Increased mast cell density and protease content in actinic cheilitis

BACKGROUND: Actinic cheilitis (AC) is a pre-malignant lesion caused by ultraviolet (UV) radiation and characterized by epithelial and connective tissue alterations. Mast cells (MCs), key contributors to solar elastosis in murine UV-irradiated skin, were characterized in order to assess their potential contribution to connective tissue degeneration in AC. METHODS: Actinic cheilitis (n = 15) and normal lip (n = 8) biopsies were stained immunohistochemically for tryptase and enzymehistochemically for chymase to determine MC density and protease content. MC subpopulations (i.e. MC(T) containing only tryptase, and MC(TC) containing chymase and tryptase) and their distribution were also determined. RESULTS: Mast cells and their proteases were increased in AC as compared with normal lip (P < 0.0001), and appeared degranulated especially around elastotic areas. MC(T) predominated over MC(TC) in AC and normal lip (P < 0.05). However, in AC MC(T) were increased in the epithelium/connective junction and connective area (P < 0.05), while in normal lip MC(T) predominated in connective and submucosal areas (P < 0.05). CONCLUSION: The results suggest that increased MC density and protease content may contribute to elastosis formation in AC. In addition, changes in MC(T) distribution may favor AC malignization.     

Increase of mast cells and tumor angiogenesis in oral squamous cell carcinoma

BACKGROUND: Although mast cells (MCs) have been implicated in promoting angiogenesis in some malignant tumors, especially of the aerodigestive tract, little is known in oral squamous cell carcinoma (SCC). METHODS: A retrospective study was conducted to elaborate upon the correlation between MCs and tumor angiogenesis in 26 cases of oral SCC, six cases of oral pre-malignant dysplasia, 10 cases of oral hyperkeratosis, and six cases of normal oral mucosa by means of immunohistochemical technique. RESULTS: The MCs in all lesions and normal oral mucosa strongly expressed tryptase. The densities of MCs and microvessels appeared to increase with disease progression. The MC and microvascular counts were significantly higher in oral SCC than in hyperkeratosis and normal oral mucosa (P < 0.05). A significant correlation between MC and microvascular densities was observed in oral SCC (r = 0.5; P = 0.012). CONCLUSIONS: These findings suggest that MCs may upregulate tumor angiogenesis in oral SCC, perhaps via MC tryptase.     

Role of angiogenic and non-angiogenic mechanisms in oral squamous cell carcinoma: correlation with histologic differentiation and tumor progression

BACKGROUND: Angiogenesis has been demonstrated to associate with various measures of tumor aggressiveness in many human malignancies. However, studies of tumor angiogenesis in oral squamous cell carcinoma (SCC) are still unclear. Recent studies indicate non-angiogenesis mechanism (tumor-lined vessel) may exist in certain tumors. Therefore, we investigate microvessel density (MVD) and tumor-lined vessel in oral SCC. METHODS: Peritumoral and intratumoral MVD were measured by immunohistochemical staining. Tumor-lined vessels were identified by double staining. Statistical analysis of peritumoral and intratumoral MVD and presence of tumor-lined vessels with clinicopathologic parameters was performed. RESULTS: The results showed peritumoral MVD increased with disease progression and further increases of intratumoral MVD was detected by CD31 and CD34. Non-angiogenesis, tumor-lined vessel, presented in oral SCC and correlated significantly with tumor size, stage, and histologic differentiation. CONCLUSION: Our results suggest at the initiation of oral SCC, increasing vascularity is observed at the periphery of the tumor. As the tumor continues to grow, further increases of intratumoral vascularity and the presence of tumor-lined vessels are associated with cancer progression.     

Regional difference in intratumoral lymphangiogenesis of oral squamous cell carcinomas evaluated by immunohistochemistry using D2-40 and podoplanin antibody: an analysis in comparison with angiogenesis

BACKGROUND: Whether tumor cells induce lymphangiogenesis intratumorally or permeate pre-existing lymphatic vessels in the peritumoral area still remains unclear. In this study, we investigated in detail the intratumoral lymphangiogenesis of oral squamous cell carcinomas (SCC) in comparison with tumor angiogenesis. METHODS: Immunohistochemistry with D2-40, podoplanin antibody, and CD34 antibody were used to evaluate the lymphatic vessel density (LVD) and blood microvessel density (MVD). Vascular endothelial growth factor (VEGF) and VEGF-C expressions of oral SCC were also assessed by immunohistochemistry. RESULTS: LVD significantly increased in the superficial area of tumor tissue compared with normal mucosa, whereas it decreased in the deep area of intratumoral tissue near the invasion front, in sharp contrast to MVD, which significantly increased throughout tumor tissue. Consistent with the decreased intratumoral LVD and increased intratumoral MVD, VEGF-C expression of tumor cells was down-regulated in the deep area of tumor tissue, while VEGF expression of tumor cells was up-regulated throughout the tumor tissue. CONCLUSIONS: Lymphangiogenesis in oral SCC varies depending on the region within the tumor tissue. It is not induced in the genuine tumor stroma near the invasion front, probably due to the down-regulation of VEGF-C expression of tumor cells, which is different from VEGF-mediated induction of intratumoral angiogenesis.     

Mast cell subpopulations in gingival overgrowth induced by immunosuppressive and nifedipine medication

BACKGROUND: An immunohistochemical study was conducted to compare distributions of mast cell subpopulations in normal human gingiva and in gingival overgrowth induced by nifedipine and immunosuppressive medication. METHODS: Gingival samples were collected from 12 triple-medicated organ transplant recipients (immunosuppression group), 11 triple-medicated organ transplant recipients taking nifedipine (immunosuppression plus nifedipine group), 11 nifedipine-medicated cardiac outpatients (nifedipine group), and 20 generally healthy individuals (control group). Cryostat sections were stained with mAbs for tryptase and chymase, and an avidin-biotin enzyme complex method was used to detect tryptase-positive mast cells (MC(T)), tryptase- and chymase-positive mast cells (MC(TC)), and chymase-positive mast cells (MC(C)). Total numbers of labeled cells were determined in connective tissue beneath the sulcular epithelium, connective tissue beneath the oral epithelium, and middle connective tissue. Statistical analyses were conducted using the Kruskal-Wallis test, the Mann-Whitney U-test, and Pearson's correlation test. RESULTS: In the three counting zones combined, numbers of MC(TC) cells and MC(C) cells were lower (P = 0.001 and P = 0.048, respectively) in the immunosuppression group than in the control group. The difference in numbers of MC(TC) cells was most marked in the middle connective tissue. Nifedipine medication had no effect on numbers of the mast cell subclasses. CONCLUSIONS: Immunosuppressive medication without concomitant nifedipine decreases the numbers of MC(TC) and MC(C) in overgrown gingiva. Chymase-positive mast cells may play a role in formation of gingival overgrowth, especially in patients receiving cyclosporin A (CsA) medication with no concomitant nifedipine. In this respect, nifedipine and CsA are different.     

Reduction of syndecan-1 expression during lip carcinogenesis

Background:  Actinic cheilitis (AC) is an oral pre-cancerous lesion that sometimes develops into lip squamous cell carcinoma (SCC). Syndecan-1, a transmembrane heparan sulfate proteoglycan, modulates cell-proliferation, adhesion, migration and angiogenesis. Malignant epithelial cells often down-regulate their own syndecan-1 production, and are capable of inducing aberrant syndecan-1 expression in stromal cells. The aim of this study was to evaluate the variations in syndecan-1 expression during lip carcinogenesis, in normal lip (NL), AC and well-differentiated lip SCC.
Methods:  Biopsies of NL vermillion ( n  = 19), AC ( n  = 23) and lip SCC ( n  = 24) were stained immunohistochemically for syndecan-1.
Results:  Syndecan-1 expression was significantly reduced in AC and lip SCC as compared to NL ( P  < 0.05), with a significant reduction in lip SCC as compared to AC ( P  < 0.0001). In lip SCC lesions, syndecan-1 expression at the epithelium overlying the tumor was increased when compared to the tumor itself ( P  < 0.03), but was significantly reduced as compared to AC and NL ( P  < 0.001).
Conclusion:  The results showed that epithelial syndecan-1 expression is reduced as lip carcinogenesis progresses (NL>AC>lip SCC), suggesting that syndecan-1 could be a useful marker of malignant transformation in the lip.     

唇癌微血管密度和血管内皮生长因子表达的意义

目的　研究唇鳞状细胞癌组织中微血管密度 (MVD)和血管内皮生长因子 (VEGF)的表达和意义。方法　采用CD34和VEGF单克隆抗体 ,用免疫组化S P法对 4 2例唇鳞状细胞癌标本进行免疫组化染色。结果　唇癌组织MVD显著高于正常对照唇组织MVD(P <0 .0 0 1)。有淋巴结转移唇癌的MVD高于无淋巴结转移的MVD ,但两者之间无显著性差异 (P >0 .0 5 )。唇癌组织和正常组织中VEGF表达阳性率分别为 6 1.90 %和 10 .0 0 % ,两者间有显著性差异 (P <0 .0 0 1)。有淋巴结转移组VEGF阳性率 (80 .0 0 % )高于无淋巴结转移组VEGF阳性率 (5 6 .2 5 % ) ,但两者间无显著性差异 (P >0 .2 5 )。VEGF阳性表达唇癌的MVD高于VEGF阴性表达唇癌的MVD ,两者间有显著性差异 (P <0 .0 2 )。结论　唇癌中VEGF的表达与MVD有密切的联系 ,说明VEGF能较好地反映唇癌微血管生成的活跃程度 ,是一个重要促血管生成因子     

口腔鳞癌间质微血管的特征及意义

目的观察口腔鳞癌间质微血管的空间分布和形态学特征，分析它们与临床病理学参数间的关系，探讨抗血管生成治疗在口腔鳞癌治疗中的作用。方法应用双标免疫组织化学及计算机图像分析技术，检测和分析62例口腔鳞癌及30例癌旁正常组织和10例正常口腔黏膜的微血管分布及形态。结果口腔鳞癌间质微血管与癌旁和正常口腔黏膜微血管相比，前者具有血管密度高、不成熟、形态不规则、血管周长较小的特点（P〈0．01）；口腔鳞癌癌灶边缘的血管与癌灶内血管相比，血管密度更高（P〈0．01）、更不成熟（P〈0．05）；微血管密度与肿瘤的淋巴结转移有关（P〈0．01）。结论口腔鳞癌间质微血管与正常口腔组织血管比较，差异有统计学意义，该差异有利于抗血管生成治疗的应用。癌灶边缘可能是抗血管生成治疗的重要靶区。微血管密度可望成为判断肿瘤恶性程度的一项指标。     

Differential infiltration of CD8+ and NK cells in lip and oral cavity squamous cell carcinoma

J Oral Pathol Med (2010) 39 162–167 Background: CD8⁺ and natural killer (NK) cells have been considered the most effective cells in the combat of cancer, contributing to better prognosis and longer survival. Methods: The aim of this study was to evaluate the population of CD8⁺ and NK cells, by immunohistochemistry, in samples of oral cavity squamous cell carcinoma (OCSCC) and lip squamous cell carcinoma (LSCC), leukoplakia, actinic cheilitis, and healthy oral mucosa (control). The relationship of CD8⁺ and NK cells with survival data, lymph node metastasis, tumor size, and proliferative index was also evaluated. Results: The number of peritumoral and intratumoral CD8⁺ and NK cells was significantly higher in LSCC, when compared with control, pre‐malignant lesions, and OCSCC. A higher proportion of peritumoral CD8⁺ cells demonstrated correlation with a lower neoplastic proliferative index. Moreover, patients with OCSCC with a high density of peritumoral CD8⁺ cells showed a tendency towards a longer survival time. Conclusions: The differential CD8⁺ and NK cells infiltration in oral SCC might reflect a distinctive tumor microenvironment with a favorable local cytotoxic immune response against neoplastic cells.     

舌鳞癌淋巴管生成与颈淋巴结转移的关系

目的：研究舌鳞癌淋巴管生成及淋巴管密度／淋巴管相对面积（LVD／LVA）与颈淋巴结转移的关系，为术前准确判断颈淋巴结状况提供参考。方法：口腔颌面外科接受舌癌切除及颈淋巴清扫术的标本63例：对HE染色阴性的淋巴结，应用细胞角蛋白CK（AE1／AE3）标记检测微转移，以免疫组织化学检测结果判断淋巴结转移；以LYVE—1作为淋巴管内皮标志物，研究舌癌淋巴管生成参数——淋巴管密度（LVD）和淋巴管面积（LVA）与颈淋巴结转移及其他临床病理变量（年龄、性别、T分类、病理分级、浸润方式）之间的关系。应用SPSS10．0统计软件包对所得数据进行Mann-whitney U检验。结果：应用细胞角蛋白CK（AE1／AE3）标记免疫组化法检测微转移，提高了淋巴结转移的检出率；舌癌实质内未见到LYVE—1^＋的脉管结构，LYVE—1^＋脉管多位于癌周，癌周LVD、LVA与颈淋巴结转移及其他临床病理变量均无关。结论：舌癌癌周淋巴管密度（LVD）、淋巴管面积（LVA）与颈淋巴结转移及其他临床病理变量均无关，不宜作为术前评估淋巴结状况的指标。     

Immunohistochemical evaluation of angiogenesis and tryptase-positive mast cell infiltration in periapical lesions

Introduction

Several studies have linked mast cells (MCs) with angiogenesis. The aim of this study was to correlate angiogenesis with MCs in radicular cyst (RC) and periapical granuloma (PG) cases.

Methods

Forty-eight samples of periapical lesions, diagnosed as RC (n = 24) and PG (n = 24), were included. The microvessel density and microvessel area measured through the immunoexpression of CD105 and CD34 and the MC density measured through the immunoexpression of tryptase were performed.

Results

MCs were detected in all RCs and PGs (P = .888), mainly in perivascular location and within fibrous stroma. CD34 stained all vessels present in all RC and PG cases. CD105 revealed differential expression, stained preferentially vessels of greater lumen, and showed variable location inside fibrous stroma in both lesions. There was a significant difference of microvessel density determinate by CD34 and CD105 in RCs (r = 0.634, P = .002) and in PGs (r = 0.5709, P = .0036). The difference was also observed when comparing age of the patient in both lesions. Considering the microscopic association between highest concentration of MCs and vascularization, CD105-positive vessels in 50% of RCs and 70.8% of PGs and CD34-positive vessels in 66.7% of RCs and 87.5% of PGs showed areas of close association with MCs.

Conclusions

These results suggest differential expression of CD105 within RC and PG. There is no difference in angiogenesis and MC density between RC and PG. Moreover, because of the association between MCs with vessels and fibrous stroma, other possible roles of tryptase, in addition to the angiogenic properties, should also be considered.     

Intratumoral lymphangiogenesis in oral squamous cell carcinoma and its clinicopathological significance

Lymphatic metastasis has always been regarded as a major prognostic indicator for disease progression and as a guide for therapeutic strategies to oral squamous cell carcinoma (OSCC), but to date, how tumor cells access and spread via the lymphatics have not been fully elucidated. Whether tumor cells metastasize by expansion and invasion of pre‐existing peritumoral lymphatics or by the induction and invasion of newly formed lymphatics within tumors is controversial. In order to address this issue and find out the clinicopathological significance of intratumoral lymphangiogenesis, we investigated 86 archival specimens from patients with OSCC, quantitating lymph vessels by immunostaining with D2‐40. We also quantified lymphatic invasion and examined the possible associations of all the above parameters with clinicopathological features and outcome. Higher intratumoral lymphatic density (ILD) and peritumoral lymphatic density (PLD) were both significantly associated with the presence of lymph node metastasis at the time of diagnosis and the outcome of the post‐operation biopsy of 77 patients (P = 0.001). Higher ILD was significantly associated with a higher incidence of intratumoral lymphatic invasion, peritumoral lymphatic invasion and recurrence of tumor (P = 0.001 and P = 0.041 and P = 0.001, respectively). Patients with higher ILD exhibited shorter 5‐year cumulative and disease‐free survival (P = 0.001). Thus, lymphangiogenesis indeed occurs in oral squamous cell carcinoma; ILD might be used as an index to inflect the aggression of the disease, to evaluate the status of lymphatic metastasis, to separate patients at higher risk of an adverse clinical outcome.     

Immunohistochemical analysis of lymphatic vessel density and mast cells in oral tongue squamous cell carcinoma

The aim of this study was to analyze lymphangiogenesis and the presence of mast cells in oral tongue squamous cell carcinoma (OTSCC), correlating the findings with clinicopathological parameters (clinical stage, tumor size, nodal metastasis, histological grade of malignancy, local recurrence, and clinical outcome). Fifty-six cases of primary OTSCC were selected. Lymphatic vessels and mast cells were identified by immunostaining with anti-podoplanin (D2-40) and anti-tryptase antibody, respectively. Lymphatic vessel density (LVD) and mast cell density (MCD) were determined in the intratumoral and peritumoral areas. Intratumoral LVD was higher in advanced clinical stages (III/IV) when compared to early-stage (p = 0.017) and in metastatic cases compared to non-metastatic tumors (p = 0.013). Peritumoral LVD and intratumoral or peritumoral MCD did not differ significantly according to the clinicopathological parameters of OTSCCs (p > 0.05). No significant correlations between LVD and MCD were observed at the intratumoral (r = ?0.014; p = 0.918) or peritumoral level (r = 0.156; p = 0.251). Our findings suggest that intratumoral lymphatic vessels, compared to peritumoral lymphatic vessels, appear to be more related to the progression of OTSCC. MCD alone does not seem to be determinant for lymphangiogenesis or for the biological behavior of OTSCC, indicating multiple pro- and antitumor effects of these inflammatory cells.     

High interstitial fluid pressure in rat tongue cancer is related to increased lymph vessel area, tumor size, invasiveness and decreased body weight

Background:  Interstitial fluid pressure (IFP) in most tumors is high, and this high pressure has been correlated with poor prognosis. Measurements of IFP in normal tongue and in tongue cancer are lacking. Recent research suggests the existence of a relationship between increased peritumoral lymph vessels (PTLV) and survival, and a correlation of increased lymphatic vessel density with an unfavorable prognosis has been reported.
Materials and methods:  In the present study, tongue squamous cell carcinoma (SCC) was induced by adding the carcinogen 4-nitroquinoline oxide in drinking water for 19 weeks. The IFP was measured by micropuncture and immunohistochemistry was used to visualize lymph vessels.
Results:  In normal tongue, IFP averaged 3.1 ± 0.3 mmHg. The IFP, both in the tumor (29.1 ± 2.9 mmHg) and 0.5 cm anterior to it (15.4 ± 2.1 mmHg) was consistently increased ( P  <   0.005) with values ranging from 10 to 40 mmHg. The highest IFP values were measured in rats with large tumors ( P  <   0.05) and low body weight ( P  <   0.001), suggesting that IFP increases with cancer progression. Lymphatic vessel area (%), as determined with the lymphatic specific marker LYVE-1 antibody, was significantly increased in the peritumoral area when compared to intratumoral and control mucosa ( P  <   0.05). There was a significant positive correlation between IFP, PTLV area, tumor size and invasiveness.
Conclusions:  Our data show that IFP is increased in tongue cancer. Corresponding changes in PTLV area, invasiveness, tumor area and IFP suggest that the increased pressure is caused by defective lymph drainage and solid stress generated by tumor cells growing in a low compliant environment.     

透明质酸在口腔鳞状细胞癌组织中的表达

目的 本研究旨在探讨透明质酸在不同分化口腔鳞状细胞癌中的表达及意义.方法 应用免疫组织化学法检测37例不同分化程度口腔鳞状细胞癌组织中透明质酸的表达.结果 按阴性(-)、弱阳性( )、阳性( )、强阳性( )表示,并进行统计学分析.结果 透明质酸主要表达于肿瘤间质和细胞外基质,细胞膜和胞浆中染色相对较少.37例口腔鳞状细胞癌组织中,低分化鳞癌透明质酸的表达明显高于高分化鳞癌(P＜0.05),表达随肿瘤分化程度降低而增强.结论 透明质酸的表达与口腔鳞状细胞癌的分化程度有关,分化越低,其表达越强.透明质酸的高表达可能有利于病变的侵袭和转移.     

Mast cells – a role in periodontal diseases?

OBJECTIVES: Limited attention has been given to the role mast cells may play in periodontal diseases. BACKGROUND: Mast cells are indeed found abundantly below and within several types of mucosal epithelia. On the basis of their proteinase content, mast cells are divided into connective tissue (CT) and mucosal phenotypes. The CT phenotype contains both tryptase and chymase (MC(TC)), while the mucosal phenotype contains only tryptase (MC(T)). The in vivo significance of different mast cell phenotypes has not yet been fully established. Mast cells are able to phagocytose, process and present antigens as effectively as macrophages. RESULTS: Recently mast cells were found in high numbers in chronically inflamed gingival tissue taken from patients with chronic marginal periodontitis (CMP). The number of mast cells was found to be even higher in HIV(+) patients with CMP. Furthermore, mast cells also express strongly matrix metalloproteinases (MMPs), which are key enzymes in degradation of gingival extracellular matrix. Mast cells may release preformed cytokines directing local innate and adaptive immune responses. The present review will focus on possible roles for mast cells in periodontal diseases. CONCLUSIONS: We certainly feel that this is a key cell in inflamed periodontal tissue and its role in periodontitis needs to be revisited.     

Differentiated expression of membrane type metalloproteinases (MMP‐14, MMP‐15) and pro‐MMP2 in laryngeal squamous cell carcinoma. A novel mechanism

Cancer progression involves multiple proteolytic interactions, with metalloproteinases (MMPs) performing a crucial role. MMP‐2, a major MMP, plays a key role in the degradation of basement membranes. Mechanisms underlying MMP‐2 activation had to be investigated. Membrane‐type matrix metalloproteinases are not only responsible for the regulation of extracellular matrix remodeling, but also involved in the activation of several inactive MMPs. The aim of this study was to evaluate the expression of pro‐MMP2, MMP‐14, and MMP‐15 in tumor cells and tumor stroma. Immunohistochemical studies were performed on paraffin‐embedded tissue sections including laryngeal squamous cell carcinoma (SCC). We found the expression of pro‐MMP2 in 58% of cases, MMP‐14 in 78%, and MMP‐15 in 98% of cases of SCC. In all tumor cases, we revealed a higher expression of pro‐MMP2 in tumor stoma than in tumor cells. The expression of MMP‐14 and MMP‐15 was higher in tumor cells than in the stroma. Moreover, we found a statistically significant difference between the expression of MMP‐14 and MMP‐15 in the tumor in comparison with the surrounding stroma (P < 0.05). An analysis of expression levels of MT‐MMPs by classification trees showed that the probability of metastases was related to decreased expression of MMP‐14 and increased expression of MMP‐15. Our results may suggest that tumor cells with low MMP‐14 expression invade tumor stroma and form metastases. Probably, in such cases, tumor progression is stimulated by MMP‐15 in an MMP‐14 independent pathway, a novel (alternative) mechanism.     

The presence of Merkel cells and CD10‐ and CD34‐positive stromal cells compared in benign and malignant oral tumors

Background: To describe sequential changes in Merkel cells (MC), and CD10⁺ and CD34⁺ stromal cells (SC) during the transition from benign to malignant oral lesions and correlate with clinicopathologic parameters. Materials and methods: Changes in cytokeratin 20‐positive (CK20⁺) Merkel cells, CD10⁺ and CD34⁺ SC were immunohistochemically examined in specimens of 28 oral verrucous carcinomas (VC), 32 squamous cell carcinomas (SCC) and 36 benign squamous lesions (BSL). Immunoreactivity and localized inflammation were measured quantitatively and/or semiquantitatively, and between‐group results were statistically compared. Results: The mean number of CD34⁺ SC was significantly lower in VC (57.36) and SCC (33.81) than BSL (351.56, P < 0.001). However, the three tumor types had similar staining level and number of CD10⁺ SC. We found a significant difference in the density of MC between BSL and VC (P < 0.001) or SCC (P < 0.001). The number of CK20⁺ MC was significantly lower in highly inflamed specimens than mildly inflamed specimens (P = 0.001). Conclusion: CD34⁺ SC and to a lesser extent MC, but not CD10⁺ SC, reveal statistically different density during the transition from benign to malignant oral lesions. The correlations between the CD34⁺ SC expression and squamous lesions may be associated with epithelial dysplasia and/or tumor invasion.     

Podoplanin在口腔鳞状细胞癌中的表达及与淋巴结转移的关系

目的:采用淋巴管特异性标志物podoplanin标记口腔鳞癌组织和正常口腔组织中的淋巴管,并计数淋巴管密度(lymphatic vessel density,LVD)值,探讨口腔鳞癌及癌周淋巴管密度与淋巴结转移的相关性及可能机制。方法:采用免疫组织化学方法检测21例正常口腔黏膜组织和88例口腔鳞癌患者组织的podoplanin表达;用podoplanin标记淋巴管,并计数口腔鳞癌和癌周组织的淋巴管密度。采用SPSS13.0软件包对数据进行t检验,分析正常组织和癌组织、淋巴结转移组和未转移组的淋巴管密度(癌周、癌内)。结果:口腔鳞癌及癌周组织的淋巴管密度均高于正常口腔黏膜组织,有显著差异(P<0.05)。癌组织内淋巴管小而闭锁,癌组织周围的淋巴管大而扩张;淋巴结转移组的癌周淋巴管密度(14.270±4.610)显著高于无转移组(9.450±2.411),差异具有显著性(P<0.05),癌组织淋巴管密度在2组间无显著差异。结论:口腔鳞癌患者癌周淋巴管的生成可能是影响区域淋巴结转移的重要因素。     

Mast Cell Degranulation in Human Periodontitis

Background: Mast cells are tissue‐resident immune cells that participate in a variety of allergic and inflammatory conditions. Limited attention has been given to the role of mast cells in periodontal diseases, and the effects of mast cell degranulation on the chronic stages of non‐allergic inflammation, particularly in periodontitis, are not known. The present study analyzes the relationship between the mast cell degranulation and human periodontal disease progression. Methods: A total of 50 clinical specimens including moderate periodontitis (n = 17), advanced periodontitis (n = 18), and healthy control tissues (n = 15) were used in this study. All specimens were fixed in 10% buffered formalin and stained with hematoxylin and eosin for histopathology, with toluidine blue for identifying mast cells, and by immunohistochemistry for the expressions of mast cell tryptase in periodontal tissues. The total and degranulated mast cell densities (per high‐power field) were quantified in the specimens. Results: Compared with healthy controls, there were significantly increased both total and degranulated mast cell densities in human moderate (P <0.01) and advanced (P <0.01) periodontitis groups by toluidine blue staining, and there were significantly higher densities of both total and degranulated tryptase‐positive mast cell subpopulation in the moderate periodontitis group (P <0.01) and even significantly higher subpopulation densities in the advanced periodontitis group by immunohistochemical staining, in which both total and degranulated mast cell densities were significantly higher in the advanced periodontitis group than those in the moderate periodontitis group (P <0.01) by both toluidine blue staining and immunohistochemical staining. There was significantly more severe periodontal inflammatory pathology in the advanced periodontitis group than in the moderate periodontitis group (P <0.01). Conclusion: These findings indicate a significant correlation among tryptase‐positive mast cell density, the degree of their degranulation, and the human periodontitis severity, and the results of this study further indicate that mast cell degranulation appears to be associated with human periodontal disease.