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Matrix Damage (matrix + damage)
Selected AbstractsComplications of Nail Surgery: A Review of the LiteratureDERMATOLOGIC SURGERY, Issue 3 2001Meena Moossavi MD Background. The realm of nail unit surgery encompasses the dermatologist as well as the hand surgeon. Nail surgery complications may include allergy to anesthetic, infection, hematoma, nail deformity, and persistent pain and swelling. Objective. To review the pertinent literature regarding nail unit surgery complications. Methods. A Medline literature search was performed for relevant publications. Results. Nail unit surgery complications appear to be relatively infrequent. The majority of postoperative nail deformity complications result from nail matrix damage. Conclusion. Complications may be reduced to a minimum by preventive measures, such as careful patient selection, sterile technique, and gentle treatment of the nail matrix. [source] Loss of Osteocyte Integrity in Association with Microdamage and Bone Remodeling After Fatigue In Vivo,JOURNAL OF BONE AND MINERAL RESEARCH, Issue 1 2000Olivier Verborgt Abstract As a result of fatigue, bone sustains microdamage, which is then repaired by bone-remodeling processes. How osteoclastic activity is targeted at the removal of microdamaged regions of bone matrix is unknown. In the current studies, we tested the hypothesis that changes in osteocyte integrity, through the initiation of regulated cell death (apoptosis), are associated with fatigue-related microdamage and bone resorption. Ulnae of adult rats were fatigue-loaded to produce a known degree of matrix damage. Osteocyte integrity was then assessed histomorphometrically from terminal deoxynucleotidyl transferase,mediated deoxyuridine triphosphate,nick end labeling (TUNEL),stained sections to detect cells undergoing DNA fragmentation associated with apoptosis; toluidine blue,stained sections were used for secondary morphological confirmation. Ten days after loading, large numbers of TUNEL-positive osteocytes were found in bone surrounding microcracks and in bone surrounding intracortical resorption spaces (,300% increases over controls, p < 0.005). TUNEL labeling in loaded ulnae at sites distant from microcracks or resorption foci did not differ from that in control bone. Osteocytes in toluidine blue,stained sections showed equivalent trends to TUNEL-stained sections, with significant increases in pyknotic nuclei and empty lacunae associated with microcracks and intracortical resorption spaces. TUNEL-positive osteocytes were observed around bone microdamage by 1 day after loading (p < 0.01 relative to baseline), and their number remained elevated throughout the entire experimental period. Increases in empty lacunae and decreases in normal osteocyte numbers were observed over time as well. These studies show that (1) osteocyte apoptosis is induced by bone fatigue, (2) this apoptosis is localized to regions of bone that contain microcracks, and (3) osteoclastic resorption after fatigue also coincides with regions of osteocyte apoptosis. The strong associations between microdamage, osteocyte apoptosis, and subsequent bone remodeling support the hypothesis that osteocyte apoptosis provides a key part of the activation or signaling mechanisms by which osteoclasts target bone for removal after fatigue-induced matrix injury. [source] Mechanical loading stimulates ecto-ATPase activity in human tendon cellsJOURNAL OF CELLULAR BIOCHEMISTRY, Issue 1 2005M. Tsuzaki Abstract Response to external stimuli such as mechanical signals is critical for normal function of cells, especially when subjected to repetitive motion. Tenocytes receive mechanical stimuli from the load-bearing matrix as tension, compression, and shear stress during tendon gliding. Overloading a tendon by high strain, shear, or repetitive motion can cause matrix damage. Injury may induce cytokine expression, matrix metalloproteinase (MMP) expression and activation resulting in loss of biomechanical properties. These changes may result in tendinosis or tendinopathy. Alternatively, an immediate effector molecule may exist that acts in a signal-dampening pathway. Adenosine 5,-triphosphate (ATP) is a candidate signal blocker of mechanical stimuli. ATP suppresses load-inducible inflammatory genes in human tendon cells in vitro. ATP and other extracellular nucleotide signaling are regulated efficiently by two distinct mechanisms: purinoceptors via specific receptor,ligand binding and ecto-nucleotidases via the hydrolysis of specific nucleotide substrates. ATP is released from tendon cells by mechanical loading or by uridine 5,-triphosphate (UTP) stimulation. We hypothesized that mechanical loading might stimulate ecto-ATPase activity. Human tendon cells of surface epitenon (TSC) and internal compartment (TIF) were cyclically stretched (1 Hz, 0.035 strain, 2 h) with or without ATP. Aliquots of the supernatant fluids were collected at various time points, and ATP concentration (ATP) was determined by a luciferin-luciferase bioluminescence assay. Total RNA was isolated from TSC and TIF (three patients) and mRNA expression for ecto-nucleotidase was analyzed by RT-PCR. Human tendon cells secreted ATP in vitro (0.5,1 nM). Exogenous ATP was hydrolyzed within minutes. Mechanical load stimulated ATPase activity. ATP was hydrolyzed in mechanically loaded cultures at a significantly greater rate compared to no load controls. Tenocytes (TSC and TIF) expressed ecto-nucleotidase mRNA (ENTPD3 and ENPP1, ENPP2). These data suggest that motion may release ATP from tendon cells in vivo, where ecto-ATPase may also be activated to hydrolyze ATP quickly. Ecto-ATPase may act as a co-modulator in ATP load-signal modulation by regulating the half-life of extracellular purine nucleotides. The extracellular ATP/ATPase system may be important for tendon homeostasis by protecting tendon cells from responding to excessive load signals and activating injurious pathways. © 2005 Wiley-Liss, Inc. [source] Effects of Thermal Aging on the Mechanical Properties of a Porous-Matrix Ceramic CompositeJOURNAL OF THE AMERICAN CERAMIC SOCIETY, Issue 3 2002Eric A. V. Carelli The present article focuses on changes in the mechanical properties of an all-oxide fiber-reinforced composite following long-term exposure (1000 h) at temperatures of 1000,1200°C in air. The composite of interest derives its damage tolerance from a highly porous matrix, precluding the need for an interphase at the fiber,matrix boundary. The key issue involves the stability of the porosity against densification and the associated implications for long-term durability of the composite at elevated temperatures. For this purpose, comparisons are made in the tensile properties and fracture characteristics of a 2D woven fiber composite both along the fiber direction and at 45° to the fiber axes before and after the aging treatments. Additionally, changes in the state of the matrix are probed through measurements of matrix hardness by Vickers indentation and through the determination of the matrix Young's modulus, using the measured composite moduli coupled with classical laminate theory. The study reveals that, despite evidence of some strengthening of the matrix and the fiber,matrix interfaces during aging, the key tensile properties in the 0°/90° orientation, including strength and failure strain, are unchanged. This strengthening is manifested to a more significant extent in the composite properties in the ±45° orientation, wherein the modulus and the tensile strength each exhibit a twofold increase after the 1200°C aging treatment. It also results in a change in the failure mechanism, from one involving predominantly matrix damage and interply delamination to one which is dominated by fiber fracture. Additionally, salient changes in the mechanical response beyond the maximum load suggest the existence of an optimum matrix strength at which the fracture energy in the ±45° orientation attains a maximum. The implications for long-term durability of this class of composite are discussed. [source] Vulnerability of the superficial zone of immature articular cartilage to compressive injuryARTHRITIS & RHEUMATISM, Issue 10 2010Bernd Rolauffs Objective The zonal composition and functioning of adult articular cartilage causes depth-dependent responses to compressive injury. In immature cartilage, shear and compressive moduli as well as collagen and sulfated glycosaminoglycan (sGAG) content also vary with depth. However, there is little understanding of the depth-dependent damage caused by injury. Since injury to immature knee joints most often causes articular cartilage lesions, this study was undertaken to characterize the zonal dependence of biomechanical, biochemical, and matrix-associated changes caused by compressive injury. Methods Disks from the superficial and deeper zones of bovine calves were biomechanically characterized. Injury to the disks was achieved by applying a final strain of 50% compression at 100%/second, followed by biomechanical recharacterization. Tissue compaction upon injury as well as sGAG density, sGAG loss, and biosynthesis were measured. Collagen fiber orientation and matrix damage were assessed using histology, diffraction-enhanced x-ray imaging, and texture analysis. Results Injured superficial zone disks showed surface disruption, tissue compaction by 20.3 ± 4.3% (mean ± SEM), and immediate biomechanical impairment that was revealed by a mean ± SEM decrease in dynamic stiffness to 7.1 ± 3.3% of the value before injury and equilibrium moduli that were below the level of detection. Tissue areas that appeared intact on histology showed clear textural alterations. Injured deeper zone disks showed collagen crimping but remained undamaged and biomechanically intact. Superficial zone disks did not lose sGAG immediately after injury, but lost 17.8 ± 1.4% of sGAG after 48 hours; deeper zone disks lost only 2.8 ± 0.3% of sGAG content. Biomechanical impairment was associated primarily with structural damage. Conclusion The soft superficial zone of immature cartilage is vulnerable to compressive injury, causing superficial matrix disruption, extensive compaction, and textural alteration, which results in immediate loss of biomechanical function. In conjunction with delayed superficial sGAG loss, these changes may predispose the articular surface to further softening and tissue damage, thus increasing the risk of development of secondary osteoarthritis. [source] A sodium dodecyl sulfate,polyacrylamide gel electrophoresis,liquid chromatography tandem mass spectrometry analysis of bovine cartilage tissue response to mechanical compression injury and the inflammatory cytokines tumor necrosis factor , and interleukin-1,ARTHRITIS & RHEUMATISM, Issue 2 2008Anna L. Stevens Objective To compare the response of chondrocytes and cartilage matrix to injurious mechanical compression and treatment with interleukin-1, (IL-1,) and tumor necrosis factor , (TNF,), by characterizing proteins lost to the medium from cartilage explant culture. Methods Cartilage explants from young bovine stifle joints were treated with 10 ng/ml of IL-1, or 100 ng/ml of TNF, or were subjected to uniaxial, radially-unconfined injurious compression (50% strain; 100%/second strain rate) and were then cultured for 5 days. Pooled media were subjected to gel-based separation (sodium dodecyl sulfate,polyacrylamide gel electrophoresis) and analysis by liquid chromatography tandem mass spectrometry, and the data were analyzed by Spectrum Mill proteomics software, focusing on protein identification, expression levels, and matrix protein proteolysis. Results More than 250 proteins were detected, including extracellular matrix (ECM) structural proteins, pericellular matrix proteins important in cell,cell interactions, and novel cartilage proteins CD109, platelet-derived growth factor receptor,like, angiopoietin-like 7, and adipocyte enhancer binding protein 1. IL-1, and TNF, caused increased release of chitinase 3,like protein 1 (CHI3L1), CHI3L2, complement factor B, matrix metalloproteinase 3, ECM-1, haptoglobin, serum amyloid A3, and clusterin. Injurious compression caused the release of intracellular proteins, including Grp58, Grp78, ,4-actinin, pyruvate kinase, and vimentin. Injurious compression also caused increased release and evidence of proteolysis of type VI collagen subunits, cartilage oligomeric matrix protein, and fibronectin. Conclusion Overload compression injury caused a loss of cartilage integrity, including matrix damage and cell membrane disruption, which likely occurred through strain-induced mechanical disruption of cells and matrix. IL-1, and TNF, caused the release of proteins associated with an innate immune and stress response by the chondrocytes, which may play a role in host defense against pathogens or may protect cells against stress-induced damage. [source] | ||||||||||