Year : 2005 | Volume
: 9 | Issue : 1 | Page : 12--15
Incidence of mast cells in oral inflammatory lesions: A pilot study
R Sudhakar, V Ramesh, PD Balamurali, Oza Nirima, B Premalatha, V Karthikshree
Department of Oral Pathology and Microbiology, Mahatma Gandhi Dental College and Hospital, Pondicherry, India
Department of Oral Pathology and Microbiology, Mahatma Gandhi Dental College and Hospital, Pondicherry 605 006
Mast cells are also known as «DQ»unicellular endocrine glands«DQ» due to their ability to release a wide variety of chemical mediators that have a potent biological action on the target tissues. These actions include neo-angiogenesis, recruitment of inflammatory cells, stimulation of fibroblasts, etc. The role of these cells in neoangiogenesis of oral squamous cell carcinomas has been studied and these cells have been shown to promote new vessel formation. In inflammatory lesions of the oral cavity, neo-vascularization and presence of inflammatory cells is an expected finding. However, the role of mast cells in these lesions is still obscure. In this short study, we used toluidine blue as a special stain to stain mast cells in 15 cases of inflammatory lesions and correlate their presence with the state of vascularity and inflammation and probably suggest a role for mast cells in these common oral inflammatory lesions. We found that there was an inverse relationship between mast cells, vascularity, and inflammation probably suggesting a role for mast cells in these common oral inflammatory lesions. This was contradictory to earlier studies that showed a direct relationship between mast cells, vascularity, and inflammation
|How to cite this article:|
Sudhakar R, Ramesh V, Balamurali P D, Nirima O, Premalatha B, Karthikshree V. Incidence of mast cells in oral inflammatory lesions: A pilot study.J Oral Maxillofac Pathol 2005;9:12-15
|How to cite this URL:|
Sudhakar R, Ramesh V, Balamurali P D, Nirima O, Premalatha B, Karthikshree V. Incidence of mast cells in oral inflammatory lesions: A pilot study. J Oral Maxillofac Pathol [serial online] 2005 [cited 2020 Jul 2 ];9:12-15
Available from: http://www.jomfp.in/text.asp?2005/9/1/12/39052
Mast cells arise from a. multipotent CD 34+ precursor in the bone marrow and circulate in the peripheral blood as agranular, monocytic appearing cells. After migrating into tissues, these immature mast cells assume their typical granular morphology. Mast cells are normally distributed throughout connective tissues, where they may he especially numerous beneath the epithelial surfaces of the skin, in the respiratory system, in the gastrointestinal and genitourinary tracts, adjacent to blood or lymphatic vessels, and near or within peripheral nerves  . Human mast cells range from 5 to 15 μm in diameter and in histologic sections they often appear ovoid, tadpole, or spindle shaped cells [Figure 1]. The most significant feature of mast cells is their cytoplasmic granules that vary in size from 0.2 to 0.5 µ diameter.
Mast cells exert their influence locally and systemically by releasing a variety of potent mediators through degranulation [Figure 2]. Many of these mediators are stored within cytoplasmic granules (preformed mediators), while others are produced at the time of mast cell stimulation. They have been recognised as a source of a number of cytokines. While the importance and role of mast cell derived cytokines in disease is uncertain, it is conceivable that they may play an important role in both physiologic and pathologic conditions. Mast cell mediators like histamine. tryptase, tumor necrosis factor (TNF-α), interleukin-4 (IL-4) can increase fibroblast proliferation and also act as chemotacric factor for polymorphonuclear leucocytes. Other factors like heparin, fibroblast growth factor, and vascular endothelial growth factor (VEGF) can induce endothelial cell migration and new vessel formation  .
Due to the wide variety of chemical mediators that those cells produce, the role of mast cells has been extensively studied in conditions ranging from asthma. dermatological disorders to oral squamous cell carcinomas and lichen planes. In lichen planus, mast cells have been shown to recruit T-lymphocytes  . The role of those cells in bringing about neo-angiogenesis has been studied in oral squamous cell carcinomas and a positive relation has been shown  . There is also evidence that these cells, by regulating angiogenesis, can influence growth and progression in human cancers  . On the contrary, an inverse relationship has also been observed between the number of mast cells and the amount of tumor tissue 
In the oral cavity mast cells may modulate the pathogensis of apical periodontitis and may be responsible for stimulating the formation of granuloma with the resorption of underlying bone  . Pyogenic granuloma, inflammatory hyperplasias, and granulation tissue are some of the more commonly encountered reactive lesions in the oral cavity. Histopathology of these lesions usually consists of neovascularization and inflammation depending on the stage of the lesion. Since mast cells contain cytokines that can bring about these actions, their presence in these lesions might help us to have a better understanding of the pathogenesis behind these lesions. Previous studies have shown a direct correlation between mast cells and the state of vascularity and inflammation , . In this study we planned to see the relationship of mast cells in some of these common oral inflammatory lesions.
Materials and Methods
Serial sections of 5-micron thickness were made from paraffin embedded tissue blocks of 15 active inflammatory lesions. One group of sections were stained routinely for hematoxylin and eosin to confirm the diagnosis and also for comparison. The other group of sections were stained specifically for mast cells using the metachromatic dye-toluidine blue as per the method of Churukian and Schenk  , The lesions were studied for the distribution of mast cells in relation to vascularity and inflammatory areas under toluidine blue staining only. Each of these features were labeled as mild or moderate severe. The observations were tabulated in [Table 1] .
It has been observed that mast cell distribution was seen in all the 15 cases of inflammatory lesions. The distribution was predominantly mild in most of the cases (80%, 12/ 15 cases) and moderate / severe in only 3 out of 15 cases (20%) (Chart 1). The severe distribution of mast cells were noticed only in 3 of the 6 inflammatory hyperplasias.
The distribution of vascularity was found to be mild only in 2 cases (13.4%). whereas in rest of the 13 cases (86.6%), the vascularity was markedly elevated (Chart 2). This is in contrast to the distribution of mast cells, which is noticed, in a milder form.
Similarly, the inflammatory features were predominant in 14 cases (93.3%), while only one case (6.7%) showed mild inflammatory changes (Chart 3 ).
The above results only show the role of mast cells being less once the neo-vascularization and inflammation has already set in. The continued presence of mast cells in 3 of the inflammatory hyperplasia cases showing marked inflammatory changes probably indicates the continuity of the inflammatory phenomenon.
Volumes of previous literature have evolved pertaining to the role of mast cells in the development of inflammation in oral mucosa and dental pulp, especially in early vasoinductive events and in the transforming stage from acute to chronic inflammation  . The mast cell forms the first step in the mechanism of neo-vascularization and further inflammatory reactions. Degranulation of mast cell activates endothelium through TNF - dependent mechanism which may be critical to the elicitation phase of inflammation  . Mast cell tryptase has been shown to promote neo-angiogenesis in premalignant and malignant stages of the uterine cervix  . Hence, it is more important to know the role of mast cells and their contents in any stage of control ling inflammation and subsequent reactions. It is pertinent to know the multiple interactions between mast cells, endothelial cells, and other immune related system that could provide the basis for future therapies to target the mast cell responses. Interestingly, corticosteroids, which are used Frequently for treatment of oral mucosal inflammatory lesions have been shown to deplete mast cells locally  . Hence a detailed study has been taken up to understand the relation of mast cells with the other related target tissues.
The findings in our study were in stark contrast to those reported earlier which showed a direct relation between the number of toast cells. vascularity, and inflammation , . In cases of moderate / severe vascularity, the distribution of' mast cells were predominantly low as shown in our study [Figure 3],[Figure 4]. Similarly, in cases of established inflammation, the mast cell distribution was only mild in most of the cases [Figure 5],[Figure 6]. This disparity could be explained as follows
It has been reported in earlier literature that mast cells have got variable mediators within their granules. Once the mast cells were stimulated, they degranulate and bring about the required biological action. So it is only reasonable to presume that the predominance of mast cell under degranulation would take place in a stage much before the active stimulation of angiogenesis and subsequent inflammatory - reaction. This early stage could be defined as a pre-inflammatory stage before the active vascularity and inflammatory cells are increased. Hence, there is a clear reduction in the number of mast cells in most of the well established inflammatory lesions in our study.
We propose that this pre-inflammatory stage could be an ideal stage for studying the mast cells rather than the active stage of vascularity and inflammation. However, this could he further ascertained with the study of more number of such cases.
Summary and Conclusion
Our short study of 15 cases of oral inflammatory lesions for the distribution of mast cells showed an inverse relationship existing between vascularization and inflammation. We propose to state that there might exist a stage - pro-inflammatory, during which the active role of mast cell begin. Once the inflammation and vascularization has established, the role of mast cells may diminish.
Hence, we feel that the pre-inflammatory stage could be the ideal period for intervening with mast cell action during the treatment process.
|1||Walsh LJ, Davis MF, Xu LJ, Savage NW: Relationship between mast cell degranulation and inflammation in the oral cavity. Oral. Pathol. Med. 1995;24:266-272.|
|2||Walsh LJ. Mast cells and oral inflammation. Crit. Rev. Oral Hio1. Med.2003; 14(3): 188-198.|
|3||Galli SJ. New concepts about the mast cell. N. Engl. .J. Med. 1993; 328: 257-265.|
|4||Tomita M, Matsuzaki Y, Edagawa M. Shimizu T, Hara M, Onitsuka T. Distribution of mast cells in mediastinal lymph nodes from lung cancer patients. World Journal of Surgical Oncology 2003; 1:25.|
|5||Tharp MD. Mast cell and its mediators. Www.protectingwhatprotectsyou.com|
|6||lamaroon A, Pongsiriwet S, Jittidecharaks S, Pattanaporn K. Prapayasatok S, et al. Increase of mast cells and tumor angiogenesis in oral squamous cell carcinoma. J. Oral Pathol. Med. 2003; 32: 195-199.|
|7||Zhao ZZ, Savage NW, Sugerman PH, Walsh LJ. Mast cell/ T cell interactions in oral lichen planus..J. Oral Pathol. Med.2002;31: 189-195.|
|8||Kabashima H, Nagata K„ Maeda K, Iijima T. Involvement of substance P, mast cells. TNF-alpha and ICAM-I in the infiltration of inflammatory cells in human periapical granulomas. J. Oral Pathol. Med.2002; 31: 175-180.|
|9||Klein LM, Lavker RM. Matis WL, Murphy GF. Degranulation of human mast cells induces an endothelial antigen central to leucocyte adhesion. Proc. Natl. Acad. Sci. 1989; 86: 8972-8976 (Abstract).|
|10||Benitez - Bribiesca L, Wong A, Utrera D, Castellanos E. The role of roast cell tryptase in neo-angiogenesis of premalignant and malignant lesions of the uterine cervix. J. Histochem Cytochem. 2001. 49:1061-1062.|
|11||Ch urukian CJ, Schenk EA. A toluidine blue method for demonstrating mast cells. J. Histotechnol. 1981; 4: 85-86 (Cross Ref).|