Analysis of the kinetics of osteoclastogenesis in arthritic rats

Schett, Georg; Stolina, Marina; Bolon, Brad; Middleton, Scot; Adlam, Matt; Brown, Heather; Zhu, Li; Feige, Ulrich; Zack, Debra

doi:10.1002/art.21343

Cited by 57 publications

(46 citation statements)

References 31 publications

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“…It has been reported that osteoclast development is enhanced in CIA [44]. Our data demonstrate that GSPE suppresses osteoclastogenesis in vivo and in vitro.…”

Section: Discussionsupporting

confidence: 51%

Grape seed proanthocyanidin extract (GSPE) attenuates collagen-induced arthritis

et al. 2009

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“…It has been reported that osteoclast development is enhanced in CIA [44]. Our data demonstrate that GSPE suppresses osteoclastogenesis in vivo and in vitro.…”

Section: Discussionsupporting

confidence: 51%

Grape seed proanthocyanidin extract (GSPE) attenuates collagen-induced arthritis

et al. 2009

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“…Formation of osteoclasts and their precursor cells is thus rapid, early, and triggered by continuous cytokine production and cell influx. In accordance with this, kinetic analyses of osteoclast formation in animal models of arthritis have revealed that cells form only a few days after the onset of inflammation [29]. …”

Section: Rankl In Arthritismentioning

confidence: 75%

Erosive arthritis

Schett

2007

Arthritis Res Ther

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Inflammation and degradation of bone are two closely linked processes. Chronic inflammatory arthritis not only leads to inflammatory bone loss but it also involves local erosion of articular bone. This osteo-destructive feature of chronic inflammatory arthritis is a major cause of disability in patients with rheumatoid arthritis. Osteoclasts are essential for the resorption of mineralized cartilage and subchondral bone in chronic arthritis. The observed upregulation of osteoclast differentiation factors (receptor activator of nuclear factor-κB ligand [RANKL]) in the synovial membrane of chronically inflamed joints indicates that osteoclasts are abundant in this setting, leading to rapid degradation of mineralized tissue. Blockade of osteoclast formation is thus a key strategy in preventing structural damage in arthritis. Denosumab, a humanized antibody that neutralizes RANKL, is an attractive candidate agent to inhibit inflammatory bone loss. IntroductionPathologic changes in bone mass and bone quality can be the manifestation of an intrinsic, often genetically based dysfunction of the skeletal system, which can lead to fragile or otherwise altered bone. Osteogenesis imperfecta or Paget's disease are among the best known examples of primary genetically based bone disease; the former leads to fragile bone and the latter to increased bone mass. More frequently, however, bone becomes the target of extraskeletal processes, and changes in the exogenous or endogenous environment can affect skeletal tissue, accelerate bone loss, and decrease bone quality. Lack of mobility, smoking, and drug therapy are well established exogenous environmental factors that affect bone quality. Endogenous factors include age-induced loss of muscular strength and endocrine changes, such as reduction in sex hormones during the menopause or dysfunction of the thyroid or adrenal hormone axis.Systemic inflammation is a key example of a condition that profoundly affects the skeleton but is not a primary disorder of bone itself. Recent data suggest that even a minor and subclinical increase in systemic inflammation precipitates bone disease and increases fracture risk [1]. This tight interaction between inflammation and bone is highlighted by the observation that virtually all chronic inflammatory diseases, particularly rheumatic disease and chronic inflammatory bowel disease, are associated with a high prevalence of osteoporosis and increased fracture risk [2][3][4][5][6]. In the case of a more localized inflammatory process, these systemic effects on bone are accompanied by local bone damage at the skeletal sites closest to the inflammatory focus. Similar to destruction mediated by an earthquake, bone damage is most common and most severe in the vicinity of the (inflammatory) epicenter, whereas the effects are less severe at sites distant from the epicenter, although they can still be detected (for instance, bone density measurements in the case of bone loss). Local resorption of alveolar bone in periodontal disease is a good example ...

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“…The presence and activation of osteoclasts seem to be involved in the pathogenesis of OA and other cartilage-destructive diseases, such as RA, psoriasis arthritis149 and spondyloarthropathies 120 121 150. Does this suggest that interventions that reduce bone turnover may have secondary positive effects on the progression of OA?…”

Section: Targeting Bone and Cartilage In The Treatment Of Oamentioning

confidence: 99%

The coupling of bone and cartilage turnover in osteoarthritis: opportunities for bone antiresorptives and anabolics as potential treatments?

et al. 2013

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Osteoarthritis (OA) is the most common form of arthritic disease, and a major cause of disability and impaired quality of life in the elderly. OA is a complex disease of the entire joint, affecting bone, cartilage and synovium that thereby presents multiple targets for treatment. This manuscript will summarise emerging observations from cell biology, preclinical and preliminary clinical trials that elucidate interactions between the bone and cartilage components in particular. Bone and cartilage health are tightly associated. Ample evidence has been found for bone changes during progression of OA including, but not limited to, increased turnover in the subchondral bone, undermineralisation of the trabecular structure, osteophyte formation, bone marrow lesions and sclerosis of the subchondral plate. Meanwhile, a range of investigations has shown positive effects on cartilage health when bone resorption is suppressed, or deterioration of the cartilage when resorption is increased. Known bone therapies, namely oestrogens, selective oestrogen receptor modifiers (SERMs), bisphosphonates, strontium ranelate, calcitonin and parathyroid hormone, might prove useful for treating two critical tissue components of the OA joint, the bone and the cartilage. An optimal treatment for OA likely targets at least these two tissue components. The patient subgroups for whom these therapies are most appropriate have yet to be fully defined but would likely include, at a minimum, those with high bone turnover.

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Analysis of the kinetics of osteoclastogenesis in arthritic rats

Cited by 57 publications

References 31 publications

Grape seed proanthocyanidin extract (GSPE) attenuates collagen-induced arthritis

Grape seed proanthocyanidin extract (GSPE) attenuates collagen-induced arthritis

Erosive arthritis

The coupling of bone and cartilage turnover in osteoarthritis: opportunities for bone antiresorptives and anabolics as potential treatments?

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