The pathophysiology of alveolar osteonecrosis of the jaw: anticardiolipin antibodies, thrombophilia, and hypofibrinolysis (Q28277894)

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R E McMahon

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J Bouquot

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B A Rabinovich

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A Becker

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T Tracy

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P Wang

Why is lipoprotein(a) relevant to thrombosis?

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language of work or name

English

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publication date

May 1996

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published in

Translational Research

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volume

127

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issue

5

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page(s)

481-8

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cites work

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Relationships between lipoprotein(a), lipids, apolipoproteins, basal and stimulated fibrinolytic regulators, and D-dimer.

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Avascular necrosis of bone in systemic lupus erythematosus: possible role of haemostatic abnormalities

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Avascular osteonecrosis in patients with SLE: relation to corticosteroid therapy and anticardiolipin antibodies

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Hypofibrinolysis: a common, major cause of osteonecrosis

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Thyropathic endemic dystrophy in an area of the Argeş Valley

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Association of antithrombotic factor deficiencies and hypofibrinolysis with Legg-Perthes disease

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On the role of phosphatidylethanolamine in the inhibition of activated protein C activity by antiphospholipid antibodies

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Osteonecrosis: current perspectives on pathogenesis and treatment

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Nontraumatic necrosis of bone (osteonecrosis).

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An analysis of variance test for normality (complete samples)

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Molecular studies on phospholipid-binding sites and cryptic epitopes appearing on beta 2-glycoprotein I structure recognized by anticardiolipin antibodies

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Neurological disease associated with anticardiolipin antibodies in patients without systemic lupus erythematosus: clinical and immunological features

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Cerebral ischemic events associated with endocarditis, retinal vascular disease, and lupus anticoagulant

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Neurobehavioral presentations of the antiphospholipid antibody syndrome

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Migraine and antiphospholipid antibodies

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Decreased fibrinolytic potential in patients with idiopathic avascular necrosis and transient osteoporosis of the hip

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Mutation in blood coagulation factor V associated with resistance to activated protein C.

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Resistance to activated protein C as a basis for venous thrombosis.

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Idiopathic osteonecrosis, hypofibrinolysis, high plasminogen activator inhibitor, high lipoprotein(a), and therapy with Stanozolol

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Vascular changes after experimentally-induced inflammation in the mandible

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Blood flow in jaw bones affected by chronic osteomyelitis

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Mechanism of action of angiostatic steroids: suppression of plasminogen activator activity via stimulation of plasminogen activator inhibitor synthesis

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Long-term effects of jawbone curettage on the pain of facial neuralgia

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Hypercoagulability and thrombosis.

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Thrombosis and antiphospholipid syndrome: a preliminary assessment of three antithrombotic treatments

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10.1016/S0022-2143(96)90065-7

7 January 2021

Identifiers

DOI

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Fatcat ID

release_46kp4baibratdmtd4uvho6jxmi

1 reference

Fatcat

https://api.fatcat.wiki/v0/release/46kp4baibratdmtd4uvho6jxmi