The effect of poly sterilization on wear, osteolysis and survivorship of a press-fit cup at 10-year followup.

BACKGROUND: During the mid-1990s when our institution was using a press-fit porous-coated cup without supplemental initial fixation for primary THA, the manufacturer transitioned from gamma irradiation to gas plasma for the terminal sterilization of their polyethylene liners. QUESTIONS/PURPOSES: At minimum 10-year followup, we asked whether the fixation achieved by solely relying on a press-fit would be durable and how different liner sterilization methods affected radiographic wear, osteolysis, and survivorship. PATIENTS AND METHODS: We retrospectively reviewed 373 patients who underwent 398 primary THAs with a press-fit porous-coated cup between March 1995 and December 1996. Mean age at time of surgery was 61.5 ± 13.3 years and mean followup was 10.4 ± 3.7 years. We determined reasons for revision, survivorship, femoral head penetration, osteolysis, and wear-related complications. RESULTS: Among 20 revisions involving any component, seven were associated with wear and osteolysis. Kaplan-Meier survivorship, using component revision for any reason as an end point, was 95.7% (95% confidence interval, 93.6%-97.9%) at 10 years. Noncrosslinked liners sterilized with gas plasma demonstrated a mean head penetration rate of 0.20 ± 0.09 mm/year compared with 0.13 ± 0.07 mm/year for liners sterilized with gamma irradiation in air and 0.09 ± 0.04 mm/year for liners sterilized with gamma-irradiation with barrier packaging without oxygen. THAs with increased volumetric wear tended to demonstrate larger osteolytic lesions (r = 0.40) and there tended to be less osteolysis among the liners sterilized with gamma-irradiation with barrier packaging without oxygen. However, there was no difference in survivorship among the sterilization groups and there has been no cup or stem loosening associated with osteolysis. CONCLUSIONS: Durable biologic fixation through 10-year followup can be achieved by solely relying on an initial press-fit. Noncrosslinking gas plasma for terminal sterilization of the polyethylene liners was associated with greater head penetration rate than gamma irradiation. LEVEL OF EVIDENCE: Level IV, therapeutic study. See Guidelines for Authors for a complete description of levels of evidence.

Osteolysis propensity among bilateral total hip arthroplasty patients.

Because some patients with high wear rates demonstrate extensive osteolysis whereas other patients with similarly high wear rates show little or no evidence of osteolysis, we hypothesized that both polyethylene wear and a patient-specific propensity mediate the development of osteolysis. We evaluated wear and osteolysis using computed tomography and radiographs among 46 patients who had undergone bilateral total hip arthroplasties (THAs). A radiographic patient-specific propensity for osteolysis associated with each THA was quantified by dividing the amount of osteolysis by the volumetric wear. Using a multivariate regression analysis to simultaneously consider the influence of polyethylene wear and patient propensity, we found that both factors are associated with the amount of osteolysis around a THA and that they appear to be of similar importance.

Five Duraloc locking ring failures.

We report on 5 cases that underwent revision for locking ring failure in the Duraloc product line (DePuy, Warsaw, Ind). All liner retrievals showed signs of posterior neck/liner impingement and superior edge loading or significant wear. In these cases, we believe superior head migration and neck/liner impingement due to cup anteversion contributed to these locking ring failures. More research is needed to determine the incidence of this complication. Patients with locking ring failures should be closely monitored. Full cup revision, face-changing liners, or cementing liners into well-fixed cups are all options to correct suboptimal cup positioning.

A comparison of a second- and a third-generation modular cup design: is new improved?

The highly cross-linked polyethylene liners currently used with modular uncemented cups have substantially decreased wear and osteolysis at early follow-up. However, retroacetabular osteolysis has still been reported in some cases with DePuy Orthopaedic's (Warsaw, IN) second-generation Duraloc acetabular shell. DePuy's third-generation Pinnacle cup incorporates a different shell-liner locking mechanism. We compared the clinical outcome among a matched series of 42 Duraloc and 42 Pinnacle cups at a mean follow-up of 5.9 years. Although the Harris Hip Scores and wear rates were not statistically different between the 2 cup designs, retroacetabular osteolysis behind the central hole was absent among the Pinnacle cups but noted among 19% of the Duraloc cups.

Can the volume of pelvic osteolysis be calculated without using computed tomography?

UNLABELLED: The most common method to diagnose and monitor osteolysis is the standard anteroposterior radiograph. Unfortunately, plain radiographs underestimate the incidence and extent of osteolysis. CT scans are more sensitive and accurate but also more expensive and subject patients to more radiation. To determine whether the volume of pelvic osteolysis could be accurately estimated without a CT scan, we evaluated the relationships between CT volume measurements and other variables that may be related to the size of pelvic osteolytic lesions in 78 THAs. Only the area of pelvic osteolysis measured on radiographs, heavy patient activity level, and total volume of wear were associated with the pelvic osteolysis volume measured on CT in the context of the multivariate regression analysis. Despite a strong correlation (r = 0.93, r(2) = 0.87) between these three variables and the volume of pelvic osteolysis measured on CT, estimates of pelvic osteolysis volume deviated from the actual volume measured on CT by more than 10 cm(3) among eight of the 78 THAs in this study. CT images remain our preferred modality when accurate assessments of pelvic osteolysis volume are required. LEVEL OF EVIDENCE: Level III, diagnostic study. See Guidelines for Authors for a complete description of levels of evidence.

Promotion of osteoclast survival and antagonism of bisphosphonate-induced osteoclast apoptosis by glucocorticoids.

Glucocorticoids depress bone formation by inhibiting osteoblastogenesis and increasing osteoblast apoptosis. However, the role of bone resorption in the initial rapid phase of bone loss characteristic of glucocorticoid-induced osteoporosis is unexplained, and the reason for the efficacy of bisphosphonates in this condition remains unknown. We report that in murine osteoclast cultures, glucocorticoids prolonged the baseline survival of osteoclasts and antagonized bisphosphonate-induced caspase activation and apoptosis by a glucocorticoid receptor-mediated action. Consistent with the in vitro evidence, in a murine model of glucocorticoid-induced osteoporosis, the number of cancellous osteoclasts increased, even though osteoclast progenitor number was reduced. Moreover, in mice receiving both glucocorticoids and bisphosphonates, the expected proapoptotic effect of bisphosphonates on osteoclasts was abrogated, as evidenced by maintenance of osteoclast numbers and, additionally, loss of bone density. In contrast, bisphosphonate administration prevented glucocorticoid-induced osteoblast apoptosis. These results indicate that the early loss of bone with glucocorticoid excess is caused by extension of the life span of pre-existing osteoclasts, an effect not preventable by bisphosphonates. Therefore, the early beneficial effects of these agents must be due, in part, to prolonging the life span of osteoblasts.

The skeletal effects of glucocorticoid excess override those of orchidectomy in mice.

Hypogonadism has been implicated as a contributing factor in glucocorticoid-induced osteoporosis, but evidence for this is limited. Hypogonadism and glucocorticoid excess both cause bone loss, but the cellular mechanisms responsible are distinct. Loss of gonadal steroids causes an increase in bone remodeling by up-regulating osteoblastogenesis and osteoclastogenesis. Glucocorticoid excess, conversely, suppresses remodeling by down-regulating osteoblastogenesis and osteoclastogenesis. Nonetheless, both conditions increase osteoblast apoptosis and decrease osteoclast apoptosis, and both cause bone loss due to an undersupply of osteoblasts relative to the need for cavity repair. To investigate their interactions, we compared the effects of orchidectomy, glucocorticoid excess, or both combined in mice. After 28 d, serum unbound testosterone concentration and seminal vesicle weight were not diminished when prednisolone was administered alone. Vertebral bone mineral density and compression strength decreased to the same extent in animals receiving prednisolone or after orchidectomy, but the changes were not additive. Orchidectomy induced the expected up-regulation of osteoblast and osteoclast progenitors, but these changes were prevented in orchidectomized mice simultaneously receiving glucocorticoids. Likewise, the increase in cancellous osteoid, osteoblasts, osteoclasts, bone formation, and activation frequency caused by orchidectomy were prevented by prednisolone. The prevalence of osteoblast apoptosis increased in the mice receiving prednisolone or after orchidectomy, but the increases were not additive. These data demonstrate that hypogonadism does not occur in or contribute to glucocorticoid-induced osteoporosis and that the adverse skeletal effects of glucocorticoid excess override those of orchidectomy.

Glucocorticoids act directly on osteoblasts and osteocytes to induce their apoptosis and reduce bone formation and strength.

Whether the negative impact of excess glucocorticoids on the skeleton is due to direct effects on bone cells, indirect effects on extraskeletal tissues, or both is unknown. To determine the contribution of direct effects of glucocorticoids on osteoblastic/osteocytic cells in vivo, we blocked glucocorticoid action on these cells via transgenic expression of 11beta-hydroxysteroid dehydrogenase type 2, an enzyme that inactivates glucocorticoids. Osteoblast/osteocyte-specific expression was achieved by insertion of the 11beta-hydroxysteroid dehydrogenase type 2 cDNA downstream from the osteoblast-specific osteocalcin promoter. The transgene did not affect normal bone development or turnover as demonstrated by identical bone density, strength, and histomorphometry in adult transgenic and wild-type animals. Administration of excess glucocorticoids induced equivalent bone loss in wild-type and transgenic mice. As expected, cancellous osteoclasts were unaffected by the transgene. However, the increase in osteoblast apoptosis that occurred in wild-type mice was prevented in transgenic mice. Consistent with this, osteoblasts, osteoid area, and bone formation rate were significantly higher in glucocorticoid-treated transgenic mice compared with glucocorticoid-treated wild-type mice. Glucocorticoid-induced osteocyte apoptosis was also prevented in transgenic mice. Strikingly, the loss of vertebral compression strength observed in glucocorticoid-treated wild-type mice was prevented in the transgenic mice, despite equivalent bone loss. These results demonstrate for the first time that excess glucocorticoids directly affect bone forming cells in vivo. Furthermore, our results suggest that glucocorticoid-induced loss of bone strength results in part from increased death of osteocytes, independent of bone loss.

Results of the anatomic medullary locking total hip arthroplasty at a minimum of twenty years. A concise follow-up of previous reports.

Between October 1982 and December 1984, the senior author performed 223 total hip arthroplasties in 215 patients with use of the anatomic medullary locking hip stem and TriSpike cup. We now report on 119 of these hips at a mean of 22.0 years (range, 20.0 to 25.0 years) after surgery. Of the fifty-six hips with minimum twenty-year follow-up radiographs and the original acetabular component, seventeen (30.4%) had pelvic osteolytic lesions measuring larger than 1.5 cm(2). Of the sixty-eight hips with twenty-year radiographs and the original anatomic medullary locking stem, twenty-five (36.8%) had femoral osteolytic lesions measuring larger than 1.5 cm(2). Acetabular osteolysis was significantly associated with cup loosening (p = 0.006), but the presence of femoral osteolysis was not associated with stem loosening. Kaplan-Meier analysis, with revision for any reason as the end point, revealed that the survival rate at twenty years was 85.8% +/- 5.2% for the acetabular shell and 97.8% +/- 2.2% for the stem. The most common reoperation was polyethylene exchange because of wear or osteolysis.