis usually develops as a consequence of an acute febrile illness in members of lower socioeconomic groups in developing areas of the world. The clinical setting and presence of culturable Klebsialla ozenae in the purulent, foul-smelling, nasal discharge of these patients forms the basis for diagnosis. An animal model for the disease exists in swine in which case an effective vaccine has been developed.

Secondary atrophic rhinosinusitis is a condition that follows destruction of the nasal mucosa by any of a number of inflammatory processes including inflammatory diseases nasal/sinus surgery, and antiangiogenic therapy. Diagnostic criteria include patient reported recurrent epistaxis or episodic anosmia; or physician documented nasal purulence, nasal crusting, chronic inflammatory disease involving the upper airway (e.g. sarcoidosis, Wegener's granulomatosis, etc.) or two or more sinus surgeries. Patients with two more of these have secondary atrophic rhinitis with a sensitivity of 0.95 and a specificity of 0.77.

Summary Atrophic rhinosinusitis results from destruction of the normal respiratory epithelium and transition to a nonciliated squamous epithelium, loss of mucociliary clearance, accumulation of stagnant mucous. That milieu facilitates acute and chronic infection (wet phase), and eventual sclerosis with epistaxis and chronic bloody crusts (dry phase).

aDepartment of Medicine, Division of Clinical Allergy and Immunology, USA

bDepartment of Otarlaryngology, University of Mississippi Medical Center, Jackson, Mississippi, USA

Correspondence to Richard D. deShazo, MD, Department of Medicine, University of Mississippi Medical Center, 2500 N. State Street, Jackson, MS 39216-4505, USA E-mail:

Copyright © 2011 Wolters Kluwer Health, Inc. All rights reserved.