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Histologic Assessment (histologic + assessment)
Selected AbstractsIn reference to Histologic assessment of thermal injury to tonsillectomy specimens: a comparison of electrocautery, coblation, harmonic scalpel, and tonsillotomeTHE LARYNGOSCOPE, Issue 5 2010Douglas Hetzler MD No abstract is available for this article. [source] Influence of surgical repositioning of mature permanent dog teeth following experimental intrusion: a histologic assessmentDENTAL TRAUMATOLOGY, Issue 6 2002R. F. Cunha Abstract,,, The aim of this study was to evaluate, through histologic examination, the effect of surgical repositioning of intruded dog teeth upon the pulpal and surrounding tissues. Thirty teeth in 10 adult dogs, aged 2,3 years, were used. Fifteen teeth were intruded, surgically repositioned and fixed using orthodontics wire, composite resin, and enamel acid conditioning. All these teeth served as the experimental group. The remaining intruded teeth were not treated (control group). The animals were sacrificed to allow observations at 7, 15, and 30 post-operative days. The maxillary and mandibular archs were removed and processed for histologic exam. Based on the methodology and observed results, we concluded that: pulpal necrosis, external root resorption and ankylosis were common sequelae to severe traumatic intrusion; a careful immediate surgical repositioning of severed intruded permanent tooth with complete root formation has many advantages with few disadvantages. [source] Accentuated Ovariectomy-Induced Bone Loss and Altered Osteogenesis in Heterozygous N-Cadherin Null Mice,,JOURNAL OF BONE AND MINERAL RESEARCH, Issue 12 2006Chung Fang Lai Abstract Ovariectomy-induced bone loss is accentuated in mice with germline Cdh2 haploinsufficiency, the result of a decreased osteoblastogenesis in the face of normal osteoclast number. Reduced N-cadherin abundance in these mice decreases cell,cell adhesion and alters signaling pathways important for osteoblast commitment and differentiation, thus providing in vivo evidence that N-cadherin,mediated cell,cell interactions are involved in homeostatic responses to increased bone remodeling. Introduction: We have shown that targeted expression of a dominant negative truncated form of N-cadherin (Cdh2) delays acquisition of peak bone mass in mice and retards osteoblast differentiation. We tested the role of this molecule in the skeletal homeostatic response to ovariectomy in mice with germline Cdh2 haploinsufficiency. Materials and Methods: Heterozygous Cdh2 null (Cdh2+/,) and wildtype mice were ovariectomized and followed up to 13 weeks by in vivo radiodensitometric and ex vivo histologic assessment of bone mass and turnover. Cells isolated from wildtype and Cdh2+/, mice were used to determine the alterations in bone cell function produced by partial loss of N-cadherin. Results: Bone mass was not significantly different between Cdh2+/, and wildtype littermates, but on ovariectomy, bone loss in Cdh2+/, mice was initially slower, but with time it became significantly greater than in wildtype mice. This accentuated bone loss was associated with lower osteoblast number and serum osteocalcin levels, with no differences in bone resorption. Although development of calcified nodules was faster in calvaria cells isolated from Cdh2+/, mice relative to Cdh2+/+ cells, bone marrow osteogenic precursors were lower in the former than in the latter genotypes. Cdh2 expression was downregulated with differentiation in wildtype calvaria cells, whereas cadherin-11 abundance remained unchanged. Furthermore, cell,cell adhesion (postconfluence) was decreased among heterozygous calvaria cells, as was cell proliferation (preconfluence), relative to wildtype cells. Finally, the abundance and cellular distribution of ,-catenin was minimally decreased in Cdh2+/, cells, whereas mitogen-activated protein kinase (MAPK) signaling was more active in Cdh2 insufficient cells. Conclusions:Cdh2 is involved in the homeostatic bone formation response to ovariectomy, presumably by regulating osteoprogenitors number and differentiation through stabilization of cell,cell adhesion and/or signaling modulation. [source] Laryngeal Preservation With Supracricoid Partial Laryngectomy Results in Improved Quality of Life When Compared With Total Laryngectomy,THE LARYNGOSCOPE, Issue 2 2001Gregory S. Weinstein MD Abstract Objectives/Hypotheses Study 1: To assess the oncologic outcome following supracricoid partial laryngectomy (SCPL). Study 2: To compare the quality of life (QOL) following SCPL to total laryngectomy (TL) with tracheoesophageal puncture (TEP). Study 3: To analyze whole organ TL sections to determine the percentage of lesions amenable to SCPL. Study Design Study 1: A retrospective review of patients who underwent SCPL. Study 2: A non-randomized, prospective study using QOL instruments to compare patients who underwent either SCPL or TL. Study 3: A retrospective histopathologic study of TL specimens assessed for the possibility of performing an SCPL. Methods Study 1: Twenty-five patients with carcinoma of the larynx underwent SCPL between June 1992 and June 1999. Various rates of oncologic outcome were calculated. Study 2: Thirty-one patients participated in the QOL assessment. This included the SF-36 general health status measure, the University of Michigan Head and Neck Quality of Life (HNQOL) instrument, and the University of Michigan Voice-Related Quality of Life (VRQOL) instrument. Study 3: Ninety surgical specimens were obtained and studied from the total laryngectomy cases in the Tucker Collection. Multiple sites were evaluated for the presence of carcinoma. A computer program was written to classify whether the patient was amenable to SCPL. Results Study 1: The overall local control rate was 96% (24/25). The local control rate following SCPL with cricohyoidoepiglottopexy (CHEP) was 95% (20/21). The local control rate following SCPL with cricohyoidopexy (CHP) was 100% (4/4). Study 2: The SCPL had significantly higher domain scores than TL and TEP in the following categories for the SF-36: physical function, physical limitations, general health, vitality, social functioning, emotional limitations, and physical health summary. The significantly higher domains for the SCPL when compared with the TL and TEP for the HNQOL were eating and pain. Finally, when voice-related QOL was assessed with the V-RQOL, the domains of physical functioning and the total score were significantly better with SCPL when compared with TL and TEP. Study 3: Forty of 90 (44%) laryngeal whole organ specimens were determined to be resectable by SCPL. In 16 (18%) specimens, the patients could have undergone SCPL with CHEP and in 24 (27%) specimens the patients could have undergone SCPL with CHP. Among the 40 (44%) specimens determined to be able to have undergone SCPL, 19 were glottic (1 T1, 15 T2, 3 T3) and 21 were supraglottic (9 T2, 12 T3). Conclusions 1) A review of the literature and an analysis of the data in this study indicate that excellent local control may be expected following SCPL. 2) The QOL following SCPL, as measured by three validated QOL instruments, is superior to TL with TEP. 3) A histologic assessment of whole organ sections of TL specimens indicates that many patients who have been subjected to TL may have been candidates for SCPL. 4) If the indications and contraindications are rigorously adhered to, SCPLs are reasonable alternatives to TL in selected cases. [source] Amelioration of collagen-induced arthritis and immune-associated bone loss through signaling via estrogen receptor ,, and not estrogen receptor , or G protein,coupled receptor 30ARTHRITIS & RHEUMATISM, Issue 2 2010Cecilia Engdahl Objective The effects of estrogen may be exerted via the nuclear estrogen receptors (ERs) ER, or ER, or via the recently proposed transmembrane estrogen receptor G protein,coupled receptor 30 (GPR-30). The purpose of this study was to elucidate the ER specificity for the ameliorating effects of estrogen on arthritis and bone loss in a model of postmenopausal rheumatoid arthritis (RA). Methods Female DBA/1 mice underwent ovariectomy or sham operation, and type II collagen,induced arthritis was induced. Mice were treated subcutaneously 5 days/week with the specific agonists propylpyrazoletriol (PPT; for ER,), diarylpropionitrile (DPN; for ER,), G1 (for GPR-30), or with a physiologic dose of estradiol. Clinical arthritis scores were determined continuously. At termination of the study, bone mineral density (BMD) was analyzed, paws were collected for histologic assessment, serum was analyzed for cytokines and markers of bone and cartilage turnover, and bone marrow was subjected to fluorescence-activated cell sorting. Results Treatment with PPT as well as estradiol dramatically decreased the frequency and severity of arthritis. Furthermore, estradiol and PPT treatment resulted in preservation of bone and cartilage, as demonstrated by increased BMD and decreased serum levels of bone resorption markers and cartilage degradation markers, whereas no effect was seen after DPN or G1 treatment. Conclusion In a well-established model of postmenopausal RA, ER,, but not ER, or GPR-30 signaling, was shown to ameliorate the disease and the associated development of osteoporosis. Since long-term treatment with estrogen has been associated with significant side effects, increased knowledge about the mechanisms behind the beneficial effects of estrogen is useful in the search for novel treatments of postmenopausal RA. [source] Th17 and natural Treg cell population dynamics in systemic lupus erythematosusARTHRITIS & RHEUMATISM, Issue 5 2009Ji Yang Objective To investigate the relative abundance and activities of Th17 cells and natural Treg cells in systemic lupus erythematosus (SLE). Methods Blood samples were collected from 50 adult patients with SLE. Samples were processed to detect Th17 cells and natural Treg cells by flow cytometry, and related gene expression was assessed by real-time reverse transcription,polymerase chain reaction. Skin biopsy specimens were collected for histologic assessment. The function of Th17 cells in relation to human umbilical vein endothelial cells (HUVECs) was studied in vitro. Th17 cells were also examined in lupus-prone MRL/Mp- lpr/lpr (MRL/lpr) mice. Results We demonstrated the presence of Th17 cells among the peripheral blood mononuclear cells (PBMCs) and in the involved organs of patients with active SLE. Both the percentage of circulating Th17 cells and the ability to produce interleukin-17A (IL-17A) were increased in samples derived from patients with active SLE. The number of Th17 cells increased during SLE flare, especially in patients with vasculitis, and decreased following certain treatments. We observed that IL-17A from patients with SLE could induce adhesion molecule messenger RNA expression in HUVECs and adhesion of T cells to HUVECs. An increase in the percentage of Th17 cells was correlated with natural Treg cell depletion during disease flare. Finally, expansion of the Th17 cell population was detected in MRL/lpr mice. Conclusion SLE flare might be linked to the expansion of the Th17 cell population and the depletion of natural Treg cell subpopulations. Expansion of the Th17 cell population might be related to a distinct cytokine environment in active SLE. Th17 cells and microenvironmental IL-17A are involved in vascular inflammation in SLE. Antagonism of Th17 cells by IL-17A,blocking antibodies should be explored as a treatment of SLE. [source] Genetic association of vasoactive intestinal peptide receptor with rheumatoid arthritis: Altered expression and signal in immune cellsARTHRITIS & RHEUMATISM, Issue 4 2008Mario Delgado Objective Vasoactive intestinal peptide (VIP) has been shown to be one of the endogenous factors involved in the maintenance of immune tolerance. Administration of VIP ameliorates clinical signs in various experimental autoimmune disorders. This study was undertaken to investigate whether the exacerbated inflammatory autoimmune response in rheumatoid arthritis (RA) might result directly from altered expression and/or signaling of VIP receptors in immune cells. Methods The effect of specific agonists of different VIP receptors on collagen-induced arthritis in mice was investigated by clinical and histologic assessment and measurement of cytokine and chemokine production. Expression of VIP receptor type 1 (VPAC1) in synovial cells and monocytes from RA patients was determined by flow cytometry. Potential associations of VPAC1 genetic polymorphisms with RA susceptibility were investigated. Results A VPAC1 agonist was very efficient in the treatment of experimental arthritis, and deficient expression of VPAC1 in immune cells of RA patients was associated with the predominant proinflammatory Th1 milieu found in this disease. Immune cells derived from RA patients were less responsive to VIP signaling than were cells from healthy individuals and showed reduced VIP-mediated immunosuppressive activity, rendering leukocytes and synovial cells more proinflammatory in RA. A significant association between multiple-marker haplotypes of VPAC1 and susceptibility to RA was found, suggesting that the reduced VPAC1 expression in RA-derived immune cells is associated with the described VPAC1 genetic polymorphism. Conclusion These findings are highly relevant to the understanding of RA pathogenesis. They suggest that VIP signaling through VPAC1 is critical to maintaining immune tolerance in RA. In addition, the results indicate that VPAC1 may be a novel therapeutic target in RA. [source] Cathepsin K deficiency partially inhibits, but does not prevent, bone destruction in human tumor necrosis factor,transgenic mice,ARTHRITIS & RHEUMATISM, Issue 2 2008Uta Schurigt Objective Cathepsin K is believed to have an eminent role in the pathologic resorption of bone. However, several studies have shown that other proteinases also participate in this process. In order to clarify the contribution of cathepsin K to the destruction of arthritic bone, we applied the human tumor necrosis factor (hTNF),transgenic mouse model, in which severe polyarthritis characterized by strong osteoclast-mediated bone destruction develops spontaneously. Methods Arthritis was evaluated in hTNF-transgenic mice that were either wild-type for cathepsin K (CK+/+), heterozygous for cathepsin K (CK+/,), or deficient in cathepsin K (CK,/,). Arthritic knee joints were prepared for standard histologic assessment aimed at establishing a semiquantitative score for joint destruction and quantification of the area of bone erosion. Additionally, microfocal computed tomography was performed to visualize bone destruction in mice with the different CK genotypes. CK+/+ and CK,/, osteoclasts were generated in vitro, and their proteinase expression profiles were compared by complementary DNA array analysis, real-time polymerase chain reaction, and activity assays. Results Although the area of bone erosion was significantly reduced in hTNF-transgenic CK,/, mice, the absence of cathepsin K did not completely protect against inflammatory bone lesions. Several matrix metalloproteinases (MMPs) and cathepsins were expressed by in vitro,generated CK,/, osteoclasts, without marked differences from CK+/+ osteoclasts. MMP activity was detected in CK,/, osteoclasts, and MMP-14 was localized by immunohistochemistry in inflammatory bone erosions in hTNF-transgenic CK,/, mice, suggesting MMPs as potential contributors to bone destruction. Additionally, we detected a reduction in osteoclast formation in cathepsin K,deficient mice, both in vitro and in vivo. Conclusion The results of our experiments raise doubts about a crucial role of cathepsin K in arthritic bone destruction. [source] Crucial role of macrophages in matrix metalloproteinase,mediated cartilage destruction during experimental osteoarthritis : Involvement of matrix metalloproteinase 3ARTHRITIS & RHEUMATISM, Issue 1 2007Arjen B. Blom Objective To explore the involvement of synovial macrophages in early cartilage damage in osteoarthritis (OA), and to identify the role of matrix metalloproteinase 3 (MMP-3) in the pathology of early and late OA. Methods The role of synovial macrophages in MMP-mediated damage in OA was studied by depleting synovial macrophages prior to elicitation of a collagenase-induced instability model of OA. The expression of MMP in synovium and cartilage was monitored using TaqMan analysis. In spontaneous and induced OA, cartilage pathology was scored in MMP-3,knockout mice and control mice, by histologic assessment and VDIPEN staining. Results On day 14 following induction of OA, MMP-mediated neoepitopes were detected in cartilage from mice with mild experimental OA (mean ± SD positively stained surface area 20 ± 3.2%). Remarkably, by depleting synovial macrophages prior to induction of OA, the generation of MMP-induced neoepitopes was largely prevented (mean ± SD positively stained surface area 5 ± 1%; P< 0.001), indicating an important role for synovial macrophages in the occurrence of MMP-mediated cartilage damage. We observed a strong decrease in MMP-3 and MMP-9 expression in synovial but not cartilage tissue in macrophage-depleted joints. Among 2-year-old mice, spontaneous OA,like changes in the lining layer were significantly decreased in MMP-3,knockout mice compared with control mice. Even more striking was the 67% reduction in the occurrence of severe cartilage damage in MMP-3,knockout mice. In addition, MMP-mediated VDIPEN expression was significantly decreased, indicating reduced MMP-mediated cartilage breakdown. Conclusion The results of this study prove that MMP-3 is involved in the generation of severe cartilage damage in murine OA. Synovial macrophages are crucial in early MMP activity and appear to mediate MMP production in synovium rather than cartilage. [source] | ||||||||||