1994
DOI: 10.3109/17453679409155226
|View full text |Cite
|
Sign up to set email alerts
|

Vascular aspects of degenerative joint disorders a synthesis

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
3
1
1

Citation Types

3
19
0

Year Published

1996
1996
2017
2017

Publication Types

Select...
7
1

Relationship

0
8

Authors

Journals

citations
Cited by 24 publications
(22 citation statements)
references
References 147 publications
3
19
0
Order By: Relevance
“…It is beyond the scope of this paper to validate the model further. Our interpretation of the Brix model is consistent with many other observations proposing a vascular component of OA 3438. These studies focused on venous outflow obstruction as a key pathological observation.…”
Section: Discussionsupporting
confidence: 91%
“…It is beyond the scope of this paper to validate the model further. Our interpretation of the Brix model is consistent with many other observations proposing a vascular component of OA 3438. These studies focused on venous outflow obstruction as a key pathological observation.…”
Section: Discussionsupporting
confidence: 91%
“…The elevated signal enhancement patterns seen on DCE‐MRI during the clearance phase suggest the presence of venous outflow obstruction and venous stasis. Previously, intraosseous venography has demonstrated markedly delayed venous drainage and occlusion of retinacular veins in OA of the hip with drainage of the proximal femur through diaphyseal intramedullary veins . In physiologic and anatomic studies of established human OA, circulatory alterations consisting of decreased venous drainage, venous outflow obstruction, and venous stasis have been reported, associated with intraosseous hypertension, reductions in perfusion, and relative hypoxia .…”
Section: Discussionmentioning
confidence: 99%
“…Several mechanisms exist that could suggest a functional , rather than structural , increase in venous outflow resistance. Venous stasis could have been produced by increased intraosseous extravascular pressure or extraosseous venous shunting, both of which have been demonstrated in OA . Bone venous vasculature is relatively more sensitive to vasoconstricting agents and are responsive to a number of cytokines resident in bone particularly endothelin, a vasoconstricting agent that is released from endothelial cells by hypoxia …”
Section: Discussionmentioning
confidence: 99%
“…One likely source that remains underexplored is that of intra-osseous hypertension. The pathophysiology remains unclear, although phlebographic studies in OA indicate impaired vascular clearance from bone and raised intra-osseous pressure in the bone marrow near the painful joint (3134). What may subsequently cause pain is as yet unknown.…”
Section: Local Tissue Pathologymentioning
confidence: 99%