Hypercoagulability and Hypofibrinolysis in Primary Osteoarthritis

Cheras, Phillip A; Whitaker, A N; Blackwell, Eric; Sinton, T J; Chapman, Miranda; Peacock, K. A.

doi:10.1097/00003086-199701000-00008

Cited by 48 publications

(32 citation statements)

References 34 publications

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“…However, it must be noted that there exists some controversy regarding the role of hypercoagulability and ON of the femoral head. It is not always observed in ON of the femoral head and is often seen in other conditions affecting the femoral head, namely, osteoarthritis of the hip and bone marrow edema syndrome [60,61]. Similarly, abnormalities of protein C and S, antithrombin III, or resistance to activated protein C have not been found in two studies that retrospectively examined patients with Perthes disease [62,63].…”

Section: Intravascular Occlusionmentioning

confidence: 99%

Pathophysiology and risk factors for osteonecrosis

Shah

Racine

Jones

et al. 2015

Curr Rev Musculoskelet Med

231

150

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Osteonecrosis, also known as avascular necrosis or AVN, is characterized by a stereotypical pattern of cell death and a complex repair process of bone resorption and formation. It is not the necrosis itself but rather the resorptive component of the repair process that results in loss of structural integrity and subchondral fracture. Most likely, a common pathophysiological pathway exists involving compromised subchondral microcirculation. Decreased femoral head blood flow can occur through three mechanisms: vascular interruption by fractures or dislocation, intravascular occlusion from thrombi or embolic fat, or intraosseous extravascular compression from lipocyte hypertrophy or Gaucher cells. In this review, we emphasize etiologic relationships derived mostly from longitudinal cohort studies or meta-analyses whose causal relationships to osteonecrosis can be estimated with confidence. Understanding risk factors and pathophysiology has therapeutic implications since several treatment regimens are available to optimize femoral head circulation, interrupt bone resorption, and preserve the subchondral bone.

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Section: Intravascular Occlusionmentioning

confidence: 99%

Pathophysiology and risk factors for osteonecrosis

Shah

Racine

Jones

et al. 2015

Curr Rev Musculoskelet Med

231

150

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“…[15][16][17][18][19][20][21][22] Despite numerous reports on elevated concentrations of Lp(a) in plasma from patients with rheumatoid arthritis (RA) 19,[23][24][25] or other rheumatological diseases, 23,26,27 little is known on the biology and the role of Lp(a) within the joint.…”

mentioning

confidence: 99%

Plasma Apolipoprotein(a) Co-Deposits with Fibrin in Inflammatory Arthritic Joints

Busso

Dudler

Salvi

et al. 2001

The American Journal of Pathology

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Extravascular coagulation and diminished fibrinolysis are processes that contribute to the pathology of both inflammatory arthritis and atherosclerosis. We hypothesized that, given its homology with plasminogen, apolipoprotein (apo) (a), the distinctive glycoprotein of the atherogenic lipoprotein (Lp) (a), may be equally implicated in inflammatory arthritis. We detected the presence of apo(a) as part of Lp(a) in human arthritic synovial fluid. The abundance of apo(a) in synovial fluid rose in proportion to plasma apo(a) levels and was higher in inflammatory arthritides than in osteoarthritis. In addition, apo(a) immunoreactive material, but not apo(a) transcripts, was detected in inflammatory arthritic synovial tissues. These data indicated that synovial fluid apo(a) originates from circulating Lp(a) and that diffusion of Lp(a) through synovial tissue is facilitated in inflammatory types of arthritis. In synovial tissues, apo(a) co-localized with fibrin. These observations could be reproduced in a model of antigen-induced arthritis, using transgenic mice expressing human Lp(a). Although in this mouse model the presence of apo(a) did not change the severity of arthritis, the co-localization of apo(a) with fibrin in synovial tissue suggests that, in humans, apo(a) may modulate locally the fibrinolytic activity and may thus contribute to the persistence of intra-articular fibrin in inflammatory arthritis. Patients suffering from rheumatic diseases are at increased risk for cardiovascular morbidity and mortality, 1,2 suggesting that common factors may promote the development of both atherosclerosis and arthritis.

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“…Understanding of the relationship between hypercoagulable states and ON may allow pharmacologic intervention to prevent this process. The work of Cheras and Ghosh showed that changes in coagulability of the blood might also predispose to OA (Cheras et al, 1997;Ghosh and Cheras, 2001). Cheras et al (1993) observed intraosseous intravascular lipid and thrombosis, particularly in the venous microvasculature, in femoral heads from patients with degenerative osteoarthritis, but not in non-osteoarthritic femoral heads.…”

Section: Coagulation Abnormalities In Oamentioning

confidence: 99%

Subchondral Bone in Osteoarthritis

Findlay¹

2012

Principles of Osteoarthritis- Its Definition, Character, Derivation and Modality-Related Recognition

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Hypercoagulability and Hypofibrinolysis in Primary Osteoarthritis

Cited by 48 publications

References 34 publications

Pathophysiology and risk factors for osteonecrosis

Pathophysiology and risk factors for osteonecrosis

Plasma Apolipoprotein(a) Co-Deposits with Fibrin in Inflammatory Arthritic Joints

Subchondral Bone in Osteoarthritis

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