Bone density and local growth factors in generalized osteoarthritis

Dequeker, Jan; Mokassa, Luc; Aerssens, Jeroen; Boonen, Steven

doi:10.1002/(sici)1097-0029(19970515)37:4<358::aid-jemt10>3.0.co;2-l

Cited by 71 publications

(53 citation statements)

References 77 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Quantitative CT documented increased subchondral sclerosis in Brtl mice. The contribution of more sclerotic subchondral bone to progressive cartilage damage after the onset of OA is uncertain (10,(41)(42)(43). Previous studies have shown that dense stiff bone can also alter joint biomechanics and increase the force exerted on cartilage (43), thereby fostering OA.…”

Section: Discussionmentioning

confidence: 99%

“…These results suggest that the relationship of subchondral bone and cartilage in OA is complex, with poorly mineralized weak bone initiating cartilage degeneration, whereas subsequent subchondral bone remodeling leads to increased bone density that may perpetuate the process. This latter response may explain the high incidence of OA in metabolic bone diseases such as acromegaly, osteopetrosis, and Paget's disease (43,44).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

A type I collagen defect leads to rapidly progressive osteoarthritis in a mouse model

Blair-Levy

Watts

Fiorientino

et al. 2008

Arthritis & Rheumatism

View full text Add to dashboard Cite

Objective. This study was undertaken to test the hypothesis that abnormalities of the subchondral bone can result in osteoarthritis (OA).Methods. We used a knockin model of human osteogenesis imperfecta, the Brittle IV (Brtl) mouse, in which defective type I collagen is expressed in bone. OA in individual mice was documented by micro-magnetic resonance imaging (micro-MRI) and micro-computed tomography (micro-CT). Alterations in the knee joints were confirmed by histopathologic and immunohistochemical analysis. In addition, atomic force microscopy (AFM) was used to assess the ultrastructure of the articular cartilage and subchondral bone matrix.Results. Brtl mice had decreased integrity of bone but initially normal articular cartilage. However, by the second month of life, Brtl mice developed alterations of the cartilage that were characteristic of OA, as documented by micro-CT, micro-MRI, and histologic evaluation. In addition, chondrocyte loss and breakdown of the collagen matrix in the residual cartilage were demonstrated using AFM.Conclusion. The Brtl mouse model demonstrates that progressive destruction of articular cartilage characteristic of OA may be secondary to altered architecture of the underlying subchondral bone.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

A type I collagen defect leads to rapidly progressive osteoarthritis in a mouse model

Blair-Levy

Watts

Fiorientino

et al. 2008

Arthritis & Rheumatism

View full text Add to dashboard Cite

show abstract

“…Diminished subchondral sclerosis might indicate a decreased stiffness of the subchondral bone. The improved capacity to absorb stress during joint loading reduces impact on the articular cartilage (12,29). On the other hand, cartilage repair protects subchondral bone from overload and thereby diminishes subchondral sclerosis (12,29).…”

Section: Discussionmentioning

confidence: 99%

Clinical benefit of joint distraction in the treatment of severe osteoarthritis of the ankle: Proof of concept in an open prospective study and in a randomized controlled study

Marijnissen¹,

Roermund²,

Melkebeek³

et al. 2002

Arthritis & Rheumatism

136

125

View full text Add to dashboard Cite

Objective. Osteoarthritis (OA) is a degenerative, disabling joint disease that affects >10% of the adult population. No effective disease-modifying treatment is available. In the present study, we used joint distraction, a relatively new treatment in which mechanical contact between the articular surfaces is avoided while intraarticular intermittent fluid pressure is maintained, to treat patients with severe OA of the ankle.Methods. Patients with severe ankle OA (n ‫؍‬ 57) who were being considered for joint fusion (arthrodesis) were treated with joint distraction in an open prospective study. In addition, a randomized trial was performed in 17 patients to determine whether joint distraction had a better outcome than debridement. A standardized evaluation protocol (physical examination, assessment of pain, mobility, and functional ability) was used, and changes in radiographic joint space width and subchondral sclerosis were measured. Thirtyeight patients in the open study have been followed up for >1 year, with up to 5 years of followup in 7 of them (mean ؎ SD followup 2.8 ؎ 0.3 years). Patients in the randomized study have been followed up for 1 year.Results. Significant clinical benefit was found in three-fourths of the 57 patients in the open prospective study. Most interestingly, the improvement increased over time. Radiographic evaluation showed increased joint space width and decreased subchondral sclerosis. Moreover, joint distraction showed significantly better results than debridement.Conclusion. The clinical benefit of joint distraction in the treatment of severe OA is proof of the concept. Although the followup remains relatively short and effects over time remain unpredictable, our study creates possibilities for the treatment of severe OA in general. Considering the high prevalence of OA and the lack of a cure for it, joint distraction as a treatment of severe OA may have great medical, social, and economic impact.

show abstract

“…A pathological feature of OA is irregular hypercalcification of the 'tidemark,' a calcified layer of cartilage matrix located at the junction of articular cartilage and subarticular bone. [69][70][71] During OA development, the tidemark and subchondral bone thicken, hypercalcify, and present an irregular surface to the overlying articular cartilage, resulting in abnormal transmission of mechanical stress, thus contributing to articular cartilage degeneration. 72 Ali and Griffiths 8 showed that the articular cartilage of the knees and hips in OA patients, contains more extracellular 50-250 nm-diameter MVs than normal, especially in the deep cartilage near the tidemark (Table 2).…”

Section: Cancersmentioning

confidence: 99%

Role of extracellular membrane vesicles in the pathogenesis of various diseases, including cancer, renal diseases, atherosclerosis, and arthritis

Anderson

Mulhall

Garimella

2010

Laboratory Investigation

156

143

View full text Add to dashboard Cite

Bone density and local growth factors in generalized osteoarthritis

Cited by 71 publications

References 77 publications

A type I collagen defect leads to rapidly progressive osteoarthritis in a mouse model

A type I collagen defect leads to rapidly progressive osteoarthritis in a mouse model

Clinical benefit of joint distraction in the treatment of severe osteoarthritis of the ankle: Proof of concept in an open prospective study and in a randomized controlled study

Role of extracellular membrane vesicles in the pathogenesis of various diseases, including cancer, renal diseases, atherosclerosis, and arthritis

Contact Info

Product

Resources

About