Temporomandibular joint disc; a proposed histopathological degeneration grading score system

Summary. Aims: The purpose of this study was to draw up a TMJ disc histopathological score that is a semiquantitative transcription of the entire spectrum of TMJ disc degenerative diseases related to changes in disc tissue, and then validate the proposed grading, in order to contribute to a standardized histopathological diagnosis. Methods: Sections from sixty two temporomandibular joint disc specimens affected by tissue degenerative changes and stained with Hematoxylin & Eosin (H&E) were collected from among those found in the archives of the Department of Dentistry at Catania University. Specimens, included anterior, intermediate and posterior disc bands. Based on a literature search regarding the most frequent histopathological changes detected in TMJ disc tissue a grading score was designed. This score takes into account pathological disc tissue transformation i.e. collagen bundles, non-specific degenerative changes and the presence of blood vessels. This grading system results in a score ranging from 0 up to 8 for heavily degenerated disc tissue. Two observers performed the assessment of the TMJ disc H&E stained sections. Each specimen was scored twice by each observer after a minimum interval of 1 week. Results: The average TMJ disc degeneration score of the TMJ disc sample was 3.89±1.37. There was an almost perfect agreement, between the two observers, and degeneration scores from the two observers were highly correlated. Conclusions: The introduction of this validated degeneration score system may be of major importance for future research and collaboration between different centers in order to improve knowledge in TMJ disc histopathology

An Immunohistochemical Study of Gastric Mucosa and Critical Review Indicate That the Subepithelial Telocytes Are Prelymphatic Endothelial Cells

Background and Objectives: There are only a few studies regarding gut subepithelial telocytes (TCs). The telopodes, namely peculiar TCs’ prolongations described on two-dimensional cuts, are not enough to differentiate this specific cell type. Subepithelial TCs were associated with the intestinal stem niche but a proper differential diagnosis with lymphatic endothelial cells (LECs) was not performed. In this study, we will also critically review studies suggesting that distinctive TCs could be positioned within the lamina propria. Materials and Methods: We performed an immunohistochemical study of human gastric mucosa to test the expression of D2-40, the lymphatic marker, as well as that of CD31, CD34, CD44, CD117/c-kit, α-smooth muscle actin (α-SMA) and vimentin in the gastric subepithelial niche. Results: The results support the poorly investigated anatomy of intramural gastric lymphatics, with circumferential collectors located on both sides of the muscularis mucosae (mucosal and then submucosal) and myenteric collectors in the muscularis propria. We also found superficial epithelial prelymphatic channels bordered by D2-40+ but CD31–TC-like cells. Deep epithelial lymphatic collectors drain in collectors within the lamina propria. Blood endothelial cells expressed CD31, CD34, CD44, and vimentin. Conclusions: Therefore, the positive diagnosis of TC for subepithelial CD34+ cells should be regarded with caution, as they could also be artefacts, resulting from the two-dimensional examination of three dimensional structures, or as LECs. Lymphatic markers should be routinely used to discriminate TCs from LECs

Endocardial Tip Cells in the Human Embryo – Facts and Hypotheses

<div><p>Experimental studies regarding coronary embryogenesis suggest that the endocardium is a source of endothelial cells for the myocardial networks. As this was not previously documented in human embryos, we aimed to study whether or not endothelial tip cells could be correlated with endocardial-dependent mechanisms of sprouting angiogenesis. Six human embryos (43–56 days) were obtained and processed in accordance with ethical regulations; immunohistochemistry was performed for CD105 (endoglin), CD31, CD34, α-smooth muscle actin, desmin and vimentin antibodies. Primitive main vessels were found deriving from both the <i>sinus venosus</i> and aorta, and were sought to be the primordia of the venous and arterial ends of cardiac microcirculation. Subepicardial vessels were found branching into the outer ventricular myocardium, with a pattern of recruiting α-SMA+/desmin+ vascular smooth muscle cells and pericytes. Endothelial sprouts were guided by CD31+/CD34+/CD105+/vimentin+ endothelial tip cells. Within the inner myocardium, we found endothelial networks rooted from endocardium, guided by filopodia-projecting CD31+/CD34+/CD105+/ vimentin+ endocardial tip cells. The myocardial microcirculatory bed in the atria was mostly originated from endocardium, as well. Nevertheless, endocardial tip cells were also found in cardiac cushions, but they were not related to cushion endothelial networks. A general anatomical pattern of cardiac microvascular embryogenesis was thus hypothesized; the arterial and venous ends being linked, respectively, to the aorta and <i>sinus venosus</i>. Further elongation of the vessels may be related to the epicardium and subepicardial stroma and the intramyocardial network, depending on either endothelial and endocardial filopodia-guided tip cells in ventricles, or mostly on endocardium, in atria.</p></div

Human embryonic heart (56 days), CD 34, desmin and α-SMA immune labeling.

<p>Immune labeling for CD34 (A, detail in B), desmin (C) and α-SMA (D) of the future posterior interventricular groove in a 56 days human embryonic heart, oblique-sagittal cut. Endothelial sprouts guided by tip cells (arrow, A and B) invade the outer myocardium. The subepicardial vessels are embedded in a myoid stroma, α-SMA- and desmin-positive (arrowhead in C and D). Myoid cells (arrows in C and D) contact the endothelial sprouts within the outer myocardium.</p

Human embryonic heart (56 days), CD 34 immune labeling.

<p>Immune labeling with CD34 antibodies of a 56 days human embryonic heart, oblique-sagittal cut. General view (A) with detailed area in (B), indicated by the black connector. The CD34 positive endocardial cells cover the ventricular cavity (*). Endocardial tip cells (white arrows) are identified projecting filopodia within the myocardium. The endocardially-derived endothelial networks advance towards the epicardially-derived endothelial networks. ac: <i>apex cordis</i>; P:pericardium.</p

Human embryonic heart (43 days), CD 34 immune labeling.

<p>Immune labeling with CD34 antibodies of a 43 days human embryonic heart, oblique-sagittal cut at ventricle level. Endocardial tip cells are indicated (arrows).</p

Human embryonic heart (43 days), CD 34, vimentin, CD105, desmin and CD31 immune labeling.

<p>Immune labeling with CD34 (A) and vimentin (B) antibodies of a 43 days human embryonic heart, oblique-sagittal cut at ventricle level. Corresponding epicardial vascular canals are indicated (white arrrows and white arrowheads). The walls of these canals seem to acquire a CD34-positive phenotype and are vimentin-positive. In (A) an active intramyocardial process of sprouting angiogenesis is detailed (inset), being guided by tip cells (double-headed arrows). CD105 immunolabeling of the ventricular wall (C) identifies filopodia-guided processes (arrows) of endocardial sprouting. Desmin-positive reactions were exclusively found (D) in the dorsal wall of the venous sinus (arrows) and in the atrioventricular ring (arrowheads) (VS: venous sinus; RA: right atrium; RV: right ventricle; avc: atrioventricular cushion). CD31-positive endocardial (arrows) and vascular (arrowhead) endothelia were identified. α-SMA intense labeling of the venous sinus (VS) myocardium (arrow) but not of subepicardium (arrowhead).</p

Human embryonic heart (56 days), CD105 (A, B) and vimentin (C, D) immune labeling.

<p>Intramyocardial endothelial networks result from processes of sprouting angiogenesis (arrows) of the underlying CD105-positive and vimentin-positive endocardium. The connector indicates corresponding areas of the left atrium (LA) wall.</p