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Table of Contents   
ORIGINAL RESEARCH  
Year : 2012  |  Volume : 23  |  Issue : 5  |  Page : 695-696
Evaluation of mast cells, eosinophils, blood capillaries in oral lichen planus and oral lichenoid mucositis


1 Department of Oral Pathology and Microbiology, Saraswathi Dhanawantari Dental College and Hospital, Pathri Road, Parbhani, Maharashtra, India
2 Department of Oral Pathology and Microbiology, Meenakshi Ammal Dental College and Hospital, Alapakkam Main Road, Maduravoyal, Chennai, Tamil Nadu, India
3 Department of Oral Pathology and Microbiology, Vishnu Dental College, Vishnupur, Bhimavaram, West Godavari District, Andhra Pradesh, India

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Date of Submission22-Oct-2011
Date of Decision23-May-2012
Date of Acceptance18-Jun-2012
Date of Web Publication19-Feb-2013
 

   Abstract 

Introduction: Mast cells are granule containing secretory cells present in oral mucosal and connective tissue environment. Oral lichen planus and oral lichenoid lesions are commonly occurring oral diseases and have some similarity clinically and histologically. Both are characterized by an extensive sub epithelial infiltrate of T cells, together with mast cells, eosinophils and blood capillaries. In this study mast cell and eosinophil densities along with number of blood capillaries were studied to find out if they could aid in histopathological distinction between oral lichen planus and lichenoid mucositis.
Aims: To enumerate mast cells and compare the status of Mast Cells (Intact or Degranulated) in Lichen planus, Lichenoid mucositis and normal buccal mucosa in tissue sections stained with Toluidine Blue, and also to enumerate Eosinophils and blood capillaries in tissue sections stained with H and E.
Materials and Methods: The study group included 30 cases each of oral lichen planus and oral lichenoid mucositis. 10 cases of clinically normal oral buccal mucosa formed the control group. All the sections were stained with Toluidine blue and H and E separately. Histopathological analysis was done using binocular light microscope equipped with square ocular grid to standardize the field of evaluation.
Results: The result of the study showed.

  • Significant increase in number of mast cells in oral lichen planus and oral lichenoid mucositis compared to normal buccal mucosa.
  • Significant increase of intact mast cells suepithelially within the inflammatory cell infiltrate in oral lichen planus compared to oral lichenoid mucositis.
  • Significant increase of degranulated mast cells in oral lichenoid mucositis to oral lichen planus, and increase in number of eosinophil densities in oral lichenoid mucositis compared to oral lichen planus.
  • Significant increase in number of capillaries in oral lichenoid mucositis compared to oral lichen planus.

Conclusion: The findings of increased number of intact mast cells sub epithelially in oral lichen planus to oral lichenoid mucositis and increase in number of degranulated mast cells as well as capillaries subepithelially in oral lichenoid mucositis to oral lichen planus can be used as reliable criteria for histologic distinction between these two lesions. The increase of eosinophils in oral lichenoid mucositis to oral lichen planus could be used as adjunct histologic criterion in the diagnosis of oral lichenoid mucositis.

Keywords: Blood capillaries, eosinophils, lichen mucositis, lichen planus, mast cells

How to cite this article:
Reddy D S, Sivapathasundharam B, Saraswathi T R, SriRam G. Evaluation of mast cells, eosinophils, blood capillaries in oral lichen planus and oral lichenoid mucositis. Indian J Dent Res 2012;23:695-6

How to cite this URL:
Reddy D S, Sivapathasundharam B, Saraswathi T R, SriRam G. Evaluation of mast cells, eosinophils, blood capillaries in oral lichen planus and oral lichenoid mucositis. Indian J Dent Res [serial online] 2012 [cited 2020 Aug 9];23:695-6. Available from: http://www.ijdr.in/text.asp?2012/23/5/695/107422
Oral lichen planus is a chronic inflammatory oral disease of unknown etiology, which is characterized by an extensive sub epithelial infiltrate of T cells and macrophages, together with mast cells. The subepithelial infiltrate in both oral lichen planus and in classic reactions of delayed hypersensitivity is primarily composed of T-lymphocytes. The most prevalent hypersensitivity type-IV like reactions comprises lichenoid contact lesions. The pathogenesis of lichenoid lesions or reactions seems to be complex and is still not fully understood. The oral lichenoid lesions show clinical and histopathological characteristics compatible with oral lichen planus except for their association with drugs and chemicals. Mast cells are granule containing cells present in oral mucosal and connective tissue environment [1] [Figure 1]. The mast cells participate in the resulting inflammatory and immunological reactions. [2] The role of mast cells has been extensively studied in conditions ranging from inflammatory hyperplasias to oral squamous cell carcinomas. [3]
Figure 1: Arrow indicates intact mast cells in zone-I of normal buccal mucosa. (H and E, × 400)

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Several studies have shown the presence of mast cells in lesions of oral lichen planus. [2] Recent evidence implicates an involvement of mast cells in the pathogenesis of delayed hypersensitivity like lichenoid contact lesions. In addition to elicitation of inflammatory mediators mast cells are able to synthesize components of the basement membrane such as laminin, collagen IV and heparin sulfate proteoglycan and facilitate new vessel formation. [4] Eosinophils have been reported to occur in cutaneous lichenoid drug reactions. The occurrence of a tissue eosinophilia in the presence of oral lichenoid drug reactions is poorly documented. In this study along with the mast cells, eosinophil densities and number of blood capillaries were studied to find out if they could be reliable aid in histopathological distinction between oral lichen planus and lichenoid mucositis which is very challenging even to well experienced pathologist's and also to understand their role in the pathogenesis of these lesions.


   Materials and Methods Top


This study was conducted on the archival retrieved formalin fixed paraffin embedded tissues obtained from the department of Oral and Maxillo-facial Pathology, Meenakshi Ammal Dental College and Hospital, Chennai. The study group included 30 cases of histologically diagnosed oral lichen planus and 30 cases of lichenoid mucositis. Control group consisted of 10 cases of clinically normal buccal mucosa. Tissue sections of 5μ thickness were made from all the Paraffin embedded tissues and were stained with toluidine blue and H and E separately. Histopathological analysis was done using binocular light microscope equipped with 10X eye piece fitted with (1cm 2 ) square ocular grid to standardize the field of evaluation.

Counting of cells and capillaries

The soft tissue stained sections of both H and E and toludine blue were observed under binocular light microscope equipped with 10X eye piece fitted with 1 cm 2 square ocular grid and 40X objective. The area encompassed by the graticule was taken as one microscopic field, and number of mast cells, eosinophils and capillaries within the area were counted in four different areas in the connective tissue which were selected without any overlapping and avoiding edges of sections. In each of these areas the cells and capillaries were counted at two different levels, described as Zone I and Zone II. Zone I was sub epithelial within the inflammatory cell infiltrate, whereas Zone II was beneath the inflammatory cell infiltrate in the deeper region of the connective tissue.

Criteria for identification of cells and capillaries

Mast cells

Based on the intensity of metachromasia, mast cells were categorized as:

  • Intact mast cells exhibiting intense metachromasia and dense granules obscuring the nucleus. [Figure 2]
  • Degranulated mast cells with less intense metachromasia and clear outline of the nucleus. [Figure 2]
Figure 2: Intact (green arrow) and degranulated (red arrow) mast cells in zone-I of oral lichenoid mucositis. (Toluidine Blue, × 400)

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Eosinophils

Identified as cells with bi-lobed nucleus with intense red staining of Cytoplasmic granules. [Figure 3]
Figure 3: Eosinophils (green arrow) and capillaries (blue arrow) in zone-I of oral lichenoid mucositis. (H and E, × 400)

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Capillaries

Identified by the lumen lined by flat endothelial cells. [Figure 3]


   Results Top


The result of the study showed significant increase in number of mast cells in oral lichen planus and oral lichenoid mucositis compared to normal buccal mucosa [Table 1].
Table 1: Distribution of total mast cells (Intact and degranulated)

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Significant increase of intact mast cells sub epithelially with in the inflammatory cell infiltrate in oral lichen planus compared to oral lichenoid mucositis [Table 2].
Table 2: Distribution of intact mast cells

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Significant increase of degranulated mast cells in oral lichenoid mucositis to oral lichen planus, both sub epithelally and deeper connective tissue [Table 3].
Table 3: Distribution of degranulated mast cells

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There was significant increase in number of eosinophil densities in oral lichenoid mucositis compared to oral lichen planus [Table 4].
Table 4: Distribution of eosinophils

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Significant increase in number of capillaries in oral lichenoid mucositis compared to oral lichen planus [Table 5]
Table 5: Distribution of capillaries

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   Discussion Top


Lichen planus is a disease characterized by lesions of the skin and oral mucous membrane. Lichenoid reaction clinically resembles oral lichen planus but may be unilateral, asymmetrical or occur in uncommon sites. Discrimination between OLP and OLR has always been a major challenge for both clinicians and pathologists. [5]

Recent attention has been directed towards the role of mast cells in the pathogenesis of oral lichen planus. [6] Mast cells have been studied in normal gingiva, chronic inflammatory gingivitis, desquamative gingivitis, lichen planus, OSMF and Oral Cancer. Mast cell exhibits phenotypic plasticity. There is variation in the mast cell mediators, with the change in the micro-environment, which makes the study of this cell in various studies interesting. [7]

In addition, the role of eosinophils and presence of capillaries in these conditions remain unexplored. With this in mind the present study was done to compare the number and status of mast cells present in oral lichen planus, oral lichenoid reaction and normal buccal mucosa as well as the number of eosinophils and blood capillaries in different levels of lamina propria and correlate these findings to pathogenesis and histopathological characterization of the above conditions.

There was a significant increase in total number of mast cells both in oral lichen planus and oral lichenoid mucositis compared to normal buccal mucosa.

This observation of increased mast cells in oral lichen planus compared to normal buccal mucosa is in consonance with the previous studies by Jontell M et al.[2] and Zhao ZZ et al., [8] the finding of increased mast cells both in oral lichen planus and oral lichenoid mucositis are in concordance with studies by Jose M et al.[3] and Manish Juneja et al.[9] which confirms the important role of mast cells in the pathogenesis of both these conditions.

Zhao ZZ et al.[10] reported the increased number of mast cells in oral lichen planus lesions results in increased levels of mast cell derived mediators such as TNF-α, which in turn up regulates lesional T cell RANTES (Regulated upon Activation, Normal T cell Expressed and Secreted) that provides a mechanism for the selective accumulation and activation of mast cells and T cells in oral lichen planus lesional tissues leading to mast cell degranulation. TNF-α also up regulates stromeolysin (MMP-3), constitutively secreted by fibroblasts, which involves in the degradation of extracellular matrix both in normal and pathological tissues. [10] TNF- α is secreted by oral mucosal mast cells as well as by T-lymphocytes within the oral lichen planus infiltrate. Hence, both mast cells and infiltrating T lymphocytes stimulate production of MMPs and thereby contribute to basement membrane destruction. [10]

Zhou XJ et al.[11] identified clusters of mast cells and intra epithelial CD8+ T-cells at the sites of basement membrane disruption in oral lichen planus and suggested that the destruction of epithelial basement membrane in oral lichen planus may result from the accumulation of mast cells and the release of mast cell derived mediators, especially mast cell proteases and CD8+ T cells migrate through these basement membrane breaks to enter the oral lichen planus epithelium.

Increase in total mast cell count in oral lichen planus has been attributed to the fact that mast cells helped in recruiting the T-lymphocytes to sub epithelial infiltrate as mast cells have the ability to influence the permeability of the endothelium as suggested by Jontell M et al.[2]

There was a significant increase of mast cells in deeper layers of the connective tissue in both the oral lichen planus and oral lichenoid mucositis in our study and is consistent with the finding of Jose M et al.[3] This increase of mast cells in deeper layer suggests that mast cell adhesion and migration occurs predominantly in the deep layer with subsequent migration to the transitional area of submucosa and further move towards the sub epithelial zone where they exert their biologic effect on blood vessels and help in the recruitment of inflammatory cells to the lesional area. [9]

On comparing morphological types of mast cells, there was a significant increase of intact mast cells sub epithelially with in the inflammatory cell infiltrate in oral lichen planus compared to oral lichenoid mucositis. Similarly, intact mast cells were significantly increased in oral lichen planus compared to oral lichenoid mucositis when compared combining both the sub epithelial and deeper zones of lamina propria together. This finding suggests that there is increased degranulation of mast cells in oral lichenoid mucositis compared to lichen planus.

Mucosal mast cells are associated with neurofilaments and blood vessels. Chronic stimulation of these nerves and the release of nueropeptides induce mast cells to degranulate. [10] Mast cells serve as 'gatekeepers of the microvascular bed' and may link neural networks to immune cell trafficking in oral lichen planus. [10] Degranulation of mast cells is triggered by the IgE receptor or through interaction with a variety of agonists which act directly on cell surface. [6] Both T cell derived cytokines and adhesion between mast cells and T cells may cause mast cell activation and degranulation. [6]

In the present study statistically significant increase in number of degranulated mast cells was seen in oral lichenoid mucositis over oral lichen planus. This is in consonance with the previous studies by Jose M et al.[3] but contrary to the findings of Manish Juneja et al., [8] , who observed an increase in number of degranulated mast cells in oral lichen planus compared to oral lichenoid mucositis.

Niissalo et al.[12] in a study of oral lichen planus and oral lichenoid mucositis observed that the pattern of innervations differed between the two. The nerve fibers were found to be relatively evenly distributed in oral lichenoid mucositis, whereas in oral lichen planus they were concentrated in superficial sub epithelial tissue. [8] They also suggested that nueropeptides released from the nerve fibers could cause increased degranulation in oral lichen planus. Manish Juneja et al.[8] explained the sub epithelial increase in number of degranulated mast cells on the basis of the dense innervations seen sub epithelially as reported above.

There was also significant increase in degranulated mast cells in oral lichenoid mucositis compared to oral lichen planus in deeper layers of the connective tissue a finding which could be used for histopathological distinction of the two lesions.

Increased degranulation of mast cells in oral lichenoid mucositis suggests a possible triggered degranulation of mast cells induced by chemicals or drugs associated with this condition. [3] It is thus hypothesized that oral lichenoid mucositis mimics an allergic hypersensitivity reaction where mast cell degranulation has a primary role to play. Histopathological observation of plasma cells and eosinophils in addition to lymphocytes in the sub epithelial infiltrate of these lesions also suggests this possibility. [3] Moreover the increased densities of capillaries sub epithelially in oral lichenoid mucositis over oral lichen planus as observed in this study supports the fact that, systemic medication of certain drugs play an important role in the pathogenesis of this lesion.

Winer and Leeb [13] described the presence of an eosinophilic perivascular infiltrate present in the dermis as distinguishing feature for cutaneous lichenoid drug reactions. Histopathologically Lichenoid mucositis differs from Oral Lichen planus in that the subepithelial lymphocytic infiltrate lacks the well defined "band like appearance," being more diffuse and deep, containing eosinophils and plasma cells. Perivascular infiltration is also seen in some cases. [14]

We observed maximum number of eosinophils in oral lichenoid mucositis followed by oral lichen planus compared to normal buccal mucosa and the difference is not statistically significant, this finding is in concordance with the study by Firth NA and Reade PC. [11] Increased eosinophil densities noted in oral lichenoid mucositis and oral lichen planus compared to normal buccal mucosa suggests their role in the pathogenesis of these lesions though the difference in eosinophil densities is not statistically significant it could be used as adjunct histologic criterion for establishing a diagnosis of oral lichenoid mucositis. Further, there could be a statistically significant difference in eosinophil densities if a larger sample size is used.

Eosinophil activation involves chemotactic factors for eosinophils, namely worm extracts, histamine and eosinophilic chemotactic factors A in mast cells, Eosinophils also contain histaminase that may modulate mast cell mediated inflammation. [10] This functional relationship between the Mast cell and Eosinophil population show the importance of studying eosinophils in the above lesions.

In addition to elicitation of inflammatory mediators, mast cells are able to synthesize components of the basement membrane such as laminin, collagen IV and heparin sulfate proteoglycan and facilitate new vessel formation. [9] Mast cells are found in increased numbers in pathologic states associated with angiogenesis. Ausprunk et al.[15] reported that capillary endothelial cell migration was one of the major components of growing capillary sprouts that arise in angiogenesis. Richard Azizkhan. [16] et al. reported that mast cells release a factor that stimulates migration of capillary endothelial cells and investigated the effect of isolated mast cell products on bovine capillary endothelial cell migration, and demonstrated that heparin is the mast cell factor responsible for capillary endothelial cell migration.

In the present study there is a statistically significant increase in number of capillaries sub epithelially in oral lichenoid mucositis compared to oral lichen planus. The increase of number of capillaries in oral lichen planus is consistent with study by Tao X et al., [17] who reported a significant increase of microvessel density and VEGF (Vascular Endothelial Growth Factor) expression in both the groups of erosive-atrophic and reticular oral lichen planus compared to controls. But the findings of study contradict with that of Manish Juneja et al.[18] who observed increased vascularity in oral lichen planus as compared to oral lichenoid mucositis. This particular increase of capillaries in their study could be attributed to 15% of their samples having associated habit of Pan chewing. Current knowledge suggests that oral mucosal mast cells may be important in the pathogenesis of OLP, both promoting the development of the lesion and exerting immunoregulatory effects on the established lesion via release of cytokines and other mediators. [4] The role of mast cells in OLP and OLL are studied; the findings of our study also support the same. Data accumulated over the years have indicated that eosinophils and mast cell can affect each other's viability, functionality, trafficking and activation, [18] suggesting their role in the pathogenesis of above lesions.

We observed a functional relationship between mast cells and their surrounding structures along with eosinophils and capillaries. This may eventually lead to proper diagnosis and novel therapies for managing these important conditions as they could be used as reliable parameters for histologic distinction between these lesions.


   Conclusion Top


The histological parameters of increased number of intact mast cells sub epithelially in oral lichen planus to oral lichenoid mucositis and increase in number of degranulated mast cells as well as capillaries sub epithelially in oral lichenoid mucositis to oral lichen planus can be used as reliable criteria for histologic distinction between these two lesions. These findings also lead to the conclusion that the mast cells have a significant role in the pathogenesis of these conditions. Even though the increase of eosinophils in oral lichenoid mucositis to oral lichen planus is not stastically significant in the sample size taken in this study, still it could be used as adjunct histologic criterion in the diagnosis of oral lichenoid mucositis. These findings of the study may provide an insight into the pathogenesis of these two diseases.


   Acknowledgements Top


I sincerely express my gratitude to my professor and Head of the Department, Dr. Sivapathasundharam. B, Professor Dr. Saraswthi T.R, and all my other teachers, Dr. Sivakumar. G, Dr. Eistein T. Bertin, Dr. Kavitha.B, Dr. Sri Ram. G, Dr. Spencer Lilly and my colleagues for their timely support and help.

 
   References Top

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Correspondence Address:
D Santhosh Reddy
Department of Oral Pathology and Microbiology, Saraswathi Dhanawantari Dental College and Hospital, Pathri Road, Parbhani, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0970-9290.107422

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    Figures

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    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5]

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