Relationship between bone mineral density and urine level of NTx in rheumatoid arthritis.

We analyzed the relationship between the level of type-I collagen N-telopeptide (NTx) in urine (U-NTx) and bone mineral density (BMD) in patients with rheumatoid arthritis (RA). The subjects were 62 female patients with RA who had experienced the menopause 5 years or more before the study commenced, and who had not been treated for osteoporosis. The mean age of the subjects was 61.

[Periarticular and generalized osteoporosis in rheumatoid arthritis].

Patients with rheumatoid arthritis (RA) develop both periarticular and generalized osteoporosis. Periarticular osteopenia in appendicular bones occurs early in the course of RA and is one of the earliest radiological signs of RA. Periarticular osteoporosis might be mediated through an increased productions of inflammatory cytokines and prostaglandins by synovium and bone marrow.

[Inflammatory cytokines and bone diseases].

The abnomalities in cytokines may be an pathogenetic factor in human diseases as diverse as rheumatoid arthritis (RA), some bone diseases, multiple myeloma, metastatic bone tumors. A cytokine imbalance in favour of pro-inflammatory mediators may be a central pathogenic mechanism in RA. Pro-inflammatory mediators include the cytokines TNF-alpha and IL-1, which activate osteoclasts to resorb subchondral bone.

[Mechanisms of joint destruction in rheumatoid arthritis].

A variety of destructive enzymes are secreted by pannnus. Prominent among these are the various matrix metalloproteinases (MMPs) and cathepsins. These enzymes act upon collagen and the proteoglycan matrix, thereby destroying the central structure of articular cartilage.

[SERM and quality of bone].

Now, we can prevent osteoporotic fractures by improvement of bone strength. It became clear that not only the increase of bone mineral density but also the improvement of bone quality are important factors for the mechanisms of preventing fractures. Measuring bone metabolism markers is contributing to evaluate bone quality.

[Bone quality in glucocorticoid induced osteoporosis].

The administration of oral glucocorticoids is associated with a significant decrease in bone formation (low turnover) and with generalized thinning of bone trabecula. These condition will be worse of bone quality and bone strength than high turnover state that indicate partial breakage of bone trabecula. Because the cut-off value of bone mineral density induced fracture is higher in glucocorticoid-induced osteoporosis than in postmenopausal osteoporosis.

Sjögren's syndrome with bilateral spontaneous fracture of the femoral neck following aseptic necrosis of the femoral head.

Abstract A woman with Sjögren's syndrome concurrently suffered bilateral fractures of the femoral neck without any proximate cause, while she had aseptic necrosis of the femoral head resulting from the treatment for Sjögren's syndrome. According to previous reports, fractures of the femoral neck following aseptic necrosis of the femoral head are attributed to primary diseases such as systemic lupus erythematosus (SLE) or idiopathic thrombocytopenic purpura (ITP), and steroids are administered in most cases. Heterogeneous bone regeneration after necrosis causes irregularity in its mechanical strength depending on which regions of frailty are generated.

[Treatment of osteoporosis provided from the orthopaedic surgeon's standpoint].

Osteoporosis is associated with increased risk of fractures at most skeletal sites. Hip fractures have much greater prognostic significance in terms of health than any other single type of fracture. However, symptomatic vertebral fractures and other non-hip fractures also represent enormous morbidity and economic burdens, and signal increased risk of future fractures of all types, including the hip.

Comparison of the inhibitory effects of two types (90 kDa and 190 kDa) of hyaluronic acid on the expression of fibrinolytic factors in human synovial fibroblasts.

Abstract  Hyaluronic acid (HA) has been shown to be clinically effective, and is currently used for the treatment of arthropathy. We previously reported that HA of molecular weight 90 kDa (90-HA) inhibits the fibrinolytic factors in human synovial fibroblasts. In the present study, we investigated the effect of high molecular weight (190 kDa) HA (190-HA) compared with 90-HA on the pericellular fibrinolytic system of human synovial fibroblasts in osteoarthritis (OA) and rheumatoid arthritis (RA).

Activation of histamine H1 receptor results in enhanced proteoglycan synthesis by human articular chondrocyte: involvement of protein kinase C and intracellular Ca(2+).

In earlier work, we obtained evidence for the presence of histamine H1 and H2 receptors on chondrocytes. Activation of the H1 receptor enhanced keratan sulfate synthesis, and protein kinase C (PKC) inhibitors antagonized histamine-stimulated keratan sulfate (KS) synthesis. These data do indicate the involvement of PKC in activation of H1 receptor, but precise mechanisms remained to be clarified.

Interleukin-4 reversed the Interleukin-1-inhibited proteoglycan synthesis through the inhibition of NO release: a possible involvement of intracellular calcium ion.

Interleukin-1 (IL-1) causes cartilage degradation through nitric oxide (NO) synthesis. Although Interleukin-4 (IL-4) antagonizes the IL-1-mediated cartilage degradation, the precise mechanisms are not clear. We examined the effect of IL-4 on NO synthesis in parallel with intracellular Ca levels ([Ca(2+)]i) and proteoglycan (PG) synthesis.

A role for histamine receptors in rheumatoid arthritis.

Although neurotransmitters and various chemical mediators play an important role in the pathogenesis of rheumatoid arthritis (RA), precise underlying mechanisms have yet to be determined. Histamine is a classical mediator of inflammation and three types of receptors are known. We investigated the presence and functions of histamine receptors of lymphocytes, bone marrow cells, synovial fibroblasts, and chondrocytes in experimentally-induced arthritis and human RA.

Acrodysostosis associated with spinal canal stenosis.

An adult case of acrodysostosis with striking lumbar spinal canal stenosis is reported. She complained of numbness on the right arm, intermittent claudication with numbness on both legs and pain and weakness on the left leg. Although the reduced lumbar interpedicular distance has been reported, no adult case with neurologic symptoms has been reported.

Effective treatment of mice with type II collagen induced arthritis with lethal irradiation and bone marrow transplantation.

We examined the effects of irradiation followed by bone marrow transplantation (BMT) on type II collagen induced arthritis (CIA) in mice. Either before or after the onset of arthritis, the mice were irradiated at levels lethal to cells, then given bone marrow cells from normal syngeneic or allogeneic mice. The BMT, especially allogeneic BMT, blocked the induction of CIA when administered before the onset of arthritis.

Abnormalities in bone marrow mononuclear cells in patients with rheumatoid arthritis.

We analyzed the cell surface phenotype and the function of mononuclear cells in peripheral blood and in bone marrow of patients with rheumatoid arthritis (RA). The monoclonal antibodies anti-CD45RA, anti-CD29 and anti-S6F1 identify the suppressor-inducer (CD4+CD45RA+), helper-inducer (CD4+CD29+) and killer-effector (CD8+S6F1+) subpopulations of lymphocytes, respectively. In patients with RA, peripheral blood samples showed the same percentage of CD4+CD45RA+, CD4+CD29+ and CD8+S6F1+ cells as seen in control subjects.

[Histamine receptors in arthritis].

Histamine H1 and H2 receptors in lymphocytes, bone marrow mononuclear cells, synovial fibroblasts and chondrocytes were measured by binding assay and pharmacological study. Histamine suppressed IgG production through H1 and H2 receptors and cytotoxic activity through H2 receptor in lymphocyte. Histamine increased the production of hyaluronic acid in synovial fibroblast through H1 and H2 receptors.

Phenotypic abnormalities in CD8+ T lymphocyte subsets in patients with rheumatoid arthritis.

We analyzed the cell surface phenotype of CD8+ cells in both peripheral blood and synovial fluid (SF) of patients with rheumatoid arthritis (RA) and osteoarthritis (OA). Utilizing the monoclonal antibodies anti-CD45RA, anti-CD29 and anti-S6F1-, one can define both suppressor effector (CD45RA+CD29-S6F1-) and killer effector (CD45RA-CD29+S6F1+) cells within the CD8 population. In patients with OA, normal proportions of CD8+CD45RA+, CD8+CD29+ and CD8+S6F1+ cells were found in both peripheral blood and SF.

CD4+CD45RA+ and CD4+CD45RA- T cell subsets in man maintain distinct function and CD45RA expression persists on a subpopulation of CD45RA+ cells after activation with Con A.

We have previously shown that Con A-induced suppressor T cells belong to the CD45RA+ subset. After unseparated T cells are activated with Con A, CD45RA expression increases to a maximum (Day 2), and then decreases significantly, but does not disappear entirely (Day 9), while CD29 expression increases steadily. In the present study, we examined the fate of these cell surface molecules on isolated CD4+CD45RA+ and CD4+CD45RA- cells following activation with Con A, and their relationship to the regulatory functions of these subsets.

The functional heterogeneity of CD8+ cells defined by anti-CD45RA (2H4) and anti-CD29 (4B4) antibodies.

The monoclonal antibodies, anti-2H4(CD45RA), and anti-4B4(CD29), along with UCHL1-(CD45RO), identify reciprocal populations of CD4 cells with distinct suppressor inducer (CD45RA+CD29-CD45RO-) and helper inducer (CD45RA-CD29+CD45RO+) functions. Although the CD8+ population is known to contain precytotoxic, cytotoxic, suppressor, and some natural killer cells, the exact phenotypic identities of these functional CD8 subsets has not been established. In this study, we tried to determine whether these monoclonal antibodies could distinguish functionally distinct subsets of cells within the CD8+ population.