Osteoporosis in Rheumatoid Arthritis

Dequeker, Jan; Maenaut, K; Verwilghen, J; Westhovens, René

doi:10.1007/978-1-4471-3825-9_36

Cited by 21 publications

(3 citation statements)

References 75 publications

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“…Reduction in the bone mineral density (BMD) has been observed as well as qualitative features of osteopenia, seen in radiograms as shrinking of the cortical bone, lower Singh index, more distinct (due to thinning) trabeculae or -in contrast -lack of the trabecular structure in imaging. Similar reports have been published based on observations in patients treated with MTX for collagenoses [9][10][11][12][13][14][15][16][17]. Apart from clinical symptoms, there was also described in this group of patients inhibition of osteoblast activity [13], as well as a significant reduction in osteocalcin synthesis by osteoblasts [14] -seen in both of the above studies after a weekly administration of MTX at low doses.…”

supporting

confidence: 79%

Bone tissue as the site of action of oncological drugs

Leśniewski-Kmak¹,

Radecka²,

Litwiniuk³

2011

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Anticancer therapy has multiple, sometimes life-threatening side effects, and their influence on bone is not seen as important. Data have been published confirming the existence of side effects chemotherapy has on bone, which affect patients' quality of life. They influence a bone tissue not only in a direct way, but also when suppressing the activity of gonads. We have no information on the impact of drugs on bone belonging to the "targeted therapies". There are, however, some attempts to create antibodies that target proteins involved in bone physiology. Relatively well known is the impact of anti-cancer hormone therapy on bone metabolism. Bone tissue is of special importance in the pathophysiology and the clinical course of neoplastic diseases. Metastases to bones do not pose a direct threat to the patient's life, yet they markedly lower the quality of life and may be associated with complications leading to severe disability and, in consequence, to shortening of the patient's life. In the clinical picture of certain neoplasms, such as multiple myeloma, prostate cancer, thyroid cancer or sometimes breast cancer, the dominating symptoms are those related to bone infiltration. On the other hand, there are also effects of the oncological treatment on the bone -both those concerning the physiological bone cycle (of increasing importance with the observed prolongation of patient life) and the interactions between the neoplastic cells and bone cells. Below, we present a literature review on this subject. The issue of steroid therapy's effects on bones is not addressed here as the multitude of usages of this drug class resulted in the subject being already extensively discussed in other publications. ChemotherapyAdverse effects of chemotherapy concerning bones may in a longer-term perspective lead to health complaints markedly lowering the quality of life, particularly in patients with good prognosis, even more so because this approach is often combined with different hormone and radiation therapies. As early as in 1965, a report was published presenting the results of a study on the effects of methotrexate (MTX) treatment on calcium metabolism, demonstrating elevated levels of this element in urine and stool, its lowered levels in blood serum, and indirectly its increased bone resorption [1]. The above data have been reflected in a clinical setting, in patients treated with MTX for acute myeloid leukaemia, where there have been observed pain and difficult uniting of fractures during the course of treatment and remission upon its completion [2][3][4][5][6][7][8]. Although the high doses of steroids have been of significance, the cytostatic agents have been deemed to play an important role here. Reduction in the bone mineral density (BMD) has been observed as well as qualitative features of osteopenia, seen in radiograms as shrinking of the cortical bone, lower Singh index, more distinct (due to thinning) trabeculae or -in contrast -lack of the trabecular structure in imaging. Similar reports have been published base...

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supporting

confidence: 79%

Bone tissue as the site of action of oncological drugs

Leśniewski-Kmak¹,

Radecka²,

Litwiniuk³

2011

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“…41 Apart from the muscular activity, reductions in total body potassium are also correlated with changes in BMD leading to disease severity with the production of TNF-α. 42 Apart from these processes, inflammatory cytokine prostaglandin E1 has also been identified as a potent stimulator of bone resorption. 43 It has been reported that an imbalance between the T regulatory cells and the T helper cells (TH-17) often leads to development of autoimmune disorders.…”

Section: Inflammatory Cellsmentioning

confidence: 99%

Molecular targets in arthritis and recent trends in nanotherapy

Roy¹,

Kanwar²,

Kanwar³

2015

IJN

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Due to its severity and increasing epidemiology, arthritis needs no description. There are various forms of arthritis most of which are disabling, very painful, and common. In spite of breakthroughs in the field of drug discovery, there is no cure for arthritis that can eliminate the disease permanently and ease the pain. The present review focuses on some of the most successful drugs in arthritis therapy and their side effects. Potential new targets in arthritis therapy such as interleukin-1β, interleukin-17A, tumor necrosis factor alpha, osteopontin, and several others have been discussed here, which can lead to refinement of current therapeutic modalities. Mechanisms for different forms of arthritis have been discussed along with the molecules that act as potential biomarkers for arthritis. Due to the difficulty in monitoring the disease progression to detect the advanced manifestations of the diseases, drug-induced cytotoxicity, and problems with drug delivery; nanoparticle therapy has gained the attention of the researchers. The unique properties of nanoparticles make them highly attractive for the design of novel therapeutics or diagnostic agents for arthritis. The review also focuses on the recent trends in nanoformulation development used for arthritis therapy. This review is, therefore, important because it describes the relevance and need for more arthritis research, it brings forth a critical discussion of successful drugs in arthritis and analyses the key molecular targets. The review also identifies several knowledge gaps in the published research so far along with the proposal of new ideas and future directions in arthritis therapy.

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“…RA is a disease characterized by a chronic proliferative and erosive synovitis that waxes and wanes over the lifetime of the affected individual, with a progressive course. The main characteristics of RA is the dense lymphoid infiltration into the synovial membrane associated with juxtaarticular bone loss occurring around inflamed joints and a generalized bone loss with reduced bone mass [reviewed in Gough et al, 1994;Dequeker et al, 1995;Deodhar and Woolf, 1996]. However, RA is also considered a systemic disease which includes serological and hematological signs of inflammation, subcutaneous rheumatoid nodules, high levels of circulating rheumatoid factor, vasculitis, and granulomatous and/or interstitial organ pathologies [Kinne et al, 1997].…”

mentioning

confidence: 99%

Inflammatory T cells rapidly induce differentiation of human bone marrow stromal cells into mature osteoblasts

Rifas

Arackal

Weitzmann

2003

J of Cellular Biochemistry

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Activated T cells secrete multiple osteoclastogenic cytokines which play a major role in the bone destruction associated with rheumatoid arthritis. While the role of T cells in osteoclastogenesis has received much attention recently, the effect of T cells on osteoblast formation and activity is poorly defined. In this study, we investigated the hypothesis that in chronic inflammation activated T cells contribute to enhanced bone turnover by promoting osteoblastic differentiation. We show that T cells produce soluble factors that induce alkaline phosphatase activity in bone marrow stromal cells and elevated expression of mRNA for Runx2 and osteocalcin. This data indicate that T cell derived factors have the capacity to stimulate the differentiation of bone marrow stromal cells into the osteoblast phenotype. RANKL mRNA was undetectable under any conditions in highly purified bone marrow stromal cells. In contrast, RANKL was constitutively expressed in primary osteoblasts and only moderately up-regulated by activated T cell conditioned medium. Interestingly, both bone marrow stromal cells and osteoblasts expressed mRNA for RANK, which was strongly up-regulated in both cell types by activated T cell conditioned medium. Although, mRNA for the RANKL decoy receptor, osteoprotegerin, was also up-regulated by activated T cell conditioned medium, it's inhibitory effects may be mitigated by a simultaneous rise in the osteoprotegerin competitor TNF-related apoptosis-inducing ligand. Based on our data we propose that during chronic inflammation, T cells regulate bone loss by a dual mechanism involving both direct stimulation of osteoclastogenesis, by production of osteoclastogenic cytokines, and indirectly by induction of osteoblast differentiation and up-regulation of bone turnover via coupling.

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Osteoporosis in Rheumatoid Arthritis

Cited by 21 publications

References 75 publications

Bone tissue as the site of action of oncological drugs

Bone tissue as the site of action of oncological drugs

Molecular targets in arthritis and recent trends in nanotherapy

Inflammatory T cells rapidly induce differentiation of human bone marrow stromal cells into mature osteoblasts

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Osteoporosis in Rheumatoid Arthritis

Cited by 21 publications

References 75 publications

Bone tissue as the site of action of oncological drugs

Bone tissue as the site of action of oncological drugs

Molecular targets in arthritis and recent trends in&nbsp;nanotherapy

Inflammatory T cells rapidly induce differentiation of human bone marrow stromal cells into mature osteoblasts

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Molecular targets in arthritis and recent trends in nanotherapy