Mastoiditis pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
Mastoiditis is the infection in the cavities of [[mastoid process]] of [[temporal bone]] that occurs after [[otitis media]]. At birth, the [[mastoid]] consists of a single cavity, which is connected to the [[middle ear]] by a canal. As the child grows, the [[mastoid bone]] becomes pneumatized, resulting in a series of connected cavities, lined by a [[mucosa]] diverted from respiratory epithelium. There is a relationship between the [[middle ear]], [[eustachian tube]], and the [[mastoid]]. This connection has a fundamental role in the pathogenesis of mastoiditis. In the setting of [[acute otitis media]] the [[mucosa]] that lines the middle ear and also [[mastoid air cells]] becomes inflamed. In majority cases of [[acute otitis media]] inflammation resolves, but some persist leading to bacterial and fluid accumulation within the [[mastoid air cells]]. Gradually, as a result of pressure rising in the [[mastoid]], air cell septae may be destroyed and mastoiditis could be proceed to [[Periostitis|periostitis,]] cavity [[abscess]] and [[osteomyelitis]]. Mastoid is near vital organs in head and neck and mastoid infection may cause serious complications. There is evidence of genetic predisposition to recurrent otitis media and therefore mastoiditis, with statistically significant evidence that it has high heritability. The following genes have been identified as having potential pathogenic qualities for [[otitis media]]: ''CAPN14'', ''GALNT14'', ''BPIFA3'', ''BPIFA1'', ''[[BMP5]]'', ''GALNT13'', ''[[NELL1]]'', ''TGFB3''. Up-regulation of the genes correlated to [[Otitis media|recurrent otitis media]] pathogenesis contribute to individual susceptibility to mastoiditis. | |||
== Pathophysiology == | == Pathophysiology == | ||
=== Pathogenesis === | === Pathogenesis === | ||
Mastoiditis is the infection in the cavities of [[mastoid process]] of [[temporal bone]] that occurs after [[otitis media]]. At birth, the [[mastoid]] consists of a single cavity, which is connected to the [[middle ear]] by a canal. As the child grows, the [[mastoid bone]] becomes pneumatized, resulting in a series of connected cavities, lined by a [[mucosa]] diverted from respiratory epithelium. There is a relationship between the [[middle ear]], [[eustachian tube]], and the [[mastoid]]. This connection has a fundamental role in the pathogenesis of mastoiditis. In the setting of [[acute otitis media]] the [[mucosa]] that lines the middle ear and also [[mastoid air cells]] becomes inflamed. In majority cases of [[acute otitis media]] inflammation resolves, but some persist leading to bacterial and fluid accumulation within the [[mastoid air cells]]. Gradually, as a result of pressure rising in the [[mastoid]], air cell septae may be destroyed and mastoiditis could be proceed to [[periostitis]], cavity [[abscess]] and [[osteomyelitis]]. | Mastoiditis is the infection in the cavities of [[mastoid process]] of [[temporal bone]] that occurs after [[otitis media]]. | ||
At birth, the [[mastoid]] consists of a single cavity, which is connected to the [[middle ear]] by a canal. As the child grows, the [[mastoid bone]] becomes pneumatized, resulting in a series of connected cavities, lined by a [[mucosa]] diverted from respiratory epithelium. There is a relationship between the [[middle ear]], [[eustachian tube]], and the [[mastoid]]. This connection has a fundamental role in the pathogenesis of mastoiditis. In the setting of [[acute otitis media]] the [[mucosa]] that lines the middle ear and also [[mastoid air cells]] becomes inflamed. In majority cases of [[acute otitis media]] inflammation resolves, but some persist leading to bacterial and fluid accumulation within the [[mastoid air cells]]. Gradually, as a result of pressure rising in the [[mastoid]], air cell septae may be destroyed and mastoiditis could be proceed to [[periostitis]], cavity [[abscess]] and [[osteomyelitis]]. | |||
* [[Mastoid]] is near important structures like the [[facial nerve]], [[sternocleidomastoid muscle]], [[jugular vein]], [[internal carotid artery]], [[sigmoid sinus]], [[brain]], and [[meninges]]; as a result of this proximity, spreading infection to these places may cause complications.<ref name="pmid197344392">{{cite journal|year=2010|title=Clinical strategies for the management of acute mastoiditis in the pediatric population|url=|journal=Clin Pediatr (Phila)|volume=49|issue=2|pages=110–5|doi=10.1177/0009922809344349|pmid=19734439|vauthors=Lin HW, Shargorodsky J, Gopen Q}}</ref><ref name="pmid197587112">{{cite journal|year=2009|title=Mastoiditis in a paediatric population: a review of 11 years experience in management|url=|journal=Int. J. Pediatr. Otorhinolaryngol.|volume=73|issue=11|pages=1520–4|doi=10.1016/j.ijporl.2009.07.003|pmid=19758711|vauthors=Pang LH, Barakate MS, Havas TE}}</ref> | * [[Mastoid]] is near important structures like the [[facial nerve]], [[sternocleidomastoid muscle]], [[jugular vein]], [[internal carotid artery]], [[sigmoid sinus]], [[brain]], and [[meninges]]; as a result of this proximity, spreading infection to these places may cause complications.<ref name="pmid197344392">{{cite journal|year=2010|title=Clinical strategies for the management of acute mastoiditis in the pediatric population|url=|journal=Clin Pediatr (Phila)|volume=49|issue=2|pages=110–5|doi=10.1177/0009922809344349|pmid=19734439|vauthors=Lin HW, Shargorodsky J, Gopen Q}}</ref><ref name="pmid197587112">{{cite journal|year=2009|title=Mastoiditis in a paediatric population: a review of 11 years experience in management|url=|journal=Int. J. Pediatr. Otorhinolaryngol.|volume=73|issue=11|pages=1520–4|doi=10.1016/j.ijporl.2009.07.003|pmid=19758711|vauthors=Pang LH, Barakate MS, Havas TE}}</ref> | ||
=== | ===Transmision=== | ||
Mastoiditis results from extension of adjacent infection in middle ear. | |||
===Genetics=== | ===Genetics=== | ||
*There is evidence of genetic predisposition to [[otitis media]], and thereby mastoiditis, with statistically significant evidence that it has high heritability.<ref name="pmid22018929">{{cite journal |vauthors=Hafrén L, Kentala E, Järvinen TM, Leinonen E, Onkamo P, Kere J, Mattila PS |title=Genetic background and the risk of otitis media |journal=Int. J. Pediatr. Otorhinolaryngol. |volume=76 |issue=1 |pages=41–4 |year=2012 |pmid=22018929 |doi=10.1016/j.ijporl.2011.09.026 |url=}}</ref> | *There is evidence of genetic predisposition to [[recurrent otitis media]], and thereby mastoiditis, with statistically significant evidence that it has high heritability.<ref name="pmid22018929">{{cite journal |vauthors=Hafrén L, Kentala E, Järvinen TM, Leinonen E, Onkamo P, Kere J, Mattila PS |title=Genetic background and the risk of otitis media |journal=Int. J. Pediatr. Otorhinolaryngol. |volume=76 |issue=1 |pages=41–4 |year=2012 |pmid=22018929 |doi=10.1016/j.ijporl.2011.09.026 |url=}}</ref> | ||
**Hereditary factors comprising 45-75% of risk factors for [[recurrent otitis media]], as revealed by heritability studies involving twins and triplets.<ref name="pmid23133572">{{cite journal |vauthors=Rye MS, Warrington NM, Scaman ES, Vijayasekaran S, Coates HL, Anderson D, Pennell CE, Blackwell JM, Jamieson SE |title=Genome-wide association study to identify the genetic determinants of otitis media susceptibility in childhood |journal=PLoS ONE |volume=7 |issue=10 |pages=e48215 |year=2012 |pmid=23133572 |pmc=3485007 |doi=10.1371/journal.pone.0048215 |url=}}</ref> | **Hereditary factors comprising 45-75% of risk factors for [[recurrent otitis media]], as revealed by heritability studies involving twins and triplets.<ref name="pmid23133572">{{cite journal |vauthors=Rye MS, Warrington NM, Scaman ES, Vijayasekaran S, Coates HL, Anderson D, Pennell CE, Blackwell JM, Jamieson SE |title=Genome-wide association study to identify the genetic determinants of otitis media susceptibility in childhood |journal=PLoS ONE |volume=7 |issue=10 |pages=e48215 |year=2012 |pmid=23133572 |pmc=3485007 |doi=10.1371/journal.pone.0048215 |url=}}</ref> | ||
*The following genes have been identified as having having potential pathogenic qualities for [[recurrent otitis media]] and mastoiditis:<ref name="pmid23133572">{{cite journal |vauthors=Rye MS, Warrington NM, Scaman ES, Vijayasekaran S, Coates HL, Anderson D, Pennell CE, Blackwell JM, Jamieson SE |title=Genome-wide association study to identify the genetic determinants of otitis media susceptibility in childhood |journal=PLoS ONE |volume=7 |issue=10 |pages=e48215 |year=2012 |pmid=23133572 |pmc=3485007 |doi=10.1371/journal.pone.0048215 |url=}}</ref><ref name="pmid197587112">{{cite journal|year=2009|title=Mastoiditis in a paediatric population: a review of 11 years experience in management|url=|journal=Int. J. Pediatr. Otorhinolaryngol.|volume=73|issue=11|pages=1520–4|doi=10.1016/j.ijporl.2009.07.003|pmid=19758711|vauthors=Pang LH, Barakate MS, Havas TE}}</ref> | *The following genes have been identified as having having potential pathogenic qualities for [[recurrent otitis media]] and mastoiditis:<ref name="pmid23133572">{{cite journal |vauthors=Rye MS, Warrington NM, Scaman ES, Vijayasekaran S, Coates HL, Anderson D, Pennell CE, Blackwell JM, Jamieson SE |title=Genome-wide association study to identify the genetic determinants of otitis media susceptibility in childhood |journal=PLoS ONE |volume=7 |issue=10 |pages=e48215 |year=2012 |pmid=23133572 |pmc=3485007 |doi=10.1371/journal.pone.0048215 |url=}}</ref><ref name="pmid197587112">{{cite journal|year=2009|title=Mastoiditis in a paediatric population: a review of 11 years experience in management|url=|journal=Int. J. Pediatr. Otorhinolaryngol.|volume=73|issue=11|pages=1520–4|doi=10.1016/j.ijporl.2009.07.003|pmid=19758711|vauthors=Pang LH, Barakate MS, Havas TE}}</ref> | ||
**2p23.1 | **2p23.1 | ||
*** | ***CAPN14 | ||
*** | ***GALNT14 | ||
**20q11.21 | **20q11.21 | ||
*** | ***BPIFA3 | ||
*** | ***BPIFA1 | ||
**Those that interact with the | **Those that interact with the TGFβ pathway: | ||
*** | ***BMP5 | ||
*** | ***GALNT13 | ||
*** | ***NELL1 | ||
*** | ***TGFB3 | ||
*Up-regulation of the genes correlated to [[otitis media]] pathogenesis contribute to individual susceptibility to mastoiditis. | *Up-regulation of the genes correlated to [[otitis media|recurrent otitis media]] pathogenesis contribute to individual susceptibility to mastoiditis. | ||
==Associated Conditions== | ==Associated Conditions== | ||
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{{WH}} | {{WH}} | ||
{{WS}} | {{WS}} | ||
Revision as of 13:40, 30 June 2017
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Mastoiditis Microchapters |
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Diagnosis |
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Treatment |
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Case Studies |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mehrian Jafarizade, M.D [2]
Overview
Mastoiditis is the infection in the cavities of mastoid process of temporal bone that occurs after otitis media. At birth, the mastoid consists of a single cavity, which is connected to the middle ear by a canal. As the child grows, the mastoid bone becomes pneumatized, resulting in a series of connected cavities, lined by a mucosa diverted from respiratory epithelium. There is a relationship between the middle ear, eustachian tube, and the mastoid. This connection has a fundamental role in the pathogenesis of mastoiditis. In the setting of acute otitis media the mucosa that lines the middle ear and also mastoid air cells becomes inflamed. In majority cases of acute otitis media inflammation resolves, but some persist leading to bacterial and fluid accumulation within the mastoid air cells. Gradually, as a result of pressure rising in the mastoid, air cell septae may be destroyed and mastoiditis could be proceed to periostitis, cavity abscess and osteomyelitis. Mastoid is near vital organs in head and neck and mastoid infection may cause serious complications. There is evidence of genetic predisposition to recurrent otitis media and therefore mastoiditis, with statistically significant evidence that it has high heritability. The following genes have been identified as having potential pathogenic qualities for otitis media: CAPN14, GALNT14, BPIFA3, BPIFA1, BMP5, GALNT13, NELL1, TGFB3. Up-regulation of the genes correlated to recurrent otitis media pathogenesis contribute to individual susceptibility to mastoiditis.
Pathophysiology
Pathogenesis
Mastoiditis is the infection in the cavities of mastoid process of temporal bone that occurs after otitis media.
At birth, the mastoid consists of a single cavity, which is connected to the middle ear by a canal. As the child grows, the mastoid bone becomes pneumatized, resulting in a series of connected cavities, lined by a mucosa diverted from respiratory epithelium. There is a relationship between the middle ear, eustachian tube, and the mastoid. This connection has a fundamental role in the pathogenesis of mastoiditis. In the setting of acute otitis media the mucosa that lines the middle ear and also mastoid air cells becomes inflamed. In majority cases of acute otitis media inflammation resolves, but some persist leading to bacterial and fluid accumulation within the mastoid air cells. Gradually, as a result of pressure rising in the mastoid, air cell septae may be destroyed and mastoiditis could be proceed to periostitis, cavity abscess and osteomyelitis.
- Mastoid is near important structures like the facial nerve, sternocleidomastoid muscle, jugular vein, internal carotid artery, sigmoid sinus, brain, and meninges; as a result of this proximity, spreading infection to these places may cause complications.[1][2]
Transmision
Mastoiditis results from extension of adjacent infection in middle ear.
Genetics
- There is evidence of genetic predisposition to recurrent otitis media, and thereby mastoiditis, with statistically significant evidence that it has high heritability.[3]
- Hereditary factors comprising 45-75% of risk factors for recurrent otitis media, as revealed by heritability studies involving twins and triplets.[4]
- The following genes have been identified as having having potential pathogenic qualities for recurrent otitis media and mastoiditis:[4][2]
- 2p23.1
- CAPN14
- GALNT14
- 20q11.21
- BPIFA3
- BPIFA1
- Those that interact with the TGFβ pathway:
- BMP5
- GALNT13
- NELL1
- TGFB3
- 2p23.1
- Up-regulation of the genes correlated to recurrent otitis media pathogenesis contribute to individual susceptibility to mastoiditis.
Associated Conditions
- Mastoiditis is often associated with other upper respiratory conditions caused by the nasopharynx pathogen[5][2]
- Associated conditions are also allergies-related, such as allergic rhinitis.
References
- ↑ Lin HW, Shargorodsky J, Gopen Q (2010). "Clinical strategies for the management of acute mastoiditis in the pediatric population". Clin Pediatr (Phila). 49 (2): 110–5. doi:10.1177/0009922809344349. PMID 19734439.
- ↑ 2.0 2.1 2.2 Pang LH, Barakate MS, Havas TE (2009). "Mastoiditis in a paediatric population: a review of 11 years experience in management". Int. J. Pediatr. Otorhinolaryngol. 73 (11): 1520–4. doi:10.1016/j.ijporl.2009.07.003. PMID 19758711.
- ↑ Hafrén L, Kentala E, Järvinen TM, Leinonen E, Onkamo P, Kere J, Mattila PS (2012). "Genetic background and the risk of otitis media". Int. J. Pediatr. Otorhinolaryngol. 76 (1): 41–4. doi:10.1016/j.ijporl.2011.09.026. PMID 22018929.
- ↑ 4.0 4.1 Rye MS, Warrington NM, Scaman ES, Vijayasekaran S, Coates HL, Anderson D, Pennell CE, Blackwell JM, Jamieson SE (2012). "Genome-wide association study to identify the genetic determinants of otitis media susceptibility in childhood". PLoS ONE. 7 (10): e48215. doi:10.1371/journal.pone.0048215. PMC 3485007. PMID 23133572.
- ↑ Coticchia JM, Chen M, Sachdeva L, Mutchnick S (2013). "New paradigms in the pathogenesis of otitis media in children". Front Pediatr. 1: 52. doi:10.3389/fped.2013.00052. PMC 3874850. PMID 24400296.