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Purpose: Cellular fibronectin staining is decreased in adult periodontitis, which implies elastase-mediated degradation of periodontal tissues. The purpose of this study was to determine whether failing dental implants display similar changes. Materials and Methods: Cellular fibronectin and its integrin receptors were identified by immunohistochemistry and quantified by computerized image analysis. Results: Cellular fibronectin was found in blood vessel walls, epithelial basement membranes, and fibroblasts. Quantitative results of cellular fibronectin staining were as follows: failing dental implants, median 26.5% (Q3-Q1 = 23%); adult periodontitis, median 5.5% (Q3-Q1 = 5.6%); normal controls, median 12.2% (Q3-Q1 = 7.5%). Cellular fibronectin staining was increased around failing dental implants but decreased in adult periodontitis compared to healthy controls. Discussion: The distribution of integrin receptor subunits α4, α5, and β1 of cellular fibronectin was similar in failing dental implants. The pathomechanisms in adult periodontitis and failing dental implants seem to differ. Conclusions: Adult periodontitis is characterized by proteolysis/loss of cellular fibronectin, whereas failing dental implants are characterized by increased cellular fibronectin deposition, probably as a result of titanium-induced local synthesis and relatively modest degradation. [ABSTRACT FROM AUTHOR]

The laminin composition (LMα1-α5, β1–β3, γ1 and γ2 chains) of normal corneas and corneal buttons from keratoconus, bullous keratopathy (BKP), Fuchs’ dystrophy + BKP, Fuchs’ dystrophy without BKP and scar after deep lamellar keratoplasty (DLKP) was investigated with immunohistochemistry. The epithelial basement membranes (BMs) of both normal and diseased corneas contained LMα3, α5, β1, β3, γ1 and γ2 chains. The epithelial BM morphology was altered in the different diseases. Scarring was associated with irregular BM and ectopic stromal localization of different laminin chains. The Descemet’s membrane (DM) contained LMα5, β1 and γ1 chains in all cases and additionally LMβ3 and γ2 chains in the majority of keratoconus corneas. The interface in the DLKP cornea had patches of LMα3, α4, α5, β1 and β2 chains, and an extra BM-like structure under the Bowman’s membrane. These results suggest that laminin chains participate in the process of corneal scarring and in the pathogenesis of some corneal diseases. The novel finding of LMα3, β3 and γ2 in the DM of keratoconus buttons indicates that this membrane is also involved in the disease and that some cases of keratoconus may have a congenital origin, without normal downregulation of the LMβ3 chain. [ABSTRACT FROM AUTHOR]

The endothelial cells of blood vessels assemble basement membranes that play a role in vessel formation, maintenance and function, and in the migration of inflammatory cells. However, little is known about the distribution of basement membrane constituents in lymphatic vessels. We studied the distribution of basement membrane proteins in lymphatic vessels of normal human skin, digestive tract, ovary and, as an example of tumours with abundant lymphatics, ovarian carcinomas. Basement membrane proteins were localized by immunohistochemistry with monoclonal antibodies, whereas lymphatic capillaries were detected with antibodies to the lymphatic vessel endothelial hyaluronan receptor-1, LYVE-1. In skin and ovary, fibrillar immunoreactivity for the laminin α4, β1, β2 and γ1 chains, type IV and XVIII collagens and nidogen-1 was found in the basement membrane region of the lymphatic endothelium, whereas also heterogeneous reactivity for the laminin α5 chain was detected in the digestive tract. Among ovarian carcinomas, intratumoural lymphatic vessels were found especially in endometrioid carcinomas. In addition to the laminin α4, β1, β2 and γ1 chains, type IV and XVIII collagens and nidogen-1, carcinoma lymphatics showed immunoreactivity for the laminin α5 chain and Lutheran glycoprotein, a receptor for the laminin α5 chain. In normal lymphatic capillaries, the presence of primarily α4 chain laminins may therefore compromise the formation of endothelial basement membrane, as these truncated laminins lack one of the three arms required for efficient network assembly. The localization of basement membrane proteins adjacent to lymphatic endothelia suggests a role for these proteins in lymphatic vessels. The distribution of the laminin α5 chain and Lutheran glycoprotein proposes a difference between normal and carcinoma lymphatic capillaries. [ABSTRACT FROM AUTHOR]

Objective: To analyze the microvascular network in skeletal muscle biopsies from patients with dermatomyositis (DM) and systemic sclerosis (SSc) compared to polymyositis (PM) and systemic lupus erythematosus (SLE), and non-inflammatory myopathies, and to clarify whether reparative angiogenesis-related factors are expressed in parallel to blood vessel damage. Methods: Immunohistochemical staining of muscle biopsies (10 DM, 10 SSc, 10 PM, 10 SLE, and 10 non-inflammatory myopathies) with antibodies against von Willebrand factor (vWF), hypoxia-inducible factor-1β (HIF-1β), β3 integrin subunit, and vascular endothelial growth factor receptor-1 (VEGFR-1). The TechMate. [ABSTRACT FROM AUTHOR]