This proposal is concerned with adaptive bone remodeling of the femur following cementless and cemented total hip arthroplasty. Clinically, over 50% of the periprosthetic bone mass can be lost following hip arthroplasty. The practical health-related goal is to prolong implant survivorship and facilitate potential revision surgery by minimizing bone loss attributed to stress-shielding, the initial reduction in mechanical loading of the bone in the proximal femur due to load transfer through the prosthesis. The central hypothesis is that (in the absence of osteolysis related to degradation of the implant) stress-shielding represents the most important independent variable or """"""""final common pathway"""""""" through which patient, implant and technical factors account for a large proportion of the bone loss following total hip arthroplasty. If this thesis is correct, then factors such as age and source of implant bonding (e.g., bone ingrowth versus cement fixation) play a role in the adaptive process, largely through mechanically-mediated pathways. The applicants propose to test their hypothesis by examining three of its implications: (i) individual variation in stress-shielding explains a large proportion of the individual variation in femoral bone loss following hip replacement; (ii) bone loss has the same relationship to stress-shielding in skeletally mature young and old animals following cementless hip replacement, even though the actual amount of bone loss may vary as a function of age; and (iii) bone loss has the same relationship to stress-shielding in cemented and cementless total hip arthroplasty. Individual estimates of stress-shielding will be made based on animal-specific finite element modeling of a canine model. These estimates will be correlated with measurements of change in periprosthetic bone mass made in the same animals. In this way, the actual variance in the dependent variable (change in bone mass), explained by variance in the independent variable (stress-shielding) and the nature of the relationship (linear or nonlinear), will be determined. Use of an animal model allows other causes of bone loss to be largely eliminated, thus permitting the effects of stress-shielding to be clearly defined.

Agency
National Institute of Health (NIH)
Institute
National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS)
Type
Research Project (R01)
Project #
5R01AR016485-26
Application #
6171608
Study Section
Special Emphasis Panel (ZRG4-ORTH (05))
Program Officer
Panagis, James S
Project Start
1979-05-01
Project End
2002-08-31
Budget Start
2000-09-01
Budget End
2002-08-31
Support Year
26
Fiscal Year
2000
Total Cost
$198,976
Indirect Cost
Name
Rush University Medical Center
Department
Type
DUNS #
068610245
City
Chicago
State
IL
Country
United States
Zip Code
60612
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Onsten, I; Berzins, A; Shott, S et al. (2001) Accuracy and precision of radiostereometric analysis in the measurement of THR femoral component translations: human and canine in vitro models. J Orthop Res 19:1162-7
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Sumner, D R; Turner, T M; Igloria, R et al. (1998) Functional adaptation and ingrowth of bone vary as a function of hip implant stiffness. J Biomech 31:909-17
Turner, T M; Sumner, D R; Urban, R M et al. (1997) Maintenance of proximal cortical bone with use of a less stiff femoral component in hemiarthroplasty of the hip without cement. An investigation in a canine model at six months and two years. J Bone Joint Surg Am 79:1381-90
Weinans, H; Sumner, D R (1997) Finite Element analyses to study periprosthetic bone adaptation. Stud Health Technol Inform 40:3-16
Smith, A M; Turner, T M; Sumner, D R (1996) Unilateral hip replacement causes bilateral changes in tibial bone mineral content in a canine model. J Bone Miner Res 11:693-6
Bryan, J M; Sumner, D R; Hurwitz, D E et al. (1996) Altered load history affects periprosthetic bone loss following cementless total hip arthroplasty. J Orthop Res 14:762-8
Bobyn, J D; Jacobs, J J; Tanzer, M et al. (1995) The susceptibility of smooth implant surfaces to periimplant fibrosis and migration of polyethylene wear debris. Clin Orthop Relat Res :21-39

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