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 Table of Contents  
REVIEW ARTICLE
Year : 2014  |  Volume : 4  |  Issue : 2  |  Page : 81-83

Microabscess: Revisited


Department of Oral Pathology, Rajarajeswari Dental College and Hospital, Bengaluru, Karnataka, India

Date of Web Publication11-Sep-2015

Correspondence Address:
K Shyamala
Department of Oral Pathology, Rajarajeswari Dental College and Hospital, No. 14, Ramohally Cross, Kumbalgodu, Mysore Road, Bengaluru - 560 060, Karnataka
India
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Source of Support: Nil., Conflict of Interest: There are no conflicts of interest.


DOI: 10.4103/2231-6027.165098

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  Abstract 

Inflammation is the initial response of the host to a diverse array of biological stressors including bacterial infection, burns, trauma, and invasive surgery. Most inflammatory reactions begin as a suppurative or purulent exudation process when the first line of cellular defense, the neutrophils, accumulate in the area which may lead to the formation of microabscesses. This article on microabscess is an effort in providing information available about microabscess from various sources. The matter has been extracted from internet sources with the help of Google search, dictionaries, and articles from the online journals, and textbooks. In this paper, we have discussed the mechanism behind the formation, regression of microabscess and the different types of microabscesses that have appeared in the literature related to different disease processes.

Keywords: Inflammatory reaction, microabscess, Munro microabscess, Pautrier's abscess


How to cite this article:
Shyamala K, Girish H C, Murgod S, Nayak VN. Microabscess: Revisited. Int J Oral Health Sci 2014;4:81-3

How to cite this URL:
Shyamala K, Girish H C, Murgod S, Nayak VN. Microabscess: Revisited. Int J Oral Health Sci [serial online] 2014 [cited 2017 Jul 23];4:81-3. Available from: http://www.ijohsjournal.org/text.asp?2014/4/2/81/165098


  Introduction Top


The immune system is one of the most important and complex systems of the human body. Despite great advances in recent years that shed light on its understanding and unravel the underlying key mechanisms behind its functions, there are still many functions of the human immune system (HIS) that are not well understood.[1]

Inflammation is the initial response of the host to a diverse array of biological stressors including bacterial infection, burns, trauma, and invasive surgery. Despite the growing understanding of the cellular and molecular mechanisms of inflammation, the complexity of the inflammatory response has challenged the therapeutic development.[2],[3]

Most inflammatory reactions begin as a suppurative or purulent exudation process when the first line of cellular defense, the neutrophils, accumulate in the area which may lead to the formation of microabscesses.[1]

In this article, we have discussed the mechanism behind the formation, regression of microabscess, and the different types of microabscess that have appeared in the literature related to different disease processes.


  Definition of Microabscess Top


Microabscess has been defined as a very small, localized collection of pus in Dorland's dictionary,[4] and as a very small circumscribed collection of white blood cells, in solid tissues in The American Heritage ® Medical Dictionary.[5] Etymology, as given in Mosby's Medical Dictionary, is: Gk, Mikros, small; L, abscedere, to go away, a very small abscess.[6]

In other words, a microabscess is a localized collection of dead cells, body fluids, microbes, and other cells of the HIS.


  Mechanism of Microabscess Formation Top


Initially, the bacteria penetrate through the tissue causing tissue damage without its presence to be noticed. The process of formation of a microabscess begins when a cell of the HIS encounters bacteria and warns other cells that there is a stranger in the host. Its "warn" is in the form of a class of biochemicals called cytokines, which recruit other HIS cells to come to the point of infection and surround the enemy.[1]

As soon as resting macrophages in the tissue recognize the bacteria, they start to produce proinflammatory cytokines that will diffuse through the tissue reaching the blood vessel. There is an increase in the endothelium permeability when proinflammatory cytokines interact with the endothelial cells allowing neutrophils and monocytes to migrate to the tissue. The bacteria start to die due to the presence of large numbers of neutrophils. However, the immune response cannot completely eliminate bacteria due to the formation of the microabscess pattern. In the microabscess, there are bacteria and a huge concentration of dead cells around it [Figure 1]. The cleaning process realized by macrophages is very important to allow neutrophils to reach bacteria and eliminate them. Macrophages are responsible for phagocytizing dead cells that accumulated in the microabscess.[1]
Figure 1: Neutrophilic microabscess – Munros microabscess in psoriasis courtesy: http://quizlet.com/11907102/first-aid-images-4-flash-cards

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  Molecular Mechanism in Microabscess Formation Top


The cytokines are produced primarily by resident macrophages that are the first to recognize the presence of bacteria. The cytokines will increase the endothelium permeability allowing neutrophils to migrate to the tissue. These neutrophils will produce more cytokines that will guide the movement of neutrophils and macrophage cells in the direction of high concentrations of bacteria.[1]

During the formation of the microabscess and after it, the production of cytokines is higher in the regions where neutrophils and macrophages have contact with the bacteria that is surrounding the microabscess.[1]


  Mechanism of Regression of Microabscess Top


After the formation of the microabscess, the bacteria start to die around the entire microabscess since this is the area where the immune response is acting. Once the bacteriae are dead, the neutrophils that came from the blood vessel closer to the site of infection start undergoing apoptotic cell death. This phenomenon continues until the microabscess disappears. The phagocytosis by the macrophages in that area will clear the dead and damaged tissue cells.[1]


  Site and Types of Microabscess Top


Microabscesses are found in many different diseases of different sites. Liver microabscess,[7],[8],[9],[10] heart tissue microabscess (bacterial and viral myocarditis),[11],[12] and pancreatic microabscess (pancreatic neoplasia)[13] have been reported in the literature by various authors. Microabscess has been seen to occurs both in connective tissue and epithelium. Microabscess occurring in connective tissue, as in periodontal tissue in cases of periapical infections and other general connective tissue is a natural possibility considering the mechanism of its formation as discussed above. In our opinion, the formation of microabscess in the epithelium can be due to exocytosis of various inflammatory cells, and the movement of these inflammatory cells follows the chemical gradient following invasion by a foreign body. There are different microabscesses based on the type of inflammatory cell accumulation in the epithelium.

Munro microabscess, a microscopic collection of polymorphonuclear white blood cells found in the stratum corneum in psoriasis and also called Munro's abscess in deference to William J. Munro, an Australian dermatologist, who clearly described this phenomenon in, 1898.[5],[14] Munro microabscess is also seen in benign migratory glossitis which is a variant of psoriasis.[15] Pautrier's microabscess is a collection of malignant lymphocytes in the epidermis occurring as solid intraepidermal nodules; seen in epitheliotropic lymphomas.[16] Pautrier's microabscess is named after Lucien-Marie Pautrier.[17] Epidermotropism by neoplastic CD4+ lymphocytes leads to the formation of Pautrier's microabscesses.[18] Papillary microabscess is seen in pemphigus vulgaris; dermatitis herpetiformis due to acantholytic keratinocytes with neutrophils.[19] Eosinophilic microabscesses are often seen at the luminal edge of the epithelium in cases of eosinophilic esophagitis.[20]


  Conclusion Top


Microabscess when well-developed has a wall or capsule of fibrous connective tissue or surrounding epithelial cells separating it from the surrounding tissue, helping to prevent any microbes present in the microabscess from spreading to other areas of the body. Thus, microabscesses can be considered as a natural strategy used to fight against infection. Understanding the mechanism and molecular events in microabscess formation may help in understanding the pathogenetic processes of some diseases.

 
  References Top

1.
Pigozzo AB, Macedo GC, Weber dos Santos R, Lobosco M. Computational modeling of microabscess formation. Comput Math Methods Med 2012;2012:736394.  Back to cited text no. 1
    
2.
Kerschen EJ, Fernandez JA, Cooley BC, Yang XV, Sood R, Mosnier LO, et al. Endotoxemia and sepsis mortality reduction by non-anticoagulant activated protein C. J Exp Med 2007;204:2439-48.  Back to cited text no. 2
    
3.
Klaitman V, Almog Y. Corticosteroids in sepsis: A new concept for an old drug. Isr Med Assoc J 2003;5:51-5.  Back to cited text no. 3
    
4.
Dorland's Medical Dictionary for Health Consumers. © 2007 by Saunders, an Imprint of Elsevier, Inc. Available from: http://www.medicaldictionary.thefreedictionary.com/microabscess. [Last accessed on 2014 Nov 15].  Back to cited text no. 4
    
5.
The American Heritage® Medical Dictionary Copyright © 2007, 2004 by Houghton Mifflin Company. Published by Houghton Mifflin Company. Available from: http://www. medical-dictionary.thefreedictionary.com/microabscess. [Last accessed on 2014 Nov 15].  Back to cited text no. 5
    
6.
Mosby's Medical Dictionary, 8th edition; ©2009. Available from: http://www.us.elsevierhealth.com/dictionary/ mosby-medical-dictionary. [Last accessed on 2014 Nov 15].  Back to cited text no. 6
    
7.
Seydel KB, Zhang T, Stanley SL Jr. Neutrophils play a critical role in early resistance to amebic liver abscesses in severe combined immunodeficient mice. Infect Immun 1997;65:3951-3.  Back to cited text no. 7
    
8.
Rigothier MC, Khun H, Tavares P, Cardona A, Huerre M, Guillén N. Fate of Entamoeba histolytica during establishment of amoebic liver abscess analyzed by quantitative radioimaging and histology. Infect Immun 2002;70:3208-15.  Back to cited text no. 8
    
9.
Lin JC, Chang FY, Fung CP, Yeh KM, Chen CT, Tsai YK, et al. Do neutrophils play a role in establishing liver abscesses and distant metastases caused by Klebsiella pneumoniae? PLoS One 2010;5:e15005.  Back to cited text no. 9
    
10.
Ebe Y, Hasegawa G, Takatsuka H, Umezu H, Mitsuyama M, Arakawa M, et al. The role of Kupffer cells and regulation of neutrophil migration into the liver by macrophage inflammatory protein-2 in primary listeriosis in mice. Pathol Int 1999;49:519-32.  Back to cited text no. 10
    
11.
Bhavsar J, Gordon D, Shea M. Listeria myocarditis with an atypical intracavitary vegetation/thrombus. Heart 2010;96:1637.  Back to cited text no. 11
    
12.
Oka K, Oohira K, Yatabe Y, Tanaka T, Kurano K, Kosugi R, et al. Fulminant myocarditis demonstrating uncommon morphology – A report of two autopsy cases. Virchows Arch 2005;446:259-64.  Back to cited text no. 12
    
13.
Reid MD, Basturk O, Thirabanjasak D, Hruban RH, Klimstra DS, Bagci P, et al. Tumor-infiltrating neutrophils in pancreatic neoplasia. Mod Pathol 2011;24:1612-9.  Back to cited text no. 13
    
14.
King DT, Lubran MM, King LA. Munro microabscess: Let's spell it right. Arch Dermatol 1979;115:816-7.  Back to cited text no. 14
    
15.
Rjendran R. Developmental disturbances of oral and paraoral structures. In: Rjendran R, Sivapathasundaram B, editors. Shafer's Textbook of Oral Pathology. 6th ed. New Delhi: Elsevier Publishers; 2009. p. 3-79.  Back to cited text no. 15
    
16.
Saunders Comprehensive Veterinary Dictionary, 3rd ed; ©2007 Elsevier, Inc. Available from: http://www.medical-dictionary.thefreedictionary.com/pounder. [Last accessed on 2014 Nov 15].  Back to cited text no. 16
    
17.
Steffen C. The man behind the eponym: Lucien Marie Pautrier – Pautrier's microabscess. Am J Dermatopathol 2003;25:155-8.  Back to cited text no. 17
    
18.
Cuneo A, Castoldi GL. Mycosis fungoides/Sezary's syndrome. Atlas Genet Cytogenet Oncol Haematol 2005;9:242-3.  Back to cited text no. 18
    
19.
Nag S, Manjunath K, Sriram G, Sivapathasundaram B. Know this field: Mucous membrane pemphigoid. J Oral Maxillofac Pathol 2009;13:9.  Back to cited text no. 19
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20.
Parfitt JR, Gregor JC, Suskin NG, Jawa HA, Driman DK. Eosinophilic esophagitis in adults: Distinguishing features from gastroesophageal reflux disease: A study of 41 patients. Mod Pathol 2006;19:90-6.  Back to cited text no. 20
    


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   Abstract
  Introduction
   Definition of Mi...
   Mechanism of Mic...
   Molecular Mechan...
   Mechanism of Reg...
   Site and Types o...
  Conclusion
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   Mechanism of Mic...
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