Cartilage Surface (cartilage + surface)

Distribution by Scientific Domains


Selected Abstracts


Arthroscopic reattachment of osteochondritis dissecans lesions using resorbable polydioxanone pins

EQUINE VETERINARY JOURNAL, Issue 5 2004
A. J. NIXON
Summary Reasons for performing study: Debridement of osteochondritis dissecans (OCD) cartilage lesions results in fibrocartilage and imperfect hyaline repair tissue, and forms a permanent irregularity to the subchondral bone plate. Objective: To evaluate the clinical, radiographic and outcome effects of OCD cartilage flap reattachment for select lesions as an alternative to OCD debridement. Hypothesis: Separated cartilage flaps resulting from OCD lesions may be re-incorporated into the hyaline cartilage surface by reattachment rather than debridement and removal. Methods: Resorbable polydioxanone pins were used to reattach OCD flap lesions in 16 joints of 12 horses. Criteria for attachment, rather than removal, included an unmineralised cartilage flap on preoperative radiographs and a relatively smooth surface with some residual perimeter attachment at surgery. Results: There were 12 subjects, 6 males and 6 females, 7 Thoroughbred or Standardbred weanlings, 3 Warmbloods, 1 Arabian and 1 Quarter Horse, mean age at surgery 6.8 months. All horses had effusion of the affected femoropatellar joint (n = 9), tarsocrural joint (n = 1) or fetlock (n = 2). Radiographic lesions varied in length between 1.8,6.3 cm; reattachment was used in 16 of 18 affected joints and the OCD cartilage was not satisfactory for salvage in 2 stifles. Number of pins required was 2,10. One horse was subjected to euthanasia due to a tendon laceration 8 weeks after surgery; of the remaining 11 horses, mean duration of follow-up was 3.9 years (range 4 months-8 years). Nine of these were sound and had entered work, while 2 were sound but remained unbroken 4 and 6 months post operatively, respectively. Radiographic resolution of the OCD lesion occurred in 14 of 16 pinned joints in the 9 horses with long-term follow-up. The 2 remaining joints had a 3 and a 5 mm mineralised flap in the original defect sites. Conclusions: This study indicated cartilage flap reattachment was an alternative to removal in selected OCD lesions. Potential relevance: Relatively smooth OCD cartilage flaps may be salvaged by reattachment and can result in normal radiographic subchondral contour and a high likelihood of athletic performance. Further case numbers are required to determine which lesions are too irregular or contain too much mineral for effective incorporation after reattachment. [source]


Comparison of cobalt chromium, ceramic and pyrocarbon hemiprostheses in a rabbit model: Ceramic leads to more cartilage damage than cobalt chromium

JOURNAL OF BIOMEDICAL MATERIALS RESEARCH, Issue 2 2008
Martin Jung
Abstract Cartilage wear after hemiarthroplasty remains a problem in orthopedic surgery. The main cause of cartilage wear, apart from incongruency of the joint partners, is generally considered to be the tribology of the material surfaces. This study evaluates in 27 rabbits the degree of cartilage wear of the tibia plateau after hemiarthroplasty with proximal interphalangeal prostheses made of three different materials [cobalt chromium (CoCr), pyrocarbon (PyCa), and ceramic (Cer)]. Three months after hemiarthroplasty, the articulating tibial cartilage was histomorphologically examined and degenerative damage was graded using the modified Mankin score. The mechanical capacity of the cartilage was assessed by stress relaxation testing. The biomechanical properties of the cartilage were significantly superior in the CoCr group as compared with the Cer group (p < 0.03), indicating less damage to the articulating cartilage surface. The Mankin score showed significantly lower values in the CoCr compared with Cer group (p = 0.011), whereas no differences were found between PyCa and CoCr or PyCa and Cer. In contrast to earlier reports, in this hemiarthroplasty model, the CoCr alloy showed less cartilage damage than a ceramic surface. Further, in vivo experiments are necessary to elucidate the controversial issue of the most suitable material for hemiarthroplasty. 2007 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 2008 [source]


PRG4 exchange between the articular cartilage surface and synovial fluid

JOURNAL OF ORTHOPAEDIC RESEARCH, Issue 10 2007
G.E. Nugent-Derfus
Abstract The boundary lubrication function of articular cartilage is mediated in part by proteoglycan 4 (PRG4) molecules, found both in synovial fluid (SF) and bound to the articular cartilage surface. Currently the mechanism by which PRG4 binds to the articular surface is not well understood. The objectives of this study were to determine (1) the effect of bathing fluid contents on PRG4 concentration at the articular surface ([PRG4]cart), and (2) whether native PRG4 can be removed from the surface and subsequently repleted with PRG4 from synovial fluid. In one experiment, cylindrical cartilage disks were stored in solutions of various PRG4 concentrations, either in phosphate-buffered saline (PBS) or SF as the carrier fluid. In a separate experiment, cartilage disks were stored in solutions expected to remove native PRG4 from the articular surface and allow subsequent repletion with PRG4 from SF. [PRG4]cart was independent of PRG4 concentration of the bathing fluid, and was similar for both carrier fluids. PRG4 was removed from cartilage by treatment with hyaluronidase, reduction/alkylation, and sodium dodecyl sulphate, and was repleted fully by subsequent bathing in SF. These results suggest that the articular surface is normally saturated with tightly bound PRG4, but this PRG4 can exchange with the PRG4 in SF under certain conditions. This finding suggests that all tissues surrounding the joint cavity that secrete PRG4 into the SF may help to maintain lubrication function at the articular surface. 2007 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 25:1269,1276, 2007 [source]


Phospholipid composition of articular cartilage boundary lubricant

JOURNAL OF ORTHOPAEDIC RESEARCH, Issue 4 2001
A. V. Sarma
The mechanism of lubrication in normal human joints depends on loading and velocity conditions. Boundary lubrication, a mechanism in which layers of molecules separate opposing surfaces, occurs under severe loading. This study was aimed at characterizing the phospholipid composition of the adsorbed molecular layer on the surface of normal cartilage that performs as a boundary lubricant. The different types of phospholipid adsorbed onto the surface of cartilage were isolated by extraction and identified by chromatography on silica gel paper and mass spectroscopy. The main phospholipid classes identified were quantified by a phosphate assay. Gas chromatography and electrospray ionization mass spectrometry were used to further characterize the fatty acyl chains in each major phospholipid component and to identify the molecular species present. Phosphatidylcholine (41%), phosphatidylethanolamine (27%) and sphingomyelin (32%) were the major components of the lipid layer on the normal cartilage surface. For each lipid type, a mixture of fatty acids was detected, with a higher percentage of unsaturated species compared to saturated species. The most abundant fatty acid observed with all three lipid types was oleic acid (C18:1). Additional work to further quantify the molecular species using electrospray ionization mass spectrometry is recommended. 2001 Orthopaedic Research Society. Published by Elsevier Science Ltd. All rights reserved. [source]


Evaluation of articular cartilage repair using biodegradable nanofibrous scaffolds in a swine model: a pilot study

JOURNAL OF TISSUE ENGINEERING AND REGENERATIVE MEDICINE, Issue 1 2009
Wan-Ju Li
Abstract The aim of this study was to evaluate a cell-seeded nanofibrous scaffold for cartilage repair in vivo. We used a biodegradable poly(,-caprolactone) (PCL) nanofibrous scaffold seeded with allogeneic chondrocytes or xenogeneic human mesenchymal stem cells (MSCs), or acellular PCL scaffolds, with no implant as a control to repair iatrogenic, 7 mm full-thickness cartilage defects in a swine model. Six months after implantation, MSC-seeded constructs showed the most complete repair in the defects compared to other groups. Macroscopically, the MSC-seeded constructs regenerated hyaline cartilage-like tissue and restored a smooth cartilage surface, while the chondrocyte-seeded constructs produced mostly fibrocartilage-like tissue with a discontinuous superficial cartilage contour. Incomplete repair containing fibrocartilage or fibrous tissue was found in the acellular constructs and the no-implant control group. Quantitative histological evaluation showed overall higher scores for the chondrocyte- and MSC-seeded constructs than the acellular construct and the no-implant groups. Mechanical testing showed the highest equilibrium compressive stress of 1.5 MPa in the regenerated cartilage produced by the MSC-seeded constructs, compared to 1.2 MPa in the chondrocyte-seeded constructs, 1.0 MPa in the acellular constructs and 0.2 MPa in the no-implant group. No evidence of immune reaction to the allogeneically- and xenogeneically-derived regenerated cartilage was observed, possibly related to the immunosuppressive activities of MSCs, suggesting the feasibility of allogeneic or xenogeneic transplantation of MSCs for cell-based therapy. Taken together, our results showed that biodegradable nanofibrous scaffolds seeded with MSCs effectively repair cartilage defects in vivo, and that the current approach is promising for cartilage repair. Copyright 2008 John Wiley & Sons, Ltd. [source]


Loss of cartilage structure, stiffness, and frictional properties in mice lacking PRG4

ARTHRITIS & RHEUMATISM, Issue 6 2010
Jeffrey M. Coles
Objective To assess the role of the glycoprotein PRG4 in joint lubrication and chondroprotection by measuring friction, stiffness, surface topography, and subsurface histology of the hip joints of Prg4,/, and wild-type (WT) mice. Methods Friction and elastic modulus were measured in cartilage from the femoral heads of Prg4,/, and WT mice ages 2, 4, 10, and 16 weeks using atomic force microscopy, and the surface microstructure was imaged. Histologic sections of each femoral head were stained and graded. Results Histologic analysis of the joints of Prg4,/, mice showed an enlarged, fragmented surface layer of variable thickness with Safranin O,positive formations sometimes present, a roughened underlying articular cartilage surface, and a progressive loss of pericellular proteoglycans. Friction was significantly higher on cartilage of Prg4,/, mice at age 16 weeks, but statistically significant differences in friction were not detected at younger ages. The elastic modulus of the cartilage was similar between cartilage surfaces of Prg4,/, and WT mice at young ages, but cartilage of WT mice showed increasing stiffness with age, with significantly higher moduli than cartilage of Prg4,/, mice at older ages. Conclusion Deletion of the gene Prg4 results in significant structural and biomechanical changes in the articular cartilage with age, some of which are consistent with osteoarthritic degeneration. These findings suggest that PRG4 plays a significant role in preserving normal joint structure and function. [source]


Different amplifying mechanisms of interleukin-17 and interferon-, in Fc, receptor,mediated cartilage destruction in murine immune complex,mediated arthritis

ARTHRITIS & RHEUMATISM, Issue 2 2009
Lilyanne C. Grevers
Objective Previously, we reported that interferon-, (IFN,) aggravates cartilage destruction in immune complex (IC),mediated arthritis via up-regulation of activating Fc, receptors (Fc,R). Recently, we found that interleukin-17 (IL-17) also aggravates cartilage destruction in arthritis models in which ICs are involved, but the underlying mechanism remains unknown. This study was undertaken to determine the role of IL-17 in Fc,R-mediated cartilage destruction in IC-mediated arthritis and to compare its effect with that of IFN,. Methods IC-mediated arthritis was passively induced in ,-chain,/, mice, which lack functional activating Fc,R, and in wild-type controls. AdIL-17 or a control vector was injected into the knee joints 1 day prior to induction of IC-mediated arthritis. Knee joints were isolated for histologic analysis, and synovium samples were obtained for reverse transcriptase,polymerase chain reaction (RT-PCR). Macrophage (RAW 264.7) cell lines and polymorphonuclear cell (PMN; 32Dcl3) lines were stimulated with IFN, or IL-17 for analysis of Fc,R expression using RT-PCR and fluorescence-activated cell sorting. Results IL-17 overexpression prior to induction of IC-mediated arthritis significantly aggravated cartilage destruction and inflammation, characterized by a massive influx of PMNs, which adhered to the cartilage surface. Although IL-17 overexpression increased Fc,R messenger RNA levels in the synovium, in vitro stimulation of macrophages and PMNs revealed that, in contrast to IFN,, IL-17 did not directly regulate Fc,R expression. Despite similar inflammation in AdIL-17,enhanced IC-mediated arthritis in ,-chain,/, mice and wild-type controls, severe cartilage destruction and PMN adherence were completely absent in ,-chain,/, mice. Conclusion Our findings indicate that IL-17,mediated aggravation of cartilage destruction in IC-mediated arthritis is Fc,R dependent. However, in contrast to IFN,, which directly up-regulates Fc,R expression on macrophages and PMNs, IL-17 enhances cartilage destruction by increasing the local amount of Fc,R-bearing neutrophils. [source]


Relationship of meniscal damage, meniscal extrusion, malalignment, and joint laxity to subsequent cartilage loss in osteoarthritic knees

ARTHRITIS & RHEUMATISM, Issue 6 2008
Leena Sharma
Objective Progressive knee osteoarthritis (OA) is believed to result from local factors acting in a systemic environment. Previous studies have not examined these factors concomitantly or compared quantitative and qualitative cartilage loss outcomes. The aim of this study was to test whether meniscal damage, meniscal extrusion, malalignment, and laxity each predicted tibiofemoral cartilage loss after controlling for the other factors. Methods Laxity and alignment were measured at baseline in individuals with knee OA. Magnetic resonance imaging included spin-echo coronal and sagittal imaging for meniscal scoring and axial and coronal spoiled gradient echo sequences with water excitation for cartilage quantification. Tibial and weight-bearing femoral condylar subchondral bone area and cartilage surface were segmented. Cartilage volume, denuded bone area, and cartilage thickness were quantified in each plate, with progression defined as cartilage loss >2 times the coefficient of variation for each plate. Qualitative outcome was assessed as worsening of the cartilage score. Logistic regression analysis with generalized estimating equations yielded odds ratios for each factor, adjusting for age, sex, body mass index, and the other factors. Results We studied 251 knees in 153 persons. After full adjustment, medial meniscal damage predicted medial tibial cartilage volume loss and tibial and femoral denuded bone increase, while varus malalignment predicted medial tibial cartilage volume and thickness loss and tibial and femoral denuded bone increase. Lateral meniscal damage predicted every lateral outcome. Laxity and meniscal extrusion had inconsistent effects. After full adjustment, no factor except medial laxity predicted qualitative outcome. Conclusion Using quantitative cartilage loss assessment, local factors that independently predicted tibial and femoral loss included medial meniscal damage and varus malalignment (medially) and lateral meniscal damage (laterally). A measurement of quantitative outcome was more sensitive at revealing these relationships than a qualitative approach. [source]


Loss of cartilage structure, stiffness, and frictional properties in mice lacking PRG4

ARTHRITIS & RHEUMATISM, Issue 6 2010
Jeffrey M. Coles
Objective To assess the role of the glycoprotein PRG4 in joint lubrication and chondroprotection by measuring friction, stiffness, surface topography, and subsurface histology of the hip joints of Prg4,/, and wild-type (WT) mice. Methods Friction and elastic modulus were measured in cartilage from the femoral heads of Prg4,/, and WT mice ages 2, 4, 10, and 16 weeks using atomic force microscopy, and the surface microstructure was imaged. Histologic sections of each femoral head were stained and graded. Results Histologic analysis of the joints of Prg4,/, mice showed an enlarged, fragmented surface layer of variable thickness with Safranin O,positive formations sometimes present, a roughened underlying articular cartilage surface, and a progressive loss of pericellular proteoglycans. Friction was significantly higher on cartilage of Prg4,/, mice at age 16 weeks, but statistically significant differences in friction were not detected at younger ages. The elastic modulus of the cartilage was similar between cartilage surfaces of Prg4,/, and WT mice at young ages, but cartilage of WT mice showed increasing stiffness with age, with significantly higher moduli than cartilage of Prg4,/, mice at older ages. Conclusion Deletion of the gene Prg4 results in significant structural and biomechanical changes in the articular cartilage with age, some of which are consistent with osteoarthritic degeneration. These findings suggest that PRG4 plays a significant role in preserving normal joint structure and function. [source]


Scavenger receptor class A type I/II determines matrix metalloproteinase,mediated cartilage destruction and chondrocyte death in antigen-induced arthritis

ARTHRITIS & RHEUMATISM, Issue 10 2009
P. L. E. M. van Lent
Objective Scavenger receptor class A type I (SR-AI) and SR-AII are expressed by macrophages in particular and bind and internalize a broad range of molecules (including endotoxins, apoptotic bodies, and oxidized low-density lipoprotein). This study was undertaken to investigate the role of SR-AI/II in mediating severe cartilage destruction in antigen-induced arthritis (AIA). Methods AIA was induced in the knee joints of SR-AI/II,/, mice and wild-type (WT) controls. Joint inflammation and cartilage destruction (chondrocyte death) were measured by examining the histology of total knee joints. Matrix metalloproteinase (MMP),mediated neoepitopes were measured by immunolocalization using anti-VDIPEN antibodies and chondrocyte activation with anti-S100A8 antibodies. Messenger RNA (mRNA) levels were determined in inflamed synovium using microarray analysis and quantitative reverse transcriptase,polymerase chain reaction. In synovial washouts, cytokines (interleukin-1, [IL-1,], IL-10, and tumor necrosis factor ,) and S100A8/S100A9 were measured using Luminex and enzyme-linked immunosorbent assay. Results Levels of SR-AI/II mRNA were strongly elevated in inflamed synovium in AIA. On days 2, 8, and 14 after AIA induction, joint inflammation (exudates/infiltrate) was similar between the 2 groups. In WT mice, severe cartilage destruction was found in multiple cartilage surfaces of the inflamed knee joint on day 14 after AIA induction. MMP-mediated matrix destruction ranged between 40% and 60%, and chondrocyte death was prominent in 40,75% of the cartilage surfaces. In striking contrast, in SR-AI/II,/, mice, despite comparable joint inflammation, pronounced cartilage destruction was almost completely absent. Levels of IL-1, and S100A8/S100A9 were significantly lower on days 7 and 14 after AIA induction, but levels of mRNA for various MMPs (MMP-2, MMP-3, MMP-9, and MMP-13) were comparable. Conclusion Our findings indicate that SR-AI and SR-AII are crucial receptors involved in mediating severe cartilage destruction in AIA. [source]


Prevention of cartilage degeneration in a rat model of osteoarthritis by intraarticular treatment with recombinant lubricin

ARTHRITIS & RHEUMATISM, Issue 3 2009
Carl R. Flannery
Objective Lubricin, also referred to as superficial zone protein and PRG4, is a synovial glycoprotein that supplies a friction-resistant, antiadhesive coating to the surfaces of articular cartilage, thereby protecting against arthritis-associated tissue wear and degradation. This study was undertaken to generate and characterize a novel recombinant lubricin protein construct, LUB:1, and to evaluate its therapeutic efficacy following intraarticular delivery in a rat model of osteoarthritis (OA). Methods Binding and localization of LUB:1 to cartilage surfaces was assessed by immunohistochemistry. The cartilage-lubricating properties of LUB:1 were determined using a custom friction testing apparatus. A cell-binding assay was performed to quantify the ability of LUB:1 to prevent cell adhesion. Efficacy studies were conducted in a rat meniscal tear model of OA. One week after the surgical induction of OA, LUB:1 or phosphate buffered saline vehicle was administered by intraarticular injection for 4 weeks, with dosing intervals of either once per week or 3 times per week. OA pathology scores were determined by histologic analysis. Results LUB:1 was shown to bind effectively to cartilage surfaces, and facilitated both cartilage boundary lubrication and inhibition of synovial cell adhesion. Treatment of rat knee joints with LUB:1 resulted in significant disease-modifying, chondroprotective effects during the progression of OA, by markedly reducing cartilage degeneration and structural damage. Conclusion Our findings demonstrate the potential use of recombinant lubricin molecules in novel biotherapeutic approaches to the treatment of OA and associated cartilage abnormalities. [source]


Biomechanics of cartilage articulation: Effects of lubrication and degeneration on shear deformation

ARTHRITIS & RHEUMATISM, Issue 7 2008
Benjamin L. Wong
Objective To characterize cartilage shear strain during articulation, and the effects of lubrication and degeneration. Methods Human osteochondral cores from lateral femoral condyles, characterized as normal or mildly degenerated based on surface structure, were selected. Under video microscopy, pairs of osteochondral blocks from each core were apposed, compressed 15%, and subjected to relative lateral motion with synovial fluid (SF) or phosphate buffered saline (PBS) as lubricant. When cartilage surfaces began to slide steadily, shear strain (Exz) and modulus (G) overall in the full tissue thickness and also as a function of depth from the surface were determined. Results In normal tissue with SF as lubricant, Exz was highest (0.056) near the articular surface and diminished monotonically with depth, with an overall average Exz of 0.028. In degenerated cartilage with SF as lubricant, Exz near the surface (0.28) was 5-fold that of normal cartilage and localized there, with an overall Exz of 0.041. With PBS as lubricant, Exz values near the articular surface were ,50% higher than those observed with SF, and overall Exz was 0.045 and 0.062 in normal and degenerated tissue, respectively. Near the articular surface, G was lower with degeneration (0.06 MPa, versus 0.18 MPa in normal cartilage). In both normal and degenerated cartilage, G increased with tissue depth to 3,4 MPa, with an overall G of 0.26,0.32 MPa. Conclusion During articulation, peak cartilage shear is highest near the articular surface and decreases markedly with depth. With degeneration and diminished lubrication, the markedly increased cartilage shear near the articular surface may contribute to progressive cartilage deterioration and osteoarthritis. [source]