Macrophage-osteoclast differentiation and bone resorption in osteoarthrotic subchondral acetabular cysts

Sabokbar, A; Crawford, Ross; Murray, David; Athanasou, Nicholas A.

doi:10.1080/000164700317411843

Cited by 40 publications

(22 citation statements)

References 19 publications

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“…Secondary effects, such as osteoclast resorption, then induce the cystic lesion itself (Sabokbar et al 2000). The fibrous tissue often seen in these lesions shows an upregulation of cytokines such as prostaglandin E2, which may then enhance further expansion of the cyst (von Rechenberg et al 2001).…”

Section: Discussionmentioning

confidence: 99%

The cause of subchondral bone cysts in osteoarthrosisA finite element analysis

Dürr¹,

Martin²,

Pellengahr³

et al. 2004

Acta Orthopaedica Scandinavica

108

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Background The etiology of subchondral bone cysts in arthrotic joints is unclear.Materials and methods We used two-dimensional finite element analysis to evaluate the hypothesis that subchondral bone cysts in the osteoarthrotic hip joint may be the result of microfractures caused by localized cartilage defects or a thinned layer of cartilage. We evaluated the equivalent bone stress (von Mises (VM) stress) in the cancellous bone as an indicator of potential microfractures and further development of cystic lesions.Results Cartilage defects induced stress peaks in the subchondral bone. This peak stress distribution corresponded to the clinical observation of development of acetabular and femoral subchondral cysts in a "kissing" position. A femoral subchondral bone cyst induced a stress peak at the corresponding acetabular site, whereas subchondral acetabular cysts did not increase stress in the femoral head. Acetabular cysts showed an increased level of stress at the lateral and medial border of the lesion which was much higher than the stress levels in the femoral head, indicating a tendency to faster growth.Interpretation Our study supports the theory that stress-induced bone resorption may cause development of subchondral bone cysts in osteoarthrosis.

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Section: Discussionmentioning

confidence: 99%

The cause of subchondral bone cysts in osteoarthrosisA finite element analysis

Dürr¹,

Martin²,

Pellengahr³

et al. 2004

Acta Orthopaedica Scandinavica

108

View full text Add to dashboard Cite

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“…SBCs are also shown to be associated with high bone mineralization and bone turnover [88]. Osteoclastic bone resorption, activated osteoblasts and new bone formation were detected to be present surrounding SBCs in OA [119,120] (Figure 3C, D).…”

Section: Subchondral Bone Cysts In Osteoarthritismentioning

confidence: 99%

Subchondral bone in osteoarthritis: insight into risk factors and microstructural changes

et al. 2013

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Osteoarthritis (OA) is a major cause of disability in the adult population. As a progressive degenerative joint disorder, OA is characterized by cartilage damage, changes in the subchondral bone, osteophyte formation, muscle weakness, and inflammation of the synovium tissue and tendon. Although OA has long been viewed as a primary disorder of articular cartilage, subchondral bone is attracting increasing attention. It is commonly reported to play a vital role in the pathogenesis of OA. Subchondral bone sclerosis, together with progressive cartilage degradation, is widely considered as a hallmark of OA. Despite the increase in bone volume fraction, subchondral bone is hypomineralized, due to abnormal bone remodeling. Some histopathological changes in the subchondral bone have also been detected, including microdamage, bone marrow edema-like lesions and bone cysts. This review summarizes basic features of the osteochondral junction, which comprises subchondral bone and articular cartilage. Importantly, we discuss risk factors influencing subchondral bone integrity. We also focus on the microarchitectural and histopathological changes of subchondral bone in OA, and provide an overview of their potential contribution to the progression of OA. A hypothetical model for the pathogenesis of OA is proposed.

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“…Synovial membranes can also pass through the breached cartilage (synovial herniation) and become lodged in the subchondral bone. However, in many cysts, a direct communication with the joint is not shown [9]. This finding forms the basis for the contusion model [1,6,[8][9][10][11][12][13].…”

Section: Fm -11/29/07mentioning

confidence: 99%

“…However, in many cysts, a direct communication with the joint is not shown [9]. This finding forms the basis for the contusion model [1,6,[8][9][10][11][12][13]. In the contusion model, repetitive microtrauma is thought to lead to a localized area of subchondral necrosis with secondary cyst formation.…”

Section: Fm -11/29/07mentioning

confidence: 99%