Commentary & Perspective

Bone loss around a cementless femoral stem following total hip arthroplasty is a well-described long-term phenomenon. The relative importance of this bone loss, however, remains debated. No physician wants to observe substantially diminished bone density immediately adjacent to the femoral stem following hip arthroplasty. However, stress-shielding, which is a more diffuse loss of bone density in the proximal aspect of the femur, is a well-described favorable finding indicating that the femoral stem is well fixed distal to this area. In one study, no negative consequence of such proximal bone loss, such as periprosthetic fracture or femoral stem loosening, was observed at twenty years of follow-up. If the bone in this region (Gruen zones 1 and 7) is in fact ‘‘shielded from stress,’’ why would increasing the bone density in this region by risedronate treatment be expected to make a substantial clinical difference? Regardless, most surgeons today have accepted that stiffer implants cause relative greater proximal bone loss and therefore use implants that have a modulus of elasticity closer to that of native bone in an effort to preserve proximal bone stock. On the other hand, bone loss in the form of osteolysis, especially around the greater trochanter, has been shown to lead to periprosthetic fracture that can compromise the patient’s functional outcome and lead to reoperation. In one study, the prevalence of these fractures was 4.3% at 12.2 years of follow-up, and these fractures can be particularly difficult to manage. These fractures are primarily a consequence of wear debris rather than stress-shielding, and with recent improvements in bearing surfaces, this prevalence may decrease in the future. Despite the substantial reductions in implant wear and osteolysis associated with modern bearing surfaces, wear and osteolysis have not been reduced to zero, and if bisphosphonates could be shown to further reduce osteolysis, they could be an attractive option for young, active patients with the need for a long implant life expectancy. The authors of this study examined the reduction in bone loss that occurred in patients taking bisphosphonates following total hip arthroplasty and noted that a comparable reduction in patients who had not undergone hip arthroplasty has been shown to be associated with a clinically important reduction in the risk of hip fracture. What remains unclear, however, is our ability to equate the reduction in the hip fracture risk in patients who have undergone hip arthroplasty and in patients who have not. Is it rational to assume that a reduction in periprosthetic fractures will occur because unstressed bone in the medial calcar is now stronger? We also need to be sensitive to the possible adverse events associated with any new intervention, especially when such adverse effects could influence the already outstanding long-term results associated with total hip arthroplasty. This study demonstrated a withdrawal rate of 11% (four of thirty-six) in the bisphosphonate group due to adverse events (in this case, urticaria and nausea), which would not improve patient or physician satisfaction with total hip arthroplasty if this intervention were introduced today. The association of femoral shaft fractures with long-term bisphosphonate use is of even greater concern. One area of bone that is under increased stress is just distal to a well-fixed stem, and increasing the fracture risk in this region of bone remains undesirable. Nevertheless, this study represents an important piece of work that demonstrates ‘‘proof of concept’’ as stated by the authors. By showing that reducing bone loss around a cementless implant is possible, it opens the door for further study regarding this subject. If an agent could be shown to reduce bone loss without increasing undesirable side effects, patients and physicians alike may benefit. The authors and their institution should be commended for completing a well-designed prospective, randomized, double-blinded study. William G. Hamilton, MD* Anderson Orthopaedic Research Institute, Alexandria, Virginia