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Fatigue fracture of high-strength steels often occurs from small defect on the surface of a material or from non-metallic inclusion in the subsurface zone of a material. Under rotating bending loading, the S-N curve of high-strength steels consists of two curves corresponding to surface defect-induced fracture and internal inclusion-induced fracture. The surface defect-induced fracture occurs at high stress amplitude levels and low cycles. However, the subsurface inclusion-induced fracture occurs at low stress amplitude levels and high-cycle region of more than 106 cycles (giga-cycle fatigue life). There is a definite stress range in the S-N curve obtained from the rotating bending, where the crack initiation site changes from surface to subsurface, giving a stepwise S-N curve or a duplex S-N curve. On the other hand, under cyclic axial loading, the S-N curve of high-strength steels displays a continuous decline and surface defect-induced or internal inclusion-induced fracture occur in the whole range of amplitudes. In this paper, influence factors on S-N curve characteristics of high-strength steels, including size of inclusions and the stress gradient of bending fatigue, were investigated for rotating bending and cyclic axial loading in the giga-cycle fatigue regime. Then, based on the estimated subsurface crack growth rate from the S-N data, effect of inclusion size on the dispersion of fatigue life was explained, and it was clarified that the shape of S-N curve for subsurface inclusion-induced fracture depends on the inclusion size. [ABSTRACT FROM AUTHOR]

OBJECTIVE. To examine the promoter activity and protein expression of the death receptor 3 gene DR3, a member of the apoptosis-inducing Fas gene family, with particular reference to the methylation status of its promoter region in rheumatoid arthritis (RA). METHODS: Genomic DNA was prepared from peripheral blood mononuclear cells obtained from healthy individuals and from patients with RA and synovial cells obtained from patients with RA and osteoarthritis. The methylation status of the DR3 promoter was analyzed by bisulfite genomic sequencing and methylation-specific polymerase chain reaction techniques. Gene promoter activity and protein expression were examined using the luciferase reporter and Western blotting techniques. RESULTS: The promoter region of the DR3 gene contained many CpG motifs, including one CpG island that was specifically hypermethylated in synovial cells from patients with RA. Promoter assays showed that the promoter CpG island was essential for the transactivation of the DR3 gene and that forced hypermethylation of the CpG island with the bacterial methylase Sss I in vitro resulted in inhibition of the DR3 gene expression. Furthermore, the expression of DR-3 protein was down-modulated in association with methylation of the promoter CpG island in RA synovial cells. CONCLUSION: The CpG island in the DR3 gene promoter was specifically methylated to down-modulate the expression of DR-3 protein in rheumatoid synovial cells, which may provide resistance to apoptosis in RA synovial cells. [ABSTRACT FROM AUTHOR]

ABSTRACT Effect of shot-peening on fatigue behaviour in the gigacycle regime was investigated in order to clarify the duplex S–N curve characteristics. Cantilever-type rotary bending fatigue tests were performed in laboratory air at room temperature by using hourglass-shaped specimens of high-carbon–chromium bearing steel, JIS SUJ2. Fatigue crack initiation site changed from the surface of untreated specimen to the subsurface of the specimen because of hardening and compressive residual stress with shot-peening in the region of high-stress amplitude. On the other hand, no difference in fatigue life controlled by the subsurface crack initiation between untreated specimen and shot-peening one was observed in high-cycle region. It was suggested that the S–N curve corresponding to the internal fracture mode is inherent in the material, as compared with the S–N curve of surface fracture mode, which is affected by surface conditions, environmental conditions and so on. Subsurface crack initiation and propagation behaviour were discussed under the detailed measurement of crack initiation area and shape of the fish-eye fracture surface. [ABSTRACT FROM AUTHOR]

The S–N curve obtained from cantilever-type rotary bending fatigue tests using hour-glass-shaped specimens of high carbon-chromium bearing steel clearly distinguished the fracture modes into two groups each having a different crack origin. One was governed by crystal slip on the specimen surface, which occurred in the region of short fatigue life and a high stress amplitude level. The other was governed by a non-metallic inclusion at a subsurface level which occurred in the region of long fatigue life and low stress amplitude. The inclusion developed a fish-eye fracture mode that was distributed over a wide range of stress amplitude not only below the fatigue limit defined as the threshold for fracture due to the surface slip mode but also above the fatigue limit. This remarkable shape of the S–N curve was different from the step-wise one reported in previous literature and is characterized as a duplex S–N curve composed of two different S–N curves corresponding to the respective fracture modes. From detailed observations of the fracture surface and the fatigue crack origin, the mechanisms for the internal fracture mode and the characteristics of the S–N curve are discussed. [ABSTRACT FROM AUTHOR]

Ozawa T, Nakano M, Sugimura H, Kurayama H, Tahata K, Nakamura J, Shiozawa K. Effects of endodontic instrument handle diameter on electromyographic activity of forearm and hand muscles. International Endodontic Journal , 34 , 100–106, 2001. --> Aim: To determine the influence of the handle diameter of endodontic instruments on forearm and hand muscle activity using electromyographic (EMG) recording. Methodology: Size 45 K‐type files were fitted with four different handle diameters; 3.5, 4.0, 5.0, and 6.0 mm. Seven dentists then attempted to negotiate to the working length acrylic resin root canals with each of the four handle sizes using a reaming motion. EMG activities were recorded from the flexor pollicis brevis muscle (f.p.b.), the flexor carpi radialis muscle (f.c.r.), and the brachioradialis muscle (b) with bipolar surface electrodes. The time taken to negotiate the canals, the area of integrated EMG that corresponded to the amount of EMG activity required during penetration and the maximum amplitude of EMG were measured using the EMG data. Results were analysed statistically using a one‐way factorial anova test and multiple comparison tests. Results: Reaming time and integrated EMG area of each muscle decreased with an increase in handle diameter. The most significant difference in time and area of integrated EMG was detected between handles of 6 mm and 3.5 mm diameter (time: P < 0.01, area of the f.p.b.: P < 0.01, area of the f.c.r. and b: P < 0.05), and between handles of 5 mm and 3.5 mm diameter (P < 0.05). Both 5 mm and 6 mm handles significantly decreased the maximum amplitude of EMG recorded from the f.p.b. compared with 3.5 mm handles (between 3.5 mm and 6 mm: P < 0.01, between 3.5 mm and 5 mm: P < 0.05). Conclusion: The results indicate that handle diameter has an effect on reaming time as well as on muscle activity. As a consequence, handle diameter influenced operator performance during instrumentation. [ABSTRACT FROM AUTHOR]

The effect of 1α,25-dihydroxyvitamin D3 (1 ,25-(OH)2D3) on pokeweed mitogen-induced generation of human immunoglobulin-secreting cells (ISC) was studied in serum-free culture. Human peripheral blood mononuclear cells (1.75 × 106/ml) were cultured in 200 μ1 microculture wells containing Iscove's MEM supplemented with 20 μg/ml of human transferrin, 20 μg/ml of soybean lecithin and 1 mg/ml of delipidated bovine albumin. The culture supported ISC generation of all isotypes, and the optimal concentration of pokeweed mitogen was 1 μg/ml. After stimulation with a suboptimal concentration (0.3 μg/ml) of pokeweed mitogen, 1,25-(OH)2D3 suppressed the ISC generation at a dose range between 10-9M and 10-7 M, and maximal inhibition was obtained at 10-9 M. 1,25-(OH)2D3 had no effect on the spontaneous ISC generation. The effect was specific for 1,25-(OH)2D3 and no suppression was obtained by 24R,25-dihydroxyvitamin D3 or 25-hydroxyvitamin D3. [ABSTRACT FROM AUTHOR]

The HLA-DR antigen was investigated in synovial epithelia of rheumatoid arthritis, osteoarthritis and normal traumatic joints, using monoclonal anti-human HLA-DR antibody and horseradish per- oxidase-conjugated antibody. The HLA-DR staining was observed in an electron microscope. ElLA-DR antigen was observed to be present on the surface of both macrophage-like (type A) and fibroblast-like (type B) cells in synovial epithelia in all rheumatoid arthritis, osteoarthritis and normal joints. Since type A and B cells are ultrastructurally considered to be of synovial origin, the findings suggest that the ex- pression of HLA-DR antigen on the surface is one of the common attributes of type A and B cells in synovial epithelia, even before cellular infiltration of chronic inflammation in rheumatoid arthritis. These cells may play an important role in the initiation of rheumatoid inflammation, since HLA-DR antigen is considered equivalent to murine Ia antigen. [ABSTRACT FROM AUTHOR]

New Findings: What is the central question of this study? Increased work of breathing and the accumulation of metabolites have neural and cardiovascular consequences through a respiratory muscle-induced metaboreflex. The influence of the respiratory muscle-induced metaboreflex on splanchnic blood flow in humans remains unknown. What is the main finding and its importance? Coeliac artery blood flow decreased gradually during inspiratory resistive breathing, accompanied by a progressive increase in arterial blood pressure. It is possible that the respiratory muscle-induced metaboreflex contributes to splanchnic blood flow regulation., Abstract: The purpose of this study was to clarify the effect of increasing inspiratory muscle work on coeliac artery blood flow. Eleven healthy young males completed the study. The subjects performed voluntary hyperventilation with or without inspiratory resistance (loading or non-loading trial; tidal volume of 40% of vital capacity and breathing frequency of 20 breaths/min). The loading trial was conducted with inspiratory resistance (40% of maximal inspiratory pressure) and was terminated when the subjects could no longer maintain the target tidal volume or breathing frequency. The non-loading trial was conducted without inspiratory resistance and was of the same duration as the loading trial. Arterial blood pressure was recorded using finger photoplethysmography, and coeliac artery blood flow was measured using Doppler ultrasound. Mean arterial blood pressure increased gradually during the loading trial (mean ± SD; from 89.0 ± 10.8 to 103.9 ± 17.3 mmHg) but not in the non-loading trial (from 88.7 ± 5.9 to 90.4 ± 9.9 mmHg). Coeliac artery blood flow and coeliac vascular conductance decreased gradually during the loading trial (from 601.2 ± 155.7 to 482.6 ± 149.5 mL/min and from 6.9 ± 2.2 to 4.8 ± 1.7 mL/min/mmHg, respectively) but were unchanged in the non-loading trial (from 630.7 ± 157.1 to 635.6 ± 195.7 mL/min and from 7.1 ± 1.8 to 7.2 ± 2.9 mL/min/mmHg, respectively). These results show that increasing inspiratory muscle work affects splanchnic blood flow regulation, and we suggest that this might be mediated by the inspiratory muscle-induced metaboreflex., (© 2022 The Authors. Experimental Physiology © 2022 The Physiological Society.)

New Findings: What is the central question of this study? Sympathetic vasomotor outflow is reduced during low-intensity dynamic leg exercise in younger individuals: does ageing influence the sympathoinhibitory effect during low-intensity leg cycling? What is the main finding and its importance? Muscle sympathetic nerve activity during low-intensity cycling decreased in older males, as seen in young males. It is possible that cardiopulmonary baroreflex-mediated inhibition of sympathetic vasomotor outflow during dynamic leg exercise is preserved in healthy older males., Abstract: Muscle sympathetic nerve activity (MSNA) is reduced during low-intensity dynamic leg exercise in young males. It is suggested that this inhibition is mediated by loading of the cardiopulmonary baroreceptors. The purpose of this study was to clarify the impact of age on MSNA during dynamic leg exercise. Nine younger males (YM, mean ± SD, 20 ± 1 years) and nine older males (OM, 72 ± 3 years) completed the study. The subjects performed two 4-min cycling exercises at 10% of their heart rate reserve using a cycle ergometer in a semirecumbent position (MSNA and estimated central venous pressure (eCVP) trials). MSNA was recorded via microneurography of the left radial nerve. The CVP was estimated based on peripheral venous pressure, which was monitored using a cannula in the right large antecubital vein. The magnitude of the increase in mean arterial blood pressure during leg cycling was larger in OM (+9.3 ± 5.5 mmHg) compared with YM (+2.8 ± 4.7 mmHg). MSNA burst frequency was decreased during cycling in both YM (-8.1 ± 3.8 bursts/min) and OM (-10.6 ± 3.3 bursts/min), but no significant difference was found between the two groups. The eCVP increased during exercise in both groups, and there was no difference in the changes in eCVP between YM (+1.1 ± 0.4 mmHg) and OM (+1.2 ± 0.7 mmHg). These data indicate that inhibition of sympathetic vasomotor outflow during low-intensity cycling appears in OM as seen in YM. It is possible that the muscle pump-induced loading of the cardiopulmonary baroreflex is preserved during cycling in healthy older males., (© 2022 The Authors. Experimental Physiology © 2022 The Physiological Society.)

New Findings: What is the central question of this study? Increased respiratory muscle activation is associated with neural and cardiovascular consequences via the respiratory muscle-induced metaboreflex. Does ageing and/or sex influence the arterial blood pressure response during voluntary normocapnic incremental hyperpnoea? What is the main finding and its importance? The increase in blood pressure during hyperpnoea was smaller in younger females than in older females, whereas no difference was found between older males and older females. The blunted respiratory muscle-induced metaboreflex in younger females is normalized with advancing age, whereas ageing has no such effect in males., Abstract: We hypothesized that older females (OF) have a greater arterial blood pressure response to increased respiratory muscle work compared with younger females (YF) and that no such difference exists between older males (OM) and younger males (YM). To test these hypotheses, cardiovascular responses during voluntary normocapnic incremental hyperpnoea were evaluated and compared between older and younger subjects. An incremental respiratory endurance test (IRET) was performed as follows: target minute ventilation was initially set at 30% of the maximal voluntary ventilation (MVV12) and was increased by 10% of MVV12 every 3 min. The test was terminated when the subject could not maintain the target percentage of MVV12. Heart rate and mean arterial blood pressure (MAP) were recorded continuously. The increase in MAP from baseline (ΔMAP) during the IRET in OM (+24.0 ± 14.7 mmHg, mean ± SD) did not differ (P = 0.144) from that in YM (+24.3 ± 13.4 mmHg), but it was greater (P = 0.004) in OF (+31.2 ± 11.6 mmHg) than in YF (+10.3 ± 5.5 mmHg). No significant difference in ΔMAP during the IRET was observed between OM and OF (P = 0.975). These results suggest that the respiratory muscle-induced metaboreflex is blunted in YF, but it could be normalized with advancing age. In males, ageing has little effect on the respiratory muscle-induced metaboreflex. These results show no sex difference in the respiratory muscle-induced metaboreflex in older adults., (© 2021 The Authors. Experimental Physiology © 2021 The Physiological Society.)

New Findings: What is the central question of this study? Increased respiratory muscle activation is associated with neural and cardiovascular consequences via the respiratory muscle metaboreflex. Does increased sympathetic vasoconstriction originating from the respiratory musculature elicit a reduction in blood flow to an inactive limb in order to maintain blood flow to an active limb? What is the main finding and its importance? Arm blood flow was reduced whereas leg blood flow was preserved during mild leg exercise with inspiratory resistance. Blood flow to the active limb is maintained via sympathetic control of blood flow redistribution when the respiratory muscle-induced metaboreflex is activated., Abstract: The purpose of this study was to elucidate the effect of increasing inspiratory muscle work on blood flow to inactive and active limbs. Healthy young men (n = 10, 20 ± 2 years of age) performed two bilateral dynamic knee-extension and knee-flexion exercise tests at 40% peak oxygen uptake for 10 min. The trials consisted of spontaneous breathing for 5 min followed by voluntary hyperventilation either with or without inspiratory resistance for 5 min (40% of maximal inspiratory mouth pressure, inspiratory duty cycle of 50% and a breathing frequency of 40 breaths min -1 ). Mean arterial blood pressure was acquired using finger photoplethysmography. Blood flow in the brachial artery (inactive limb) and in the femoral artery (active limb) were monitored using Doppler ultrasound. Mean arterial blood pressure during exercise was higher (P < 0.05) with inspiratory resistance (121 ± 7 mmHg) than without resistance (99 ± 5 mmHg). Brachial artery blood flow increased during exercise without inspiratory resistance (120 ± 31 ml min -1 ) compared with the resting level, whereas it was attenuated with inspiratory resistance (65 ± 43 ml min -1 ). Femoral artery blood flow increased at the onset of exercise and was maintained throughout exercise without inspiratory resistance (2576 ± 640 ml min -1 ) and was unchanged when inspiratory resistance was added (2634 ± 659 ml min -1 ; P > 0.05). These results suggest that sympathetic control of blood redistribution to active limbs is facilitated, in part, by the respiratory muscle-induced metaboreflex., (© 2018 The Authors. Experimental Physiology © 2018 The Physiological Society.)

Objective: To study the genetic contribution of major histocompatibility complex class I polypeptide-related sequence A (MICA), important in natural killer (NK) cell function, in patients with systemic lupus erythematosus (SLE)., Methods: Japanese patients with SLE (n=716), those with rheumatoid arthritis (RA) (n=327), and healthy control subjects (n=351) were genotyped for the Val129 Met polymorphism (rs1051792) and transmembrane (TM) alanine-encoding GCT repeats, termed A4, A5, A5.1, A6, and A9, in the MICA gene. Recombinant human MICA-GST fusion proteins were tested on the NK cell line NK92MI for the expression of NK group 2, member D (NKG2-D), NK cell-mediated cytotoxicity, and interferon-γ (IFNγ) production., Results: The MICA 129Met allele, TMA9 allele, and 129Met/Met genotype were positively associated with SLE (corrected P [Pcorr]=0.01 and odds ratio [OR] 1.3, Pcorr=0.003 and OR 1.6, and Pcorr=0.02 and OR 1.8, respectively), while the MICA 129Val allele was negatively associated with SLE (Pcorr=0.01, OR 0.8). The MICA 129Met;A9 haplotype was also associated with SLE (Pcorr=0.0006, OR 1.8), and there was an additive genetic effect between the MICA 129Met;A9 haplotype and HLA-DRB1*15:01. When NK92MI cells were incubated in vitro with recombinant human disease-associated 129Met;A9 (the combination of polymorphisms at 129Met and TMA9), expression of NKG2-D on NK92MI cells and cytotoxicity of the NK cells were inhibited, but production of IFNγ from NK92MI cells was enhanced., Conclusion: The MICA polymorphism is genetically associated with SLE, and MICA appears to contribute to the pathogenesis of SLE by modulating NK cell function., (Copyright © 2011 by the American College of Rheumatology.)

Objective: To determine whether angiopoietin 1 (Ang-1) potentiates overgrowth of the synovium and joint degradation in rheumatoid arthritis (RA), and to clarify the cell-signaling mechanisms of Ang-1 in the rheumatoid joint., Methods: Expression of Ang-1, TIE-2 (a receptor for Ang-1), and matrix metalloproteinase 3 (MMP-3) was studied by immunohistochemistry. Activation of the ERK/MAPK and phosphatidylinositol (PI) 3-kinase/Akt pathways and of NF-kappaB was determined by Western blotting and an NF-kappaB p65 DNA binding activity assay, respectively. Induction of apoptosis was evaluated by nuclear staining, cell viability assay, and Western blotting of caspases. Synovial cell migration was evaluated by actin polymerization, Western blotting of Rho family proteins, and affinity purification with Rhotekin-Rho and p21-activated kinase 1. Matrix degradation was examined by induction of proMMP-3 secretion from synovial cells followed by in vitro cartilaginous matrix degradation assay., Results: Ang-1 stimulated the ERK/MAPK and PI 3-kinase/Akt pathways in a cooperative but independent manner, which enhanced rheumatoid synovium overgrowth and joint destruction. In addition, Ang-1 activated NF-kappaB via Akt to promote cell growth, but also inhibited cell apoptosis via ERK and Akt. Ang-1 directly potentiated the extension of synovial cells in an ERK- and Akt-dependent manner by up-regulating Rho family proteins, which attenuated Rac signaling and led to membrane ruffling. Ang-1 induced proMMP-3 secretion from synovial cells, which resulted in direct degradation of the cartilaginous matrix., Conclusion: Ang-1 stimulates the ERK/MAPK and PI 3-kinase/Akt pathways cooperatively, but in a manner independent of each other, to directly potentiate synovium overgrowth and joint destruction in RA. In addition to inflammatory cytokines, Ang-1/TIE-2 signaling appears to be an independent factor that contributes to the destruction of the rheumatoid joint.

A topological analysis of the experimental electron density in racemic ethylenebis(1-indenyl)zirconium dichloride, C20H16Cl2Zr, measured at 100 (1) K, has been performed. The atomic charges calculated by the numerical integration of the electron density over the zero-flux atomic basins demonstrate the charge transfer of 2.25 e from the Zr atom to the two indenyl ligands (0.19 e to each) and two Cl atoms (0.93 e to each). All the atomic interactions were quantitatively characterized in terms of the electron density and the electronic energy-density features at the bond critical points. The Zr-C2 bond paths significantly curved towards the C1-C2 bond were found; no other bond paths connecting the Zr atom and indenyl ligand were located. At the same time, the pi-electrons of the C1-C2 bond are significantly involved in the metal-ligand interaction. The electron density features indicate that the indenyl coordination can be approximately described as eta1 with slippage towards eta2. The ;ligand-opposed' charge concentrations around the Zr atom were revealed using the Laplacian of the electron density and the one-particle potential; they were linked to the orbital representations. Bonds in the indenyl ligand were characterized using the Cioslowski-Mixon bond-order indices calculated directly from the experimental electron density.

Peroxisomal enzymes are responsible for several primary metabolism pathways, including beta-oxidation and lipid biosynthesis. PEX1 and PEX6 are hexameric AAA-type ATPases and both are necessary for the import of more than 50 peroxisomal resident proteins from the cytosol into peroxisomes. In this study, PEX1 N-terminal domain crystals have been prepared. The crystals belong to space group P3(1) or P3(2), with unit-cell parameters a = b = 63.5 A, c = 33.5 A, and contain one protein molecule per crystallographic asymmetric unit. An intensity data set was collected to a resolution of 2.05 A.

Objective: To investigate the role of EDA-containing fibronectin (EDA+ FN), a splice variant of FN detectable in association with cellular transformation, in the adherence of synovial cells (SC) on rheumatoid cartilage surface., Methods: The number of SC adherent on cartilage slices or on culture plates containing either EDA+ FN or plasma FN (pFN) was enumerated under a phase-contrast microscope. The portion of the FN molecule responsible for adherence of SC onto EDA+ FN was investigated by inhibition studies using antibodies or peptide fragments., Results: SC adhered more strongly on the surfaces containing EDA+ FN than on those containing pFN (P < 0.01). When monoclonal antibodies against the EDA or the carboxyl-terminal heparin-binding (Hep2) domains were used, adhesion of SC onto EDA+ FN was reduced to a level comparable with that onto pFN. FN fragments containing Hep2 or heparan sulfate inhibited the adhesion of SC onto EDA+ FN. Treatment of SC with heparitinase, but not heparinase, reduced the adhesion of SC onto EDA+ FN., Conclusion: EDA+ FN enhances adherence of SC on the matrix via the Hep2 region of EDA+ FN.

Objective: To identify the cells that synthesize EDA-containing fibronectin (FN) and examine the role of EDA+FN in the pathogenesis of rheumatoid joint lesions., Methods: Localization of EDA+FN and c-Fos protein in rheumatoid joints was studied immunohistochemically by utilizing antibodies for EDA+FN and c-Fos. Expression of EDA+FN was studied by immunoelectron microscopy and in situ hybridization. The amount of EDA+FN was measured by enzyme-linked immunosorbent assay., Results: EDA+FN was specifically localized in the synovial lining layer of synovium with active rheumatoid arthritis (RA) (n = 17), but not in that with osteoarthritis (n = 4) or with inactive fibrous RA (n = 2). EDA+FN messenger RNA was localized in the synovial lining layer. EDA+FN was immunoelectron microscopically localized in the synovial lining fibroblast-like (type B) cells. EDA+FN was also detected at the cartilage-pannus junction and on the surface of RA cartilage. Double staining showed that EDA+FN colocalized with c-Fos protein in the rheumatoid synovial lining layer. Quantification of EDA+FN showed that it was highly concentrated in rheumatoid synovial fluids., Conclusion: EDA+FN is synthesized by the synovial lining fibroblast-like (type B) cells in situ in rheumatoid synovium, and appears to be expressed in association with activated or transformed states of synovium.

The early phase of cartilage destruction by active cellular pannus in rheumatoid joints was observed under light and electron microscopy. In the early phase of pannus formation, cartilage was covered by several layers of fibroblast-like cells. This was also the case at the advancing edge of the pannus. Invasion of the cartilage by macrophage-like cells has been observed to start beneath this layer. Observations under electron microscope demonstrated that the main cells participating in the cartilage destruction at the cartilage-pannus junction were either fibroblast-like or macrophage-like cells, and suggested the possibility that these two types of cells were derived from synovial type A and type B cells. Morphologic observations also suggested a possibility of transformation of the fibroblast-like cell into the macrophage-like cell at the cartilage-pannus junction.

The presence of fibronectin on the surface of articular cartilage in rheumatoid arthritis (RA) was investigated. Cartilage samples were stained by the immunoperoxidase method using anti-human fibronectin antibody, and observed under light and electron microscopy. Fibronectin was present on the articular surface in 7 of 8 RA patients. The degree of staining varied greatly among the patients. Five of 8 patients were positive for fibronectin in 50% or more of the cartilage areas studied. In total, fibronectin was observed in RA. Fibronectin was not observed in cartilage samples of osteoarthritic joints or joints which were not diseased but had undergone trauma. Ultrastructurally, it was observed to be associated with collagen fibrils and amorphous substance in the matrix. The fibronectin-negative surface of the rheumatoid cartilage was usually thick ultrastructurally, compared with the fibronectin-positive surface, and the staining for fibronectin roughly correlated with decreased proteoglycans on the surface. The presence of fibronectin in the matrix appeared to be revealed by partial degradation of proteoglycans with proteolytic enzymes in the synovial fluid, as well as by the deposition of fibronectin onto the surface of rheumatoid cartilage. Fibronectin on the articular surface may play an important role in promoting pannus extension onto the articular surface in RA.

The pathogenesis of periarticular osteopenia in rheumatoid arthritis (RA) was investigated by histomorphometry on juxtaarticular bone removed during joint surgery. Twenty areas from 12 RA patients were compared with 14 areas from 6 osteoarthritis (OA) patients. There was no difference between the 2 groups in the percent of total bone volume. However, increased bone formation was suggested by an increase in the percent of active osteoid surface in RA compared with that in OA. Bone resorption was also increased in RA, as evidenced by increases versus OA in percent total resorptive surface, percent active resorptive surface, and number of osteoclasts. These results demonstrate increased turnover of bone in RA, especially in the resorptive phase of the periarticular trabecular bone. It is proposed that soluble factor(s) synthesized in the contiguous rheumatoid synovium may be transferred to the periarticular bone space, stimulating osteoclasts to resorb bone.