15d-PGJ2 as an endoplasmic reticulum stress manipulator in multiple myeloma in vitro and in vivo.

Multiple myeloma (MM) is characterised by intense protein folding and, consequently endoplasmic reticulum (ER) stress. The prostaglandin 15d-PGJ2 is able to raise oxidative stress levels within the cell and potentially trigger cell death. The aim of this study was to evaluate the antineoplastic effect of 15d-PGJ2 on MM in vitro and in vivo via ER and oxidative stress pathways. MM.1R and MM.1S cell lines were treated with 15d-PGJ2 at 1-10µM and evaluated with regard to proliferation, mRNA expression of PRDX1, PRDX4, GRP78, GRP94, CHOP, BCL-2 and BAX. Stress data was validated via oxidized glutathione assays. MM.1R cells were inoculated into NOD/SCID mice, which were subsequently treated daily with 15d-PGJ2 at 4mg/kg or vehicle (control), with tumour volume being monitored for 14days. 15d-PGJ2 reduced cell proliferation, induced cell death and apoptosis at 5µM and 10µM and Stress-related genes were upregulated at the same doses. Oxidized glutathione levels were also increased. 15d-PGJ2 at 4mg/kg in vivo halted tumour growth. In conclusion, 15d-PGJ2 induced myeloma cell death via ER stress in vitro. 15d-PGJ2 in vivo also inhibited tumour growth.

Evaluation of Inflammatory Response to Endodontic Sealers in a Bone Defect Animal Model.

AIM: The aim of this study was to evaluate the inflammatory response to MTA Fillapex, AH Plus, and Pulp Canal Sealer Extensive Work Time (EWT), in a murine bone defect grafting model. MATERIALS AND METHODS: Bilateral mandibular critical defects were produced in 45 Wistar rats with a trephine bur#2 and filled with the endodontic sealers. After 7, 14, and 28 days, the rats were euthanized and their jaws were histologically prepared. RESULTS: For the 7-day group, no statistical significance was observed among all studied groups (p > 0.05), and high levels of inflammatory infiltrate were detected. After 14 and 28 days, Pulp Canal Sealer EWT showed statistically lower inflammatory response in comparison to other sealers (p < 0.05) except for the control group (no sealers). CONCLUSION: Pulp Canal Sealer EWT presented the lowest levels of inflammatory response. The critical defect grafting model was an effective method to detect differences among differences on the biological response to endodontic sealers. CLINICAL SIGNIFICANCE: Knowing the biocompatibility of endodontics sealers that will be used in filling the root canal.

Tubular variant of basal cell adenoma shares immunophenotypical features with normal intercalated ducts and is closely related to intercalated duct lesions of salivary gland.

AIMS: The morphological criteria for identification of intercalated duct lesions (IDLs) of salivary glands have been defined recently. It has been hypothesised that IDL could be a precursor of basal cell adenoma (BCA). BCAs show a variety of histological patterns, and the tubular variant is the one that presents the strongest resemblance with IDLs. The aim of this study was to analyse the morphological and immunohistochemical profiles of IDLs and BCAs classified into tubular and non-tubular subtypes, to determine whether or not IDL and tubular BCA represent distinct entities. METHODS AND RESULTS: Eight IDLs, nine tubular BCAs and 19 non-tubular BCAs were studied. All tubular BCAs contained IDL-like areas, which represented 20-70% of the tumour. In non-tubular BCA, IDL-like areas were occasional and small (<5%). One patient presented IDLs, tubular BCAs and IDL/tubular BCA combined lesions. Luminal ductal cells of IDLs and tubular BCAs exhibited positivity for CK7, lysozyme, S100 and DOG1. In the non-tubular BCA group, few luminal cells exhibited such an immunoprofile; they were mainly CK14-positive. Basal/myoepithelial cells of IDLs, tubular BCAs and non-tubular BCAs were positive for CK14, calponin, α-SMA and p63; they were more numerous in BCA lesions. CONCLUSIONS: IDL, tubular BCA and non-tubular BCA form a continuum of lesions in which IDLs are related closely to tubular BCA. In both, the immunoprofile of luminal and myoepithelial cells recapitulates the normal intercalated duct. The difference between the adenoma-like subset of IDLs and tubular BCA rests mainly on the larger numbers of myoepithelial cells in the latter. Our findings indicate that at least some BCAs can arise via IDLs.

In-vitro analysis of rhBMP-2 effects in human osteogenic cells.

This study evaluated the in vitro expression of bone-related proteins by osteoblasts in the presence of different concentrations of human recombinant bone morphogenetic protein-2 (rhBMP-2). Immortalized human fetal osteoblastic cell line 1.19 (hFOB) were exposed to different concentrations of rhBMP-2 (10, 50, or 100 ng/mL) for 72 h. Cell proliferation and viability (MTT assay), as well as the expression of fibronectin, osteonectin, and osteopontin were assessed by indirect immunofluorescence and Western blot. Neither of the 3 concentrations of rhBMP-2 caused statistically significant alterations in cell proliferation and viability, although the concentration of 100 ng/mL showed lower values for both assays after both 48 and 72 h of exposure. There was no alteration in the expression of noncollagenous proteins, as analyzed by immunofluorescence, when compared with the control group. Furthermore, in the Western blot assay we observed a statistically significant decrease in fibronectin and osteonectin at 100 ng rhBMP-2/mL (p < 0.05) by comparison with the medium alone. The expression of osteopontin decreased slightly in all 3 concentrations of rhBMP-2 tested; however, the change was not statistically significant (p > 0.05). In this in-vitro study, the tested concentrations of rhBMP-2 appeared to decrease the expression of important bone-related molecules in pre-osteoblast cells.

Levels and patterns of expression of hypoxia-inducible factor-1α, vascular endothelial growth factor, glucose transporter-1 and CD105 in adenoid cystic carcinomas with high-grade transformation.

AIMS: To compare the expression of proteins regulated by hypoxia between adenoid cystic carcinoma (ACC) with and without high-grade transformation (HGT). METHODS AND RESULTS: In eight ACC-HGT and 18 ACC without HGT, expression of hypoxia-inducible factor-1 (HIF-1α), vascular endothelial growth factor (VEGF), glucose transporter-1 (GLUT-1) and microvascular density (MVD) by CD105 (a hypoxia-inducible protein expressed in angiogenic endothelial cells) was determined. Expression levels of HIF-1α and VEGF as well as CD105-MVD did not differ significantly between: (i) transformed and conventional areas (TA and CA, respectively) of ACC-HGT, (ii) CA and ordinary ACC. HIF-1α was detected in 100% of cases and presented a diffuse expression pattern. No significant association was found between levels of HIF-1α expression and tumour size, metastasis and recurrence. GLUT-1 showed a prostromal expression pattern and was observed exclusively in TA (three of six cases) and in only three of 14 ACC. CONCLUSIONS: Both the absence of significant alterations in levels of expression of HIF-1α, VEGF and CD105 and the patterns of expression of HIF-1α and GLUT-1 suggest that hypoxia may not play a key role in the process of high-grade transformation of ACC. Although HIF-1α expression is a common finding in ACC, it cannot be used as a marker of tumour aggressiveness.

Glucose transporter protein 1 expression in mucoepidermoid carcinoma of salivary gland: correlation with grade of malignancy.

Mucoepidermoid carcinoma (MEC), the most common primary salivary malignancy, shows great variability in clinical behaviour, thus demanding investigation to identify of prognostic markers. Since Warburg's studies, unrestricted cell growth during tumorigenesis has been linked to altered metabolism, implying hypoxic stimulation of glycolysis and diminished contribution of mitochondrial oxidative phosphorylation to cellular ATP supply. Hypothesizing that the study of MEC metabolic status could lead to the discovery of prognostic markers, we investigated by immunohistochemistry the expression of glucose transporter 1 (Glut-1), mitochondrial antigen and peroxiredoxin I (Prx I) in samples of MEC from different histological grades. Our results showed that mitochondrial antigen and Prx I were expressed in the majority of the MEC cases independent of the histological grade. In contrast Glut-1 expression increased significantly as the tumours became more aggressive. These results suggested that oxidative phosphorylation may contribute to ATP supply in all stages of MEC progression, and that the relative contribution of glycolysis over mitochondria for cellular ATP supply increases during MEC progression, favouring growth under low oxygen concentration. In addition, the observed high Prx I protein levels could provide protection to tumour cells against reactive oxygen species generated as a consequence of mitochondrial function and hypoxia-reoxygenation cycling. Altogether our findings suggest that upregulation of Glut-1 and Prx I constitute successful adaptive strategies of MEC cells conferring a growth advantage over normal salivary gland cells in the unstable oxygenation tumour environment.

Angiogenic and lymphangiogenic microvessel density in recurrent pleomorphic adenoma.

BACKGROUND: Recurrent pleomorphic adenoma (RPA) is an uncommon and challenging disease. The aim of this study was to determine if there is a difference between RPA and the pleomorphic adenoma (PA) without recurrence related to tumor blood and lymphatic vascularization. Moreover, we compared the microvessel density (MVD) between cell-rich areas (predominance of epithelial cells) and cell-poor areas (predominance of myxoid and chondroid areas) of the stroma of PA and RPA. In addition, immunohistochemical staining for the Ki-67 antigen was conducted simultaneously to evaluate cell proliferation in PA and RPA. METHODS: A total of 19 cases of PA and 24 cases of RPA, blood, and lymphatic vessels were analyzed by immunohistochemical technique using the antibodies CD34, CD105, D2-40, and Ki-67. RESULTS: Comparing no recurrent with recurrent tumor, no significant difference was found in terms of lymphatic vessel density, MVD, and proliferation index. When MVD and proliferation index were compared with different areas in cellular composition (cell-rich and cell-poor areas), there was a significant difference in PA, as well as in RPA. CONCLUSION: This study shows that although RPA presents more aggressive clinical behavior than PA, there is no difference between tumor blood and lymphatic vascularization, suggesting that there is no correlation between vascularity and risk of recurrence. Furthermore, vascularized stroma in PA, as well as RPA, depends on the proportion of the cellular composition.

Peroxiredoxin I is overexpressed in oncocytic lesions of salivary glands.

BACKGROUND: Oncocytic lesions, particularly frequent in the salivary glands, are characterized by cells with an atypical accumulation of mitochondria. This accumulation has been recognized as a compensatory mechanism to intrinsic functional defects of these organelles, resulting in energy production impairment and increased generation of reactive oxygen species (ROS), including hydrogen peroxide (H(2)O(2)). Peroxiredoxin I (Prx I) is a H(2)O(2) scavenging protein and the expression of its yeast homolog was reported to be influenced by mitochondrial function. METHODS: In this study, we evaluated Prx I expression in oncocytic lesions of salivary glands by immunohistochemistry. RESULTS: Our results showed that Prx I is overexpressed in oncocytes regardless of the salivary gland lesion where they appear. CONCLUSIONS: These results suggest that Prx I expression in oncocytes is related to its ability to decompose mitochondrial-derived H(2)O(2) and that it could provide to the cells a protective role in an environment that, by continuously producing potential DNA-damaging ROS, predisposes to genome instability and cellular transformation.

Antigen-presenting cells in human immunosuppressive drug-induced gingival enlargement.

An immunoperoxidase technique was used to compare the number of CD1a+ and factor XIIIa+ dendritic cells (DCs), and CD68+ Macrophages (M) in 30 gingival samples from subjects with clinically healthy periodontitium (HP) and 10 samples from subjects with drug-induced gingival enlargement (DIGE). Fewer CD1a+ and factor XIIIa+ DCs were found in areas with inflammatory infiltration (II) of the lamina propria (LP) in the group with immunosuppressed DIGE (IDIGE) compared to the group with HP. In the sulcular and junctional/pocket epithelia, the number of CD1a+ DCs was decreased in the group with IDIGE (p<0.05). There was a tendency toward a reduced number of CD1a+ DCs and CD68+ M in areas without inflammatory infiltrate of the LP in the group with IDIGE. The alterations in the number of antigen-presenting cells (APCs) may be the reason for the decreased periodontal inflammation and breakdown clinically observed in subjects who are immunosuppressed.

SOFAT as a Putative Marker of Osteoclasts in Bone Lesions.

Secreted osteoclastogenic factor of activated T cells (SOFAT) is a novel activated human T-cell-secreted cytokine that induce osteoclastogenesis in a RANKL-independent manner. The aim of this study was to evaluate the immunohistochemical expression of SOFAT in intraosseous and extraosseous lesions. Thirty-two oral biopsies were divided into 2 groups: (1) intraosseous lesions-4 cases of cherubism, 5 central giant cell lesions, 3 osteoblastomas, 3 cementoblastomas, 2 periapical lesions and (2) extraosseous lesions-5 peripheral giant cell lesions, 5 cases of oral paracoccidioidomycosis, and 5 foreign body reactions. Immunohistochemistry was performed for SOFAT and tartrate-resistant acid phosphatase. Image analysis consisted of a descriptive evaluation of the immunohistochemical staining pattern observed. Tartrate-resistant acid phosphatase-positive lesions included those containing multinucleated giant cells (MGC) from both groups. SOFAT was positive in MGC of the intraosseous lesions group, except in periapical foreign body reactions as well as extraosseous lesions. SOFAT was shown to be a putative marker of osteoclasts, which proved useful to differentiate them from multinucleated macrophages. Osteoclast induction may be both dependent and independent from the RANK/RANKL/OPG pathway and independent from the bone microenvironment.

Effect of meloxicam and diclofenac sodium on peri-implant bone healing in rats.

BACKGROUND: This study evaluated the effects of diclofenac sodium and meloxicam on peri-implant bone healing. METHODS: Thirty male rats were divided into three groups: the control group (CG) received no drug; the diclofenac sodium group (DSG) received 1.07 mg/kg twice a day for 5 days; and the meloxicam group (MG) received 0.2 mg/kg daily for 5 days. A screw-shaped titanium implant was placed in the tibia. Fluorochromes, oxytetracycline (OxT), calcein (CA), and alizarin (AL), were injected at 7, 14, and 21 days, respectively, after implantation, and the animals were sacrificed 28 days after implant placement. The percentages of OxT-, CA-, and AL-labeled bone as well as the percentages of bone-to-implant contact (BIC), cortical bone area (CBA), and trabecular bone area (TBA) within the implant threads were evaluated. RESULTS: Bone healing was delayed in the DSG during the first 14 days after implant placement (OxT-labeled bone: DSG: 5.3% +/- 7.3% versus CG: 13.2% +/- 9.8%, P = 0.002, and versus MG:14.4% +/- 13.1%, P = 0.05). The percentages of BIC (DSG: 49.6% +/- 21.9%; MG: 67.1% +/- 22.8%; and CG: 68.1% +/- 22.8%) and CBA (DSG: 63.7% +/- 21.2%; MG: 82.7% +/- 12.4%; CG: 84.9% +/- 10.6%) were lower in the DSG compared to the MG and CG (P <0.001). The percentage of TBA was significantly greater in the DSG compared to the MG and CG (DSG: 36.3% +/- 21.2% versus MG: 17.3% +/- 12.7% and versus CG: 15.1% +/- 10.6%; P <0.001). CONCLUSION: Diclofenac sodium seemed to delay peri-implant bone healing and to decrease BIC, whereas meloxicam had no negative effect on peri-implant bone healing.

Hydrocortisone affects the expression of matrix metalloproteinases (MMP-1, -2, -3, -7, and -11) and tissue inhibitor of matrix metalloproteinases (TIMP-1) in human gingival fibroblasts.

BACKGROUND: There is a positive correlation between the course of periodontal disease and psychosocial stress status. Stress leads to activation of the hypothalamic-pituitary-adrenal axis, resulting in increased cortisol release. The present study evaluates the effect of two different hydrocortisone concentrations on mRNA expression of matrix metalloproteinases (MMPs) and tissue inhibitor of matrix metalloproteinases (TIMPs) in cultured, human gingival fibroblasts. METHODS: Gingival fibroblasts were stimulated with 10(-7) or 10(-9) M hydrocortisone for 24 hours; untreated cells served as controls. Alterations in the expression of MMP-1, -2, -3, -7, -11 and TIMP-1 and -2 were evaluated using real-time polymerase chain reaction and Western blotting. beta-actin mRNA expression was used as a reference to normalize gene expression. RESULTS: Although the higher hydrocortisone concentration upregulated MMP-1, -2, -7, -11, and TIMP-1 (P <0.05) expression, the lower concentration induced downregulation or diminished upregulation. The lower hydrocortisone concentration induced a 23-fold increase in MMP-3 gene expression, whereas the higher concentration induced less upregulation; however, protein expression was regulated similarly by both hydrocortisone concentrations. The effect of hydrocortisone on TIMP-2 expression was not significant (P >0.05). CONCLUSIONS: Hydrocortisone produced a dose-dependent regulation of MMP and TIMP expression. The higher hydrocortisone concentration significantly upregulated expression of MMP-1, -2, -7, and -11 and TIMP-1 in human gingival fibroblasts, which may constitute a mechanism underlying the increased periodontal breakdown associated with psychosocial stress status.

Use of anorganic bovine-derived hydroxyapatite matrix/cell-binding peptide (P-15) in the treatment of class II furcation defects: a clinical and radiographic study in humans.

BACKGROUND: This study compared clinical and radiographic findings for the treatment of Class II furcation defects in human mandibular molars using anorganic bovine-derived hydroxyapatite matrix (ABM)/cell-binding peptide (P-15) or open flap debridement (OFD). METHODS: Twelve subjects showing two comparable Class II furcation defects in their mandibular molars were enrolled. The defects in each subject were assigned randomly to the test (ABM/P-15) or the control (OFD) group. Clinical measurements and standardized radiographs were taken at baseline and 6 to 7 months after surgery. RESULTS: There were no statistically significant differences between the test and control groups for any clinical or radiographic parameter (P >0.05). On comparing the baseline and final measurements, the gain in horizontal clinical attachment level and reduction in gingival recession were significant only in the test group (P < or =0.02), whereas the gain in the vertical clinical attachment level was significant in both groups (P < or =0.04). In the test group, four of 12 sites showed complete closure, and five showed partial closure; in the control group, three defects showed complete closure, and four showed partial closure (P = 0.42). Subtraction radiography revealed similar gains in bone height and increases in mean bone density with both treatments (P >0.05). CONCLUSIONS: ABM/P-15 yielded favorable results in the treatment of Class II furcation defects over a 6-month evaluation period; however, there was no difference compared to OFD. Further studies using a larger sample size are needed to confirm the present findings.

TGF-beta1 enhances the expression of alpha-smooth muscle actin in cultured human pulpal fibroblasts: immunochemical and ultrastructural analyses.

Transforming growth factor-beta 1 (TGF-beta1) has been related to induce the expression of alpha-smooth muscle actin (alpha-SMA) in fibroblasts during repair. Because pulpal fibroblasts seem to be somewhat different from other fibroblasts, the present study investigated in vitro whether TGF-beta1 enhances the expression of alpha-SMA in human pulpal fibroblasts. TGF-beta1 was added in doses between 5-10 ng/mL to cultures of both dental pulp and gingival human fibroblasts. The expression of alpha-SMA was analyzed by immunofluorescence and Western blotting, whereas the ultrastructure was evaluated by electron microscopy. In addition, the expression of tenascin, osteonectin, and vimentin was also investigated. Both cell types were immunoreactive for alpha-SMA even without TGF-beta1. When TGF-beta1 was added to cell cultures, the expression of alpha-SMA increased dramatically in pulpal fibroblasts, independent of the concentration used. It was confirmed by the Western blotting analysis. Ultrastructure revealed myofilaments and indented nuclei in both fibroblasts treated with TGF-beta1. Tenascin and osteonectin were only immunolabeled in pulpal fibroblasts treated or not with TGF-beta1. Both fibroblast types were positive for vimentin. The present findings showed that TGF-beta1 up-regulated the expression of alpha-SMA, thus inducing pulpal fibroblasts to acquire the myofibroblast phenotype.

The effect of epidermal growth factor on matrix metalloproteinases and tissue inhibitors of metalloproteinase gene expression in cultured human gingival fibroblasts.

OBJECTIVE: Matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) play a role in the breakdown of the extracellular matrix during normal physiological processes, and in pathological processes, including periodontitis. The aim of this study was to evaluate the effect of epidermal growth factor (EGF) on the expression of MMPs and TIMPs in cultured human gingival fibroblasts. METHODS: Fibroblasts were stimulated with 10(-3), 10(-6) or 10(-12)M EGF for 24h; untreated fibroblasts served as controls. Alterations in the expression of MMP-1, 2, 3, 7, 11, TIMP-1 and 2 were evaluated using real-time PCR and Western blotting. beta-Actin expression was used as a reference to normalize gene expression. RESULTS: Increased MMP-1, 3, 7 and 11 expressions were observed at all EGF concentrations (p<0.05). At the lowest EGF concentration, MMP-1, 3 and 7 presented the lowest expression and MMP-11 presented the greatest expression; at higher EGF concentrations, MMP-1, 3 and 7 presented greater up-regulation, and MMP-11 lower up-regulation (p<0.05). Protein expression was similarly regulated by EGF: increased up-regulation of MMP-1, 3 and 7 was observed with increasing EGF concentrations, except for MMP-11 that exhibited greater up-regulation at the lower EGF concentration. The gene expression of MMP-2, TIMP-1 and 2 was not affected by EGF (p<0.05). CONCLUSIONS: We conclude that EGF regulates expression for MMP-1, 3, 7 and 11 in a dose-dependent manner, suggesting that EGF may play a role in periodontal destruction and wound repair.

Expression of SOFAT by T- and B-lineage cells may contribute to bone loss.

A novel T cell-secreted cytokine, termed secreted osteoclastogenic factor of activated T cells (SOFAT) that induces osteoclastic bone resorption in a RANKL-independent manner, has been described. Our group have previously reported that SOFAT is highly expressed in gingival tissues of patients with chronic periodontitis suggesting a putative role in the bone loss associated with periodontal disease. The aim of the present study was to identify other potential cellular sources of SOFAT in the bone resorptive lesions of patients with periodontal disease. Gingival tissues were biopsied from systemically healthy subjects without periodontal disease (n=5) and patients with chronic periodontitis (n=5), and the presence of SOFAT was analyzed by immunohistochemistry and immunofluorescence staining. The present data demonstrated marked SOFAT staining in diseased periodontal tissues that was predominantly associated with the lymphocytic infiltration of gingival tissues. Notably, in addition to CD3+ T cells, B­lineage cells including plasma cells also exhibited strong staining for SOFAT. As SOFAT has not previously been reported in B­lineage cells, splenic T cells and B cells were further purified from BALB/c mice and activated using CD3/CD28 and lipopolysaccharide, respectively. SOFAT was quantified by reverse transcription­quantitative polymerase chain reaction and was shown to be significantly expressed (P<0.05) in both activated T cells and B cells compared with unstimulated cells. These data support a putative role of SOFAT in the bone loss associated with chronic periodontal disease. In addition, to the best of our knowledge, this study demonstrates for the first time that in addition to T cells, B-lineage cells may also be a significant source of SOFAT in inflammatory states.

Biomarker analysis in carcinoma ex pleomorphic adenoma at an early phase of carcinomatous transformation.

Diagnostic criteria for intracapsular carcinoma ex pleomorphic adenoma (CXPA) are subjective and vary among authors. Biomarker analysis, which could provide more objective evaluation of these tumors, has rarely been studied in intracapsular CXPA. Immunohistochemical evaluation of c-erbB-2, p53 protein, bcl-2, and Ki-67 was performed in 8 cases of CXPA at an early phase of malignant transformation (4 intracapsular and 4 minimally invasive) and in 17 pleomorphic adenomas (PA). In all cases of CXPA, p53 and Ki-67 were demonstrated predominantly in luminal cells of benign and malignant areas, significantly more in the latter. Few benign myoepithelial cells were p53 positive. c-erbB-2 reactivity was strongly associated with atypical luminal cells. Bcl-2 expression was weak and focal in malignant areas from 2 cases. In conclusion, both p53 and c-erbB-2 proteins appear to be involved at an early stage of malignization of PA. In PA with atypical cells, evaluation of the expression of these 2 markers provides more objective criteria for the diagnosis of intracapsular CXPA.

Solitary fibrous tumor of the oral mucosa--morphological and immunohistochemical profile in the differential diagnosis with hemangiopericytoma.

The objective was to investigate two cases of solitary fibrous tumor (SFT) of oral mucosa, emphasizing the differential diagnosis with one case of oral hemangiopericytoma (HPC), in terms of their morphological and immunohistochemical features. Solitary fibrous tumors showed cellularity and collagenization varying from area to area, focal perivascular hyalinization, scattered giant nuclei cells and abundant mast cells throughout the tumor. The hemangiopericytoma case exhibited thin-walled and dilated vessels lined with flat endothelial cells, identified by "staghorn appearance". Tumoral cells of solitary fibrous tumor exhibited immunohistochemical positivity for CD34, as well as endothelial cells. The hemangiopericytoma was positive only in endothelial cells. In solitary fibrous tumor, alpha-smooth muscle actin, h-caldesmon and laminin stained the wall vessels. In hemangiopericytoma, on the other hand, the wall vessels were positive only for laminin, which staining was also observed in perivascular tumoral cells. The morphological and immunohistochemical differences observed allowed us to infer these lesions constitute distinct entities.