Rhinosinusitis pathophysiology: Difference between revisions
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Dima Nimri, M.D. [2]
Overview
The pathophysiology for both acute and chronic rhinosinusitis involves blockage of the nasal sinuses and inflammation of the nasal sinuses. However, biofilms play a role in the pathogenesis of chronic rhinosinusitis. There are many associated conditions with rhinosinusitis, but most notably are those related to allergy and immunodeficiency.
Pathophysiology
Pathogenesis
Acute Rhinosinusitis
Allergens, infections, and other disease processes can cause inflammation and swelling of the nasal mucosa. When the sinus opening becomes blocked due to swelling of the nasal mucosa, it provides a medium for an inflammatory response to ensue and prevents the clearing of pathogens. Inflammation is mediated by protease in granulocytes and if the amount of protease overwhelms the amount of protease inhibitors available, tissue destruction will take place.[1]
Chronic Rhinosinusitis
Biofilms are complex aggregates of extracellular matrix and inter-dependent microorganisms from multiple species, many of which may be difficult or impossible to isolate using standard clinical laboratory techniques. Bacteria found in biofilms may show increased antibiotic resistance when compared to free-living bacteria of the same species. It has been hypothesized that biofilm-type infections may account for many cases of antibiotic-refractory chronic sinusitis. While biofilms have been implicated in the pathogenesis of chronic sinusitis, their role in causing inflammation and disease is not fully understood.[2][3][4]
Genetics
Chronic rhinosinusitis is believed to be the result of environmental and genetic factors combined. The role of genetic factors in chronic rhinosinusitis is not yet fully understood.[5] However, in chronic rhinosinusitis with and without nasal polyposis, first and second degree relatives conferred an increased risk to receiving the same diagnosis.[6]
Associated Conditions
- Allergies, such as hay fever[7]
- Asthma[8]
- Nasal Polyposis[9]
- Cilia disorders, such as cystic fibrosis and Kartagener Syndrome[10]
- Wegener's Granulomatosis[11]
- Humoral immunodefiency, such as IgA deficiency and X-linked agammaglobulinemia[11]
Gross Pathology
On gross examination of the sinuses, polyps may appear as transparent and pedunculated masses. In sinusitis, changes include minimal edema and thickening of the mucosa.[12]
Microscopic Pathology
Rhinosinusitis can present with the following microscopic findings;[12]
- Acute Bacterial Sinusitis: Inflammatory infiltrate is dominated by neutrophils.
- Allergic Rhinosinusitis: Inflammatory infiltrate is dominated by eosinophils.
- Chronic Rhinosinusitis: Mixed inflammatory infiltrate of lymphocytes, plasma cells, eosinophils, neutrophils, and macrophages.
References
- ↑ Lundberg C, Engquist S (1983). "Pathogenesis of maxillary sinusitis". Scand J Infect Dis Suppl. 39: 53–5. PMID 6580734.
- ↑ Harvey RJ, Lund VJ (2007). "Biofilms and chronic rhinosinusitis: systematic review of evidence, current concepts and directions for research". Rhinology. 45 (1): 3–13. PMID 17432062.
- ↑ Palmer JN (2005). "Bacterial biofilms: do they play a role in chronic sinusitis?". Otolaryngol. Clin. North Am. 38 (6): 1193–201, viii. PMID 16326178.
- ↑ Sanclement J, Webster P, Thomas J, Ramadan H (2005). "Bacterial biofilms in surgical specimens of patients with chronic rhinosinusitis". Laryngoscope. 115 (4): 578–82. PMID 15805862.
- ↑ Al-Shemari H, Bossé Y, Hudson TJ, Cabaluna M, Duval M, Lemire M, Vallee-Smedja S, Frenkiel S, Desrosiers M (2008). "Influence of leukotriene gene polymorphisms on chronic rhinosinusitis". BMC Med. Genet. 9: 21. doi:10.1186/1471-2350-9-21. PMC 2292155. PMID 18366797.
- ↑ Oakley GM, Curtin K, Orb Q, Schaefer C, Orlandi RR, Alt JA (2015). "Familial risk of chronic rhinosinusitis with and without nasal polyposis: genetics or environment". Int Forum Allergy Rhinol. 5 (4): 276–82. doi:10.1002/alr.21469. PMID 25677865.
- ↑ Christodoulopoulos P, Cameron L, Durham S, Hamid Q (2000). "Molecular pathology of allergic disease. II: Upper airway disease". J. Allergy Clin. Immunol. 105 (2 Pt 1): 211–23. PMID 10669839.
- ↑ Slavin RG (2008). "The upper and lower airways: the epidemiological and pathophysiological connection". Allergy Asthma Proc. 29 (6): 553–6. doi:10.2500/aap.2008.29.3169. PMID 19173781.
- ↑ Meltzer EO, Hamilos DL (2011). "Rhinosinusitis diagnosis and management for the clinician: a synopsis of recent consensus guidelines". Mayo Clin. Proc. 86 (5): 427–43. doi:10.4065/mcp.2010.0392. PMC 3084646. PMID 21490181.
- ↑ Le C, McCrary HC, Chang E (2016). "Cystic Fibrosis Sinusitis". Adv. Otorhinolaryngol. 79: 29–37. doi:10.1159/000444959. PMID 27466844.
- ↑ 11.0 11.1 Ryan MW (2008). "Diseases associated with chronic rhinosinusitis: what is the significance?". Curr Opin Otolaryngol Head Neck Surg. 16 (3): 231–6. doi:10.1097/MOO.0b013e3282fdc3c5. PMID 18475077.
- ↑ 12.0 12.1 Thompson, Lester D. R. Head and Neck Pathology. Elsevier Health Sciences. p. 3. ISBN 9781437726077.