Significant Difference In Microvessel Density Research Articles

Screw vs Cement-Implant–retained Restorations: An Experimental Study in the Beagle. Part 2. Immunohistochemical Evaluation of the Peri-implant Tissues

Crestal bone loss has been reported to occur around dental implants. Even if the causes of this bone loss are not completely understood, the presence of a microgap between implant and abutment with a possible contamination of the internal portion of the implants has been suggested. The aim of this study was to see if there were differences in the vascular endothelial growth factor (VEGF) expression, microvessel density (MVD), proliferative activity (MIB-1), and inflammatory infiltrate in the soft tissues around implants with screwed and cemented abutments. Sandblasted and acid-etched implants were inserted in the mandibles of 6 Beagle dogs. Ten 3.5- x 10-mm root-form implants were inserted in each mandible. A total of 60 implants (30 with screwed abutments and 30 with cemented abutments) were used. After 12 months, all the bridges were removed and all abutments were checked for mobility. A total of 8 loosened screws (27%) were found in the screwed abutments, whereas no loosening was observed in cemented abutments. A gingival biopsy was performed in 8 implants with cemented abutments, in 8 implants with screwed abutments, and in 8 implants with unscrewed abutments. No statistically significant differences were found in the inflammatory infiltrate and in the MIB-1 among the different groups. No statistically significant difference was found in the MVD between screwed and cemented abutments (P = .2111), whereas there was a statistically significant difference in MVD between screwed and unscrewed abutments (P = .0277) and between cemented and unscrewed abutments (P = .0431). A low intensity of VEGF was prevalent in screwed and in cemented abutments, whereas a high intensity of VEGF was prevalent in unscrewed abutments. These facts could be explained by the effects induced, in the abutments that underwent a screw loosening, by the presence of bacteria inside the hollow portion of the implants or by enhanced reparative processes.

Study of COX-2 expression and angiogenesis in non-small cell lung cancer

In this study the expression of COX-2 both in lung cancer tissues and tissues of benign disease of the lung is compared to explore the effect of COX-2 on occurrence and development of non-small cell lung cancer (NSCLC), and the relationship between COX-2 expression and clinical characteristics of patients with NSCLC. The COX-2 expression, vascular endothelial growth factor (VEGF) expression and microvessel density (MVD) were detected in 78 NSCLC lung cancer tissues and 14 benign tissues of the lung by immunohistochemical method. Expression of COX-2 protein was significantly higher in cancer tissues (69.2%, 54/78) than paired noncancerous tissues (14.3%, 2/14)(Chi-square=15.044, P < 0.01). There was significant difference of MVD between COX-2 positive lung cancers (19.41±8.56) and negative ones(12.00±5.37)(t=3.906, P < 0.01). There was no significant relationship between COX-2 protein expression and patients' age, sex, TNM stages and smoking status (P > 0.05); for different pathological types, COX-2 protein expression was remarkably higher in adenocarcinoma (88.9%, 32/36) than that in squamous cell carcinoma (50.0%, 20/40) (Chi-square=13.262, P < 0.01); and for squamous cell carcimoma it was significantly higher in low differentiated ones (81.0%, 17/21) than that in high differentiated ones (15.8%, 3/19) (Chi-square=16.942,P < 0.01); for adenocarcinoma it was also remarkably higher in low differentiated ones (100.0%, 18/18) than that in high differentiated ones ( 77.8% , 14/18) (Chi-square=6.046, P < 0.05).The expressions of COX-2 and VEGF in NSCLC were significantly positively correlated (r=0.509, P < 0.01), so were the expressions of VEGF and MVD (r=0.324, P < 0.01), and the expressions of COX-2 and MVD (r=0.477, P < 0.01). Controlling for VEGF, there still was significant correlation between COX-2 and MVD (r=0.383, P < 0.01). The present study suggests that there is overexpression of COX-2 in lung cancer, which is closely related to angiogenesis of lung cancer. Further studies, therefore, are needed to find the exact mechanisms.

Expression of inducible nitric oxide synthase and angiogenesis in gastric cancer

AIM:To investigate the expression of inducible NOS (iNOS) in human gastric cancer and its relationship with the angiogenesis in gastric cancer and lymphocyte metastasis. METHODS:The expression of iNOS in 50 patients with gastric cancer was studied by immunohistochemical SP method with anti-iNOS. Microvessel density (MVD) of human gastric cancer was also determined with anti-CD34 as the labels. RESULTS:The expression rate of iNOS in 50 cases was 70 %, and the rates of node negative and node positive in gastric cancer were 54.2 % and 84.6 %,respectively, with significant difference (P <0.01). There was a significant difference of MVD (P <0.01) among groups with different expression of iNOS. CONCLUSION:The expression rate of iNOS in human gastric cancer is high, and it is closely related to the carcinoangiogenesis and metastasis.

Thymidine phosphorylase expression in oral squamous cell carcinoma

Thymidine phosphorylase (TP), as an enzyme involved in DNA synthesis, catalyzes the reversible conversion of thymidine to thymine. It is also identical to the angiogenic factor, platelet-derived endothelial cell growth factor. We examined TP expression using immunohistochemistry in 66 archival samples obtained from the patients with primary oral squamous cell carcinoma (SCC) and investigated its relation to tumor vascularity, cell proliferation, apoptosis, clinicopathological features and survival. TP expression was identified in cytonucleus and/or cytoplasm in carcinomas, but was not identified in histologically normal epithelia distant to tumor in most cases. No significant difference of microvessel density (MVD) was found between the carcinomas with high TP expression (H-TP) and low TP expression (L-TP). The percentages of proliferative cells marked by Ki-67 staining in H-TP carcinomas was significantly higher than that in L-TP carcinomas (P=0.0222). The apoptotic indice (AI) in H-TP carcinomas tended to be lower than that in L-TP carcinomas (P=0.0723). Moreover, the level of TP expression was significantly correlated the pattern of tumor invasion (P=0.0146) and marginally correlated with lymph nodal metastasis (P=0.0804). Our results suggested that TP enzyme may play a role in promotion of tumor growth in oral SCC, and that its expression can be indicative of tumor aggressiveness in this tumor type.

Does a pro-angiogenic state exist in the bone-implant interface of aseptically loosened joint prosthesis?

Neovascularization is indispensable to both bone remodeling and the development of chronic inflammation. A pro-angiogenic state in the periprosthetic tissue may augment the inflammatory response to wear debris. To investigate if a pro-angiogenic state exists in the bone-implant interface of aseptically loosened joint prosthesis, the expression of vascular endothelial growth factor (VEGF) and its receptor Flk-1/KDR were studied by immunohistochemistry. The VEGF-Flk/KDR pathway has been implicated as a key signaling requirement for pathological angiogenesis. The level of vascularization in periprosthetic tissue was semi-quantitatively compared to osteoarthritic (OA) and rheumatoid arthritic (RA) synovium. The level of vascularization in areas of periprosthetic tissue with heavy or low/moderate wear debris were also compared semi-quantitatively by image analysis. High levels of VEGF expression (16/16 cases) particularly in the implant synovial-like lining layer together with Flk-1/KDR expression by endothelial cells (13/16), suggests that neovascularization is occurring. Morphometric comparison of periprosthetic tissue with RA and OA synovium revealed no significant difference in microvessel density, but did reveal significantly increased microvessel area in RA synovium (P > 0.05). Areas of high wear debris infiltrate also contained a significantly smaller microvessel area (P > 0.01). Suggesting that wear debris may cause behavioral modification of microvessels. Modifying angiogenesis in the periprosthetic tissue could be a potential therapeutic target in reducing inflammation.

Study on tumor angiogenesis in epithelial ovarian carcinoma.

To investigate tumor angiogenesis in benign, borderline and malignant epithelial ovarian tumors and its relation with the pathogenesis of ovarian carcinoma, polycolonal antibody directed against human von Willebrand factor (factor VIII) was used to measure the microvessel density (MVD) in 66 cases (11 benign, 10 borderline, and 45 malignant) of epithelial ovarian tumors by using immunohistochemistry. The results showed that the mean MVD in epithelial ovarian cancer (31.7 +/- 11.2, 400 X) was higher than in benign and borderline tumors (16.7 +/- 6.3, 20.7 +/- 8.8 respectively, P < 0.05). There was no difference in MVDs among those in different tumor grades (P > 0.05). But there was significant difference in MVDs among those in different tumor stages (P < 0.05). MVD in stage III-IV cancer was higher than that in stage I-II (P < 0.05). It is concluded that the tumor angiogenesis is an early event in ovarian tumorgenesis. The increased tumor micovessel might be responsible for tumor development.

Overexpression of Vascular Endothelial Growth Factor Is Responsible for the Hematogenous Recurrence of Early-Stage Gastric Carcinoma

Vascular endothelial growth factor (VEGF) is crucial for angiogenesis in various malignant tumors. However, it is still unclear whether VEGF is responsible for hematogenous metastasis after the curative resection of gastric carcinoma. In the present study, we evaluated the relevance of VEGF expression to the hematogenous recurrence of stage 1 or 2 primary gastric adenocarcinoma. Among 530 patients, 11 (2.1%) had hematogenous recurrence. Clinicopathological variables were compared between these 11 patients (group R) and 88 patients without intramucosal carcinoma who survived for more than 5 years (group S). Microvessel density (MVD) was assessed immunohistochemically along with VEGF protein expression in all patients from group R and 21 randomly selected patients from group S. There were significant differences in age, tumor size and VEGF expression in tumor tissue between the groups. Positive staining for VEGF protein was observed in all patients of group R, of whom 6 had strongly positive staining. On the other hand, 11 out of 21 patients in group S had positive staining and it was weak in all cases. Both the positive and strongly positive rate were significantly higher in group R than those in group S. There was no significant difference in MVD between the 2 groups (17.7 ± 11.09/field in group R vs. 14.8 ± 10.27/field in group S) and no significant correlation between VEGF expression, MVD and venous invasion, though a weak correlation between the intensity of VEGF staining and MVD was observed (negative staining 12.1 ± 10.51; weakly positive 16.67 ± 10.41; strongly positive 19.7 ± 9.97). Our results suggest that overexpression of VEGF, and not MVD or venous invasion, plays an important role in the hematogenous recurrence of curatively resected gastric carcinoma.

Angiogenesis in cutaneous lymphoproliferative disorders: microvessel density discriminates between cutaneous B-cell lymphomas and B-cell pseudolymphomas.

The role of angiogenesis in neoplastic disorders is supported by the evidence that tumor growth beyond a certain size requires induction of new blood vessels. The extent of tumor-associated angiogenesis, measured as microvessel density (MVD), has shown to correlate with aggressiveness and the prognostic outcome in several malignant neoplasms. Few data have been reported on the angiogenic response in lymphoproliferative diseases. In this study, the MVD has been assessed in benign and malignant primary cutaneous B-cell lymphoproliferative disorders. MVD was determined in formaldehyde-fixed, paraffin-embedded specimens of primary cutaneous B-cell lymphomas (CBCL; n = 18) and cutaneous B-cell pseudolymphomas (B-PSL; n = 22) according to previously described protocols but was performed using computer-aided microscopic morphometry. The endothelial cells of microvessels were identified by immunohistochemical staining for factor VIII-related antigen and CD31. The MVD was 99 dots/mm2 for CBCL and 68 dots/mm2 for PSL, and a MVD of 115 dots/mm2 for CBCL and 73 dots/mm2 for PSL by using an antibody against factor VIII-related antigen and CD31 antigen, respectively. Univariate analysis revealed statistically highly significant differences in MVD between CBCL and B-PSL (P = 0.0036 with staining for factor VIII-related antigen and P = 0.0002 with staining for CD31 antigen). This study analyzes for the first time the angiogenic response in CBCL compared with that of B-PSL and demonstrates that MVD discriminates between CBCL and B-PSL. However, because of an overlap in the ranges of MVD in CBCL and PSL, the MVD is not useful as a diagnostic tool in individual cases.

Uterine Leiomyosarcoma Has Deregulated Cell Proliferation, but Not Increased Microvessel Density Compared with Uterine Leiomyoma

Objective.To investigate the differences of biological aggressiveness in terms of proliferating cell nuclear antigen (PCNA) expression, cell proliferation, and microvessel density between uterine leiomyosarcoma and leiomyoma.Study design.All patients with uterine leiomyosarcoma undergoing surgery at National Cheng Kung University Hospital were eligible. Forty-four patients with uterine myoma were also studied as the benign counterpart. The paraffin-embedded slides were stained with hematoxylin and eosin to confirm the presence of tumor and to quantitate mitoses, PC 10 for measurement of PCNA expression, MIB 1 for measurement of cell proliferation, and factor VIII for quantitation of microvessel density. The immunohistochemical findings of the slides were correlated with clinocopathologic findings of the patients, and the data were analyzed by either χ2or unpairedttest.Results.Six patients with uterine leiomyosarcoma and 44 patients with uterine leiomyoma were studied. Statistically significant higher mean levels of PCNA and MIB 1 were observed in uterine leiomyosarcoma compared with those of uterine myoma (for PCNA expression,P= 0.0001; for MIB 1, 11.61 ± 11.42% vs 0.45 ± 0.21%,P< 0.0001). No significant difference of microvessel density was observed between these two groups (65.73 ± 48.62 vs 41.97 ± 28.20,P= 0.084). Among the six patients with leiomyosarcoma, two patients with a higher percentage of MIB 1-positive tumor cells died of recurrent disease. In contrast, two patients with lower MIB 1 counts were disease-free for 3 years or more.Conclusion.Deregulated cell growth in uterine leiomyosarcoma may account for the biological aggressiveness of this tumor. Furthermore, the percentage of MIB 1-positive tumor cells seems to be associated with the prognosis or extent of uterine leiomyosarcoma.