Identical subchondral bone microarchitecture pattern with increased bone resorption in rheumatoid arthritis as compared to osteoarthritis

Li, G.; Ma, Yuanfang; Cheng, Tak Sum; Landao-Bassonga, Euphemie; Qin, An; Pavlos, Nathan J.; Zheng, Qiujian; Zheng, Minghao

doi:10.1016/j.joca.2014.08.015

Cited by 26 publications

(25 citation statements)

References 50 publications

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“…This phenotype was consistent with data reported by a recent study, which identified a more sclerotic phenotype in the trabecular bone surrounding the subchondral bone edema/lesion compared to the trabecular bone distant to the edema/lesion in femoral heads from patients with RA. (46) The sclerotic phenotype in RA-affected subchondral bone may involve the in situ osteoblastic commitment of those MSCs/osteoprogenitors aggregating in the bone marrow as the disease progresses.…”

Section: Discussionmentioning

confidence: 99%

Aberrant Activation of TGF-β in Subchondral Bone at the Onset of Rheumatoid Arthritis Joint Destruction

Xu¹,

Zheng²,

Bian³

et al. 2015

Journal of Bone and Mineral Research

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Rheumatoid arthritis (RA) is an autoimmune disease that often leads to joint destruction. A myriad of drugs targeting the immune abnormalities and downstream inflammatory cascades have been developed, but the joint destruction is not effectively halted. Here we report that aberrant activation of TGF-β in the subchondral bone marrow by immune response increases osteoprogenitors and uncoupled bone resorption and formation in RA mouse/rat models. Importantly, either systemic or local blockade of TGF-β activity in the subchondral bone attenuated articular cartilage degeneration in RA. Moreover, conditional deletion of TGF-β receptor II (Tgfbr2) in nestin-positive cells also effectively halted progression of RA joint destruction. Our data demonstrate that aberrant activation of TGF-β in the subchondral bone is involved at the onset of RA joint cartilage degeneration. Thus, modulation of subchondral bone TGF-β activity could be a potential therapy for RA joint destruction.

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Section: Discussionmentioning

confidence: 99%

Aberrant Activation of TGF-β in Subchondral Bone at the Onset of Rheumatoid Arthritis Joint Destruction

Xu¹,

Zheng²,

Bian³

et al. 2015

Journal of Bone and Mineral Research

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“…All specimens comprised the subchondral trabecular bone (STB) and deeper trabecular bone (DTB). STB is defined as the most superficial 5 mm of the trabecular cylinder immediately under cartilage and subchondral cortical bone [22][23][24], while DTB is defined as the deepest 5 mm of the cylindrical specimen. Specimens were fixed in 4% paraformaldehyde in PBS for 5 days and stored in 70% ethanol.…”

Section: Specimen Preparationmentioning

confidence: 99%

Influence of age and gender on microarchitecture and bone remodeling in subchondral bone of the osteoarthritic femoral head

Zheng

Landao-Bassonga

et al. 2015

Bone

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“…This meta‐analysis points to the existence of a robust cross‐talk between subchondral bone and articular cartilage underlying joint diseases . Shared features in patients with rheumatoid arthritis and osteoarthritis include not only subchondral bone resorption but also microarchitecture and periarticular bone remodeling, including the subchondral bone …”

Section: Cross‐talk Between Articular Cartilage and Subchondral Bone mentioning

confidence: 89%

“…In these conditions, and unlike what occurs physiologically, one sees not a single electrical pulse (spike), but rather a series of pulses. Consequently, the threshold of neuronal activation is lowered and the neuron now becomes receptive to stimuli not normally painful (allodynia), an indication of peripheral sensitization …”

Section: Articular Mast Cellsmentioning

confidence: 99%

“…5 Shared features in patients with rheumatoid arthritis and osteoarthritis include not only subchondral bone resorption but also microarchitecture and periarticular bone remodeling, including the subchondral bone. 7 Cytokines and trophic factors released during elevated subchondral bone turnover interact with articular cartilage to create a positive feedback loop between the bone healing process and cartilage damage. On the other hand, chondrocytes, in response to stimuli such as inappropriate loads or the presence of subchondral bone catabolic factors, undergo a change in phenotype and begin producing cytokines and chemokines, which act in a paracrine fashion to initiate a vicious cycle leading to degradation of the cartilage itself.…”

Section: Cross-talk Between Articular Cartilage and Subchondral Bone mentioning

confidence: 99%

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Degenerative Joint Diseases and Neuroinflammation

Fusco¹,

Skaper

Coaccioli

et al. 2017

Pain Practice

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Rheumatic and joint diseases, as exemplified by osteoarthritis and rheumatoid arthritis, are among the most widespread painful and disabling pathologies across the globe. Given the continuing rise in life expectancy, their prevalence is destined to grow. Osteoarthritis, a degenerative joint disease, is, in particular, on its way to becoming the fourth leading cause of disability worldwide by 2020, with the rising incidence of obesity in addition to age being important factors. It is estimated that 25% of osteoarthritic individuals are unable to perform daily activities. Accompanying osteoarthritis is rheumatoid arthritis, which is a chronic systemic disease that often causes pain and deformity. At least 50% of those affected are unable to remain gainfully employed within 10 years of disease onset. A growing body of evidence now points to inflammation, locally and more systemically, as a promoter of damage to joints and bones, as well as joint-related functional deficits. The pathogenesis underlying joint diseases remains unclear; however, it is currently believed that cross-talk between cartilage and subchondral bone-and loss of balance between these two structures in joint diseases-is a critical element. This view is amplified by the presence of mast cells, whose dysregulation is associated with alterations of junction structures (cartilage, bone, synovia, matrix, nerve endings, and blood vessels). In addition, persistent activation of mast cells facilitates the development of spinal neuroinflammation mediated through their interaction with microglia. Unfortunately, current treatment strategies for rheumatic and articular disease are symptomatic and do little to limit disease progression. Research now should be directed at therapeutic modalities that target osteoarticular structural elements and thereby delaying disease progression and joint replacement.

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Identical subchondral bone microarchitecture pattern with increased bone resorption in rheumatoid arthritis as compared to osteoarthritis

Abstract: Apart from higher bone resorption in the general subchondral bone of RA samples, the peri-articular bone exhibited similar microarchitectural and bone remodeling characteristics in RA and OA.

Cited by 26 publications

References 50 publications

Aberrant Activation of TGF-β in Subchondral Bone at the Onset of Rheumatoid Arthritis Joint Destruction

Aberrant Activation of TGF-β in Subchondral Bone at the Onset of Rheumatoid Arthritis Joint Destruction

Influence of age and gender on microarchitecture and bone remodeling in subchondral bone of the osteoarthritic femoral head

Degenerative Joint Diseases and Neuroinflammation

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