No abstract

We evaluated the effects of intraosseously administered prostaglandin E2 (PGE2) within the proximal metaphysis of the goat (caprine) tibia under intraosseous normotensive and hypertensive conditions. PGE2 was administered at 0.5 or 1.0 mg (1 ml vol) twice daily for 10 days via an Osteoport which had been surgically implanted within the proximal tibial metaphysis. Intraosseous hypertension was produced when venous outflow obstruction (VOO) was created by ligation of the popliteal vein, which drained the proximal tibia, and occlusion of the diaphyseal medullary space distally with bone cement. After VOO, the intraosseous pressure measured at the metaphysis increased significantly (p < 0.05) from a baseline mean of 14.9 +/- 4.2 mm Hg to 28.6 +/- 5.3 mm Hg. Serum radioimmunoassays indicated that VOO prolonged the venous drainage of PGE2 from the tibia after an infusion. Static histomorphometric analysis indicated a marked dose-dependent increase in new bone formation in all PGE2 groups at 30 days after the PGE2 infusion. Significant (p < 0.05) formation of new bone occurred, primarily at the subperiosteal and endocortical surfaces, and moderately increased the marrow cavity of cancellous new bone as compared with the VOO-only group and the controls. Bone remodeling indices were also increased by PGE2. The PGE2 infusion, combined with VOO, produced significantly more new bone formation than the PGE2 infusion alone. Intensive marrow fibrosis was associated with the active bone remodeling.

We evaluated the in vivo animal tolerance to intraosseous infusion via the Osteoport pediatric implant (model 2005PSO, Lifequest Medical, San Antonio, TX, U.S.A.) into the proximal tibia of immature goats and investigated the osseous effects of intermittent and sustained increases in intraosseous pressure (IOP). In group 1 (n = 3) autogenous whole blood was continuously infused (CI) for 5 days at flow rates producing an IOP of 30-45 mm Hg. Group 2 animals (n = 3) underwent a 5-s high-pressure infusion (HPI) of lactated Ringer solution (LRS) producing an IOP of 90-125 mm Hg twice daily for 10 days. In group 3, the Osteoports were left in place 5 (n = 2) or 10 days (n = 2) and evaluated for patency at 72-h intervals. An IOP > 35 mm Hg produced clinical evidence of bone pain. Bone mineral density was significantly increased (p < 0.05) in all implanted tibias (mean 1.04 g/cm2; range 0.87-1.21 g/cm2) compared with controls (mean 0.67 g/cm2; range 0.65-0.71 g/cm2). A nonsignificant increase (+9% to +31%) in periosteal new bone formation occurred in all implanted tibias. In the continuously infused group, there was a significant increase (p < 0.05) in cancellous new bone formation (+483%), percentage eroded bone surface (+143%), and osteoclast covered bone surface (+255%) compared with controls. HPI of LRS did not produce significant bone changes. Seemingly, the Osteoport provided a ready means of intraosseous infusion and may be associated with less complications than current methods of continual vascular access. Bone changes correlated more with the duration than the magnitude of increased intraosseous pressures.

steofibrous dysplasia is a benign bone dysplasia in which lytic lesions occur in the cortex of the tibia and/or fibula in skeletally immature patients. Campanacci proposed the term "osteofibrous dysplasia" and described the clinical and pathologic findings 1,2 . The dysplasia may be clinically silent, so the true incidence of the disease is unknown. Symptomatic children present with anterolateral bowing of the affected bones or with pathologic fractures. As a result of the site of involvement and the propensity for pathologic fractures, this condition may be confused with congenital pseudarthrosis of the tibia.Pathologic specimens from sites affected by osteofibrous dysplasia show bland fibroblastic tissue associated with immature woven bone rimmed by osteoblasts 3-5 . While there has been a questionable association with evolution into adamantinoma, the pathologic appearance of osteofibrous dysplasia does not include neoplastic features.Osteofibrous dysplasia was not thought to be an inherited condition until a recent report, by Hunter and Jarvis, on two siblings with pathologic fractures through lesions resembling osteofibrous dysplasia 6 . We describe six individu-als, in three generations of a kindred of nineteen people, who had lytic lesions of the tibia that resembled osteofibrous dysplasia radiographically and histologically. All six patients were treated for pathologic fracture of the tibia or fibula at our institution. Materials and Methodsith institutional review board approval, a four-generation pedigree was obtained (Fig. 1). One patient presented with tibial lesions and gave a positive family history, after which medical records and radiographs were reviewed retrospectively to identify all of that patients' family members who had had lower-extremity fractures in childhood. All of the affected patients had been treated at our hospital between 1957 and the time of the study. There were twenty-two relatives from four generations; three had died before the initiation of the study.Radiographs of the tibia and fibula of the six affected patients were reviewed, and anteroposterior and lateral radiographs of the tibia and fibula of ten unaffected family members were made at the time of the study. These ten individuals O W Fig. 1 Pedigree of the family. Patients with documented tibial lesions in childhood are represented by numbers, family members with radiographic evidence of involvement are represented by shaded circles (females) or squares (males), family members with subtle radiographic findings are represented by partially shaded circles or squares, members who died before the time of the study are noted by a diagonal line. An asterisk indicates that a blood sample was obtained for DNA analysis, and a plus sign indicates that anteroposterior and lateral radiographs of the extremities were made.

No abstract