TY - JOUR
T1 - Bone changes associated with intraosseous hypertension in the caprine tibia
AU - Welch, R. D.
AU - Johnston, C. E.
AU - Waldron, M. J.
AU - Poteet, B.
PY - 1993
Y1 - 1993
N2 - We investigated the effects of increased intraosseous pressure on new- bone formation in the proximal metaphysis of the caprine tibia. Intraosseous hypertension was produced by obstruction of venous outflow by ligation of the popliteal vein draining the proximal aspect of the tibia and occlusion of the medullary space with bone cement (groups 1 and 2). After the obstruction of venous outflow (day 0), the intraosseous pressure measured at the proximal tibial metaphysis increased significantly from a mean of 15.5 millimeters of mercury before the obstruction to a mean of 28.7 millimeters of mercury in groups 1 and 2. In group 1, obstruction of venous outflow was combined with intraosseous infusion of autogenous whole blood under pressure to maintain the intraosseous pressure between thirty and forty-five millimeters of mercury during days 0 through 5. The time for venous drainage was still prolonged and intraosseous pressures were still increased on days 5 and 10 (means, 26.8 and 26.2 millimeters of mercury, respectively) in groups 1 and 2. The intraosseous hypertension produced in group 1 was associated with a significant increase in periosteal (138 per cent), endocortical (369 per cent), and cancellous new-bone formation (889 per cent) at the tibial metaphysis compared with control values. Osseous necrosis within the metaphysis was not observed. Clinical Relevance: This study suggests that intraosseous hypertension may stimulate formation of bone by an unknown mechanism. In patients who have osteoarthrosis and early stages of Legg- Perthes disease, elevated intraosseous pressure or obstructed venous outflow are thought to produce local hypoxia, resulting in necrosis of bone. Although intraosseous hypertension may contribute to the bone-remodeling observed in patients who have these conditions, factors other than venous congestion appear to be involved in the development of osseous necrosis. Hydrostatic pressure gradients secondary to intraosseous hypertension may amplify streaming potentials generated within the bone matrix and modulate bone- remodeling.
AB - We investigated the effects of increased intraosseous pressure on new- bone formation in the proximal metaphysis of the caprine tibia. Intraosseous hypertension was produced by obstruction of venous outflow by ligation of the popliteal vein draining the proximal aspect of the tibia and occlusion of the medullary space with bone cement (groups 1 and 2). After the obstruction of venous outflow (day 0), the intraosseous pressure measured at the proximal tibial metaphysis increased significantly from a mean of 15.5 millimeters of mercury before the obstruction to a mean of 28.7 millimeters of mercury in groups 1 and 2. In group 1, obstruction of venous outflow was combined with intraosseous infusion of autogenous whole blood under pressure to maintain the intraosseous pressure between thirty and forty-five millimeters of mercury during days 0 through 5. The time for venous drainage was still prolonged and intraosseous pressures were still increased on days 5 and 10 (means, 26.8 and 26.2 millimeters of mercury, respectively) in groups 1 and 2. The intraosseous hypertension produced in group 1 was associated with a significant increase in periosteal (138 per cent), endocortical (369 per cent), and cancellous new-bone formation (889 per cent) at the tibial metaphysis compared with control values. Osseous necrosis within the metaphysis was not observed. Clinical Relevance: This study suggests that intraosseous hypertension may stimulate formation of bone by an unknown mechanism. In patients who have osteoarthrosis and early stages of Legg- Perthes disease, elevated intraosseous pressure or obstructed venous outflow are thought to produce local hypoxia, resulting in necrosis of bone. Although intraosseous hypertension may contribute to the bone-remodeling observed in patients who have these conditions, factors other than venous congestion appear to be involved in the development of osseous necrosis. Hydrostatic pressure gradients secondary to intraosseous hypertension may amplify streaming potentials generated within the bone matrix and modulate bone- remodeling.
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U2 - 10.2106/00004623-199301000-00008
DO - 10.2106/00004623-199301000-00008
M3 - Article
C2 - 8419391
AN - SCOPUS:0027389109
SN - 0021-9355
VL - 75
SP - 53
EP - 60
JO - Journal of Bone and Joint Surgery - Series A
JF - Journal of Bone and Joint Surgery - Series A
IS - 1
ER -