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Angular deformities were created in cadaver forearms at proximal, middle, and distal third levels of the radius and ulna separately, and at middle and distal third levels of both bones, to determine the corresponding limitations of pronation and supination. The ranges of pronation and supination were recorded using a rotational motion measurement apparatus instrumented with a 360 degrees goniometer. These experimental results were compared to data obtained from clinical and radiographic examination of 105 patients with similar residual deformities following treatment of fractures by nonsurgical means, to evaluate the accuracy of the experimental model and to determine if loss of rotational motion could be predicted based on radiographic findings. With cadaver forearms, on the average, angulation of 10 degrees of the radius or ulna in coronal or sagittal planes limited pronation and supination by less than 24 degrees, whereas angulation of 10 degrees of both the radius and the ulna limited pronation and supination by less than 18%. Comparison of experimental results with clinical findings showed that, despite the errors involved in measuring forearm deformities in patients using biplanar radiographs, the experimental results predicted the clinical loss of pronation and supination to within 17% for the fractures of the radius, and within 8% accuracy for the fractures of the ulna.

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It is a well known entity that fractures of the tibia heal with some component of angular deformity. Ankle and subtalar joints may compensate for small degrees of angular deformities, but the exact amount of malunion that can be accepted without development of late sequalae has yet to be determined. Two recent studies from this institution have concluded that contact changes at the tibiotalar joint tend to be greater with distal third tibial fracture deformities compared to proximal and middle with the ankle in neutral, 5 degrees dorsiflexion, and 20 degrees of plantar flexion. Anterior and posterior bow deformities produced a greater change in contact area of the tibiotalar joint than with valgus or varus deformities. This phenomena may be possibly explained by the subtalar motion in the horizontal plane which averages 23 degrees. Thus, it was the primary purpose of this paper to determine the exact role, if any, in subtalar motion on tibiotalar contact in angular deformities of the tibia. To achieve this objective the subtalar joint was transfixed thereby eliminating its perceived compensatory movement. Six cadaveric lower extremities were disarticulated at the knee joint and stripped of soft tissue preserving capsular and ligamentous structures. A custom universal joint was used to create various angulatory deformities at proximal, middle, and distal third levels of the tibia.(ABSTRACT TRUNCATED AT 250 WORDS)

In this study, density, specific heat, thermal conductivity, and thermal diffusivity were measured experimentally along the lengths of human cadaveric femora. Fresh and dry bone samples were selected from both male and female specimens, and for different age groups varying between 44 and 73 years old. Measured values for specific heat vary between 1.14 and 2.37 J/gm degrees C; for thermal conductivities the range is from 0.16 to 0.34 W/m degrees C; and for thermal diffusivities the range is from 0.10 to 0.23 cm2/sec, depending on whether the bone samples were fresh or dry, cancellous or cortical. The experimental results are presented in non-dimensional coordinates and are compared with the few other data available in the literature.

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Fracture bracing is a philosophy rather than merely the use of orthotic devices in the treatment of fractures. It is predicated on the belief that immobilization of the fragments and the joints above and below the fracture is not necessary for fracture healing. It proposes also that the soft tissues of the injured extremity play a major role in providing the stability necessary to allow uninterrupted osteogenesis.The encouraged early function, weightbearing and motion of the joints and fracture fragments during treatment challenges the basic concepts of surgical as well as nonsurgical fracture management which emphasize that rest and fragment immobilization are prerequisites for fracture healing. In an effort to elucidate these conflicts and gain a better understanding of how bracing works, a series of laboratory studies was c~n d u c t e d .~~~~~~~~This article provides a synopsis of the important portions of this research as they apply to fracture bracing. VASCULARITY AND FRACTURE HEALINGAt the time of a diaphyseal fracture, the normal blood supply to the bone is disrupted and a hematoma forms at the fracture site. Medullary circulation is almost always disrupted and is slow to re-establish. Subsequently, capillaries invade the area of the fracture site from the peripheral soft tissues. The importance of the early revascularization from soft tissues is emphasized by the close association of early bone formation with vascular invasion (Fig. 1). A possible explanation for the new bone formation following the capillary invasion was offered by Trueta, who suspected endothelial metap1a~ia.I~ Much of our work has supported this theory by demonstrating the close proximity of osteoblastic and osteoclastic activity to the invading vasculature (Fig. 2 ) .Thus, one important role of function in fracture healing can well be the early vascular invasion stimulated by muscle activity. When function is introduced early in this nonsurgical management regimen, the activity level of the osteoblasts and osteoclasts is high as indicated by light and electron microscopy (Fig. 3). FRACTURE CALLUS ARCHITECTUREThe importance of the gross architecture of callus formation when healing takes place in the presence of function and muscle activity is based upon the structural role of bone. The callus architecture forms in the following manner: initially, a hematoma surrounds the area near the fracture site and the bone ends and loose fragments become necrotic. Away from the fracture site early revascularization comes from medullary circulation. The callus formation at this point is of intramembranous origin, therefore 0009-921X/80/0100/028 $00.95 0 J . B. Lippincott Co. 28