Effect of superior and superolateral relocations of the hip center on hip joint forces. An experimental and analytical analysis.

With the extensive use of uncemented acetabular components in total hip arthroplasty, relocation of the hip center has become increasingly necessary to avoid bulk grafts and to promote contact between the porous prosthetic surface and bone. Compared with the anatomic hip center, superolateral relocation theoretically results in higher hip joint forces and has been shown in cemented acetabular components to result in an increased clinical failure rate. This study experimentally and analytically compared the hip joint forces in normal, superior, and superolateral hip center locations during both single-leg stance and stairclimbing, performing this comparison over a wide range of hip joint applied flexion moments. An advanced loading fixture was designed to allow any applied moment to be set independently of femoral position, incorporating all three major muscle groups active in stairclimbing position: extensors, abductors, and adductors. For all positions and moments tested, it was found that superolateral relocation caused significant increases in the total hip joint force, but did not affect the nonsagittal force component. Also, superior-only hip center relocation did not significantly affect the total joint force magnitudes or directions. The force increase on hip center lateralization can be attributed to a corresponding increase in the adduction moment. Results from the static analytical model developed supported these findings. The results of this study suggest that superolateral hip center relocation should be avoided and that superior-only relocation may be mechanically acceptable within the confines of the osseous anatomy of the acetabulum.

Aseptic loosening in uncemented total hip arthroplasty in a canine model.

An in vivo canine model was developed to investigate the histologic and biochemical parameters associated with aseptic loosening. Thirty-eight canines had cementless total hip arthroplasty. Experimental groups were designed specifically to investigate the relative contributions of implant motion and particulate debris (cobalt chrome alloy, titanium aluminum vanadium, and polyethylene) on the resultant periprosthetic tissues. Tissues from a stable, well-ingrown prosthesis provided a control. Importantly, the histologic and biochemical characteristics of the experimentally induced membranes consistently correlated with previous in vitro reports of tissues retrieved at revision surgery for aseptic loosening. Implant motion and all 3 particulate debris groups resulted in increased numbers of macrophages in the periprosthetic membranes. The histologic findings paralleled the increase in levels of biochemical mediators of bone resorption as measured by collagenase, gelatinase, prostaglandin E2, and interleukin-1 activity. The most striking results were seen in the histology and biochemistry of the particle groups with highly cellular membranes showing increased biochemical activity when compared with controls. The clinical relevance of this work lies in the description of an in vivo model of aseptic loosening that can be used to investigate the effects of numerous variables implicated in aseptic loosening. Ultimately, the model may serve as a basis for developing therapeutic interventions.

A biochemical, histologic, and immunohistologic analysis of membranes obtained from failed cemented and cementless total knee arthroplasty.

Biochemical, histologic, and immunohistochemical analyses were performed on 34 interface membranes obtained from 33 patients during revision total knee arthroplasty. The membranes had surrounded components of cementless (n = 11) and cemented (n = 23) knee prostheses that were aseptically loose. None of these implant failures was caused by catastrophic polyethylene erosion leading to metal-to-metal contact. The histologic findings were similar in the membranes from cemented and cementless knee components: small polyethylene debris within macrophages and large birefringent polyethylene debris within foreign-body giant cells. Metallic debris was seen in membranes from both groups, but cemented membranes had more polymethylmethacrylate particles and more hyalinization. Intracytoplasmic asteroid bodies were observed in several foreign-body giant cells in both types of membranes. No significant differences were found between the two groups in levels of collagenase, prostaglandin E2 (PGE2), interleukin-1 (IL-1), interleukin-6 (IL-6), or tumor necrosis factor-alpha (TNF-alpha), nor in the population of inflammatory cells stained with IL-1, IL-6, and TNF-alpha antibodies. Membranes that had surrounded components with radiographic evidence of diffuse or localized periprosthetic bone loss released significantly more collagenase, IL-1, IL-6, and TNF than did membranes from components without bone loss. These two groups, however, did not have significantly different PGE2 levels. These findings suggest that polyethylene and metal debris may play a role in macrophage activation and the release of mediators of bone resorption in the membranes surrounding failed cemented and cementless total knee implants.