E. Rajesh, R. Jayasri Kurupaa, M. Kasthuri^* and  N. Balachander

Department of Oral Pathology, Sree Balaji Dental College and Hospital, Bharath University, Pallikaranai, Chennai-600100.

DOI : https://dx.doi.org/10.13005/bpj/1027

Abstract

In oral tissues,the mast cell releases various pro-inflammatory cytokine tumor necrosis factor alpha (TNF-Ü) which stimulate leukocyte infiltration in various inflammatory condition of oral cavity such as oral lichen planus (OLP), periapical lesions, gingivitis & periodontitis. Mast cells are the local residents of the connective tissue and plays an important role in immunopathology and producing mitogenic cytokines.These cells plays a role in pathogenesis of oral diseases.

Keywords

tissues; releases; various

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Copy the following to cite this article: Rajesh E, Kurupaa R. J, Kasthuri M, Balachander N. Role of Mast Cell in Oral Pathology. Biomed Pharmacol J 2016;9(2).

Copy the following to cite this URL: Rajesh E, Kurupaa R. J, Kasthuri M, Balachander N. Role of Mast Cell in Oral Pathology. Biomed Pharmacol J 2016;9(2). Available from: http://biomedpharmajournal.org/?p=8173

Introduction

Mast cells are granulated cells and appears as a large spherical cells which is present in all of the connective tissue elements including skin, submucosa or connective tissue of various organs and mucosal epithelial tissues & also in dental pulp^1,2. Life span of weeks to months.It is derived from bonemarrow and it contains granules granules are rich in heparin, chondroitin sulphate, proteoglycan and numerous enzymes including collagenase.These granules are metachromatic in nature and it is confirmed with staining such as Toludine blue.

Ultrastructure of Mast Cell :

Three types of mast cell :In deeper connective tissue,the cells (except that in close vicinity to blood vessels) appears as round /oval in shape & dark purple in colour. The borders of cell are well defined & nucleus is not visible due to granules called as intact cells³

In the superficial connective tissue, the mast cells appear flattened / irregular and the cytoplasm appears granular immediately below the infiltrate area and near the blood vessels . The cell borders are not defined and the nucleus is only partially appreciable; these are called spreading cells⁴.

The third type called degranulated cells found within the infiltrate & appeared paler the staining has reverted from metachromatic violet to light pink, the nucleus blue in color and well defined⁵

Role of mast cell released cytokines: –

IL-3 – induce basophil recruitment & activation

IL-5-eosinophil recruitment & activation

IL-13 – induction of IgE synthesis

Mast cell bears receptors for IgE and degranulates  this cytophilic antibody is cross-linked by antigen . Mast cell RANTES degranulation can be caused by other factors such as mechanical trauma, complement C5a, eosinophil –derived cationic protein, and bacterial products . In the absence of IgE mediated activation the mast cell can produce inflammation  and its events under many conditions⁶.

Thus, mast cell release proinflammatory mediators, promotes inflammation and angiogenesis, extracellar  matrix degeneration and tissue remodeling.

Role of MC in Oral Pathologies:

Role of MC in OLP:

Mechanism

RANTES activation

↓

Mast Cells chemotaxis and degranulation

↓

TNF- Ü

↓

Endothelium cell adhesion molecule

expression (Cd62 E, CD54, CD106)

↓

Chymase activation

↓

MMP- 9 activation

↓

Disruption of basement membrane

↓

Keratinocyte apoptosis

↓

Intra epithelial CD 8

T-cell migration through BM

↓

Survival of inflammatory cell

↓

Non-specific T-cell recruitment¹

Action of mast cell mediators in oral lichen planus leading to the following clinical

and histopathological changes⁷

Table 1

Mediators	Clinical features	Histopathologic features
Histamine . Induces vasopermeability.. . Antigen induced T-cell proliferation Inhibits the neutrophil. . Induces increased expression of E-selectin, ICAM and ICAM, which causes leukocytic margination	. Vesicles, bullae and erosive lesions Chronic persistence of the lesion.	Submucosal edema. Traffi cking of T-lymphocytes..
TNF-alpha . Increased production of matrix metalloproteinases like stromyelsin, collagenase. Destruction of basement membrane	Vesicles, bullae and erosive lesions	Necrosis and liquifactive degeneration of basal cell layer.

 

Action of mast cell mediators in oral submucous fi brosis leading to the following

clinical and histological changes⁷

Table 2

Mediators	Clinical features	Histopathologic features
Prostaglandins and leukotreines Increase the mucous gland secretion Increased venous permeability	– Excessive salivation.	Submucosal edema
Histamine Causes vasodilatation and vasopermeability.		Submucosal edema
Heparin . Causes vasoproliferation. –	Petechiae
Interleukin-5 . Causes growth and differentiation of eosinophils	Itching sensation .	In early stages of oral submucous fibrosis consists of Inflammatory infiltrate eosinophils
Eosinophilic chemotactic factor (ECF) Causing eosinophilic migration
Interleukin-1 . Stimulates fibroblastic proliferation.	Decreased mouthopening	Increased collagen fiber bundles.

 

Role of MC in angiogenesis in oral squamous cell carcinoma:

Action of mast cell mediators in oral squamous cell carcinoma leading to the following clinical and histologic

al changes⁷

Table.3

Mediators	Clinical features	Histopathologic features
IL-1 AND TNF-alpha . Causes increased epithelial cell proliferation..	Exophytic growth or a plaque	Increased thickness of the epithelium
Heparin . Causes angiogenesis and type-VIII	Tumour angiogenesis	Increased vascularity of the stroma.

 

Role of MC in oral leukoplakia:

Action mast cell mediators in oral leukoplakia leading to the following clinical and histological changes⁷

Table.4

Mediators	Clinical features	Histopathologic features
Histamine . Enhances permeability across the epithelial surface. Antigen induced T-cell proliferation.	Chronicity of the lesion	Increased mucosal permeability despite hyperkeratosis
Heparin . Causes endothelial cell proliferation and migration	Erosive leukoplakia.	Increased vascularity of the stroma and ulceration.
Interleukin-1 and TNF . Increased epithelial cell proliferation.	White patch or a plaque	Increased thickness of the epithelium.

 

Role of MC in Periapical lesions

Mechanism

Role of MC in Pyogenic Granuloma

MC + neuropeptides

neural immune network with LC  in mucosal tissue

↓

Degranulation of MC

↓

Cytokine, vasoactive amine and enzyme

↓

Inflammatory and vascular changes

↓

Pyogenic granuloma

Role of MC in wound healing

Wound healing is a dynamic process consisting of four phases:

1. Homeostasis
2. Inflammation
3. Proliferation

d. Tissue remodeling and resolution

MC  activate  fibroblast

enzyme

tryptase

↓

synthesis collagen + hyaluronic acid

↓

fibrous tissue formation

↓

MC + fibroblast13

↓

fibronectin integrin

receptor

Wound healing

Wound healing involves degradation, cell migration, synthesis of  fibronectin, fibrin and high amount of collagen type II and matrix remodeling to return the tissue to normality

 

III.  MMP – 9 from mast cell →

Wound healing¹

Role of mast cell in peripheral ossifying fibroma⁹:

 

Figure 1   Click here to view figure

 

Conclusion

This article mainly focus that all oral reactive lesions have MCs , thus having a possible role in pathogenesis of these lesions.In recent years. Mast cells have gained a lot of importance owing to the vast number of chemical mediators  released by them with wide range of actions in various disease processes. Once confirmed, it makes easier for us to target the therapeutic modalities against mast cells and the granules it contains to alter the course of disease/lesion.

Reference

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