Evidence for the dysregulated expression of TWIST1, TGFβ1 and SMAD3 in differentiating osteoblasts from primary hip osteoarthritis patients

Kumarasinghe, D.D.; Sullivan, Thomas; Kuliwaba, J.S.; Fazzalari, Nicola L.; Atkins, Gerald J.

doi:10.1016/j.joca.2012.07.005

Cited by 31 publications

(30 citation statements)

References 44 publications

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“…Radial growth of the femoral head would also require endochondral ossification to occur at the tidemark, and bone modelling to occur at the cement line. Combined with previous studies showing that OA joints have an increased trabecular and subchondral thickness, and higher volume of the femoral head 37,38 , supports the theory that OA is a disease characterized not only by decay, but also by growth 39,40 .…”

Section: Discussionsupporting

confidence: 76%

Subchondral bone turnover, but not bone volume, is increased in early stage osteoarthritic lesions in the human hip joint

Klose-Jensen

Hartlev

Boel

et al. 2015

Osteoarthritis and Cartilage

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In human end-stage hip OA, BV and bone turnover correlate with the degree of local cartilage degeneration. Subarticular bone sclerosis was only present in regions corresponding to end-stage OA. However, in regions with only none to mild cartilage degeneration the underlying bone had significantly higher turnover in OA patients compared to the control group, suggesting that high bone turnover may contribute to the early pathogenesis of OA.

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Section: Discussionsupporting

confidence: 76%

Subchondral bone turnover, but not bone volume, is increased in early stage osteoarthritic lesions in the human hip joint

Klose-Jensen

Hartlev

Boel

et al. 2015

Osteoarthritis and Cartilage

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“…However, this study did not differentiate between the gene profiles in osteoblastic and other bone cells. Further studies of OA-derived osteoblasts have shown increased expression of dickkopf-related protein 2 (DKK2), which was attributed to the autocrine effect of transforming growth factor (TGF)-β 107. This was speculated to be a component of the dysregulated osteoblast function in vivo 108.…”

Section: The Role Of Subchondral Bone Turnover and Structure In 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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“…Several transcription factors involved in the regulation of the osteogenic lineage have been found dysregulated in osteoarthritis. In fact, by using primary osteoblast cultures from bone samples of osteoarthritis patients, dysregulated expression of TWIST1, TGFβ1, and SMAD3 mRNA has been observed (Kumarasinghe, Sullivan, Kuliwaba, Fazzalari, & Atkins, ).…”

Section: Introductionmentioning

confidence: 99%

Osteoblast role in osteoarthritis pathogenesis

Maruotti

Corrado

Cantatore

2017

Journal Cellular Physiology

116

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Even if osteoarthritis pathogenesis is still poorly understood, numerous evidences suggest that osteoblasts dysregulation plays a key role in osteoarthritis pathogenesis. An abnormal expression of OPG and RANKL has been described in osteoarthritis osteoblasts, which is responsible for abnormal bone remodeling and decreased mineralization. Alterations in genes expression are involved in dysregulation of osteoblast function, bone remodeling, and mineralization, leading to osteoarthritis development. Moreover, osteoblasts produce numerous transcription factors, growth factors, and other proteic molecules which are involved in osteoarthritis pathogenesis.

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Evidence for the dysregulated expression of TWIST1, TGFβ1 and SMAD3 in differentiating osteoblasts from primary hip osteoarthritis patients

Cited by 31 publications

References 44 publications

Subchondral bone turnover, but not bone volume, is increased in early stage osteoarthritic lesions in the human hip joint

Subchondral bone turnover, but not bone volume, is increased in early stage osteoarthritic lesions in the human hip joint

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

Osteoblast role in osteoarthritis pathogenesis

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