Functional outcome of total knee replacement: a study protocol for a prospective, double-blinded, parallel-group randomized, clinical controlled trial of novel, personalized and conventional implants.

BACKGROUND: The development of total knee replacement (TKR) implant designs aims to improve outcome regarding pain, function, joint stiffness, instability, patellar problems, and ultimately wear of the implant. Recently, two major orthopaedic implant manufacturers launched a new generation of TKR implants which, according to the manufacturers, provide improved functional outcome. However, the benefits of these new TKR designs claimed by the manufacturers in terms of improved functional outcome still lack scientific documentation. The present randomized controlled trial has been designed to compare three fixed bearing, cemented cruciate-retaining (CR) designs; one of the new personalized TKR design with two conventional TKR designs with the main emphasis being on functional outcome. METHODS: The present study is a prospective, double-blinded, randomized, single-center intervention trial. A total of 240 patients will be recruited to participate in a parallel-group study at Coxa Hospital for Joint Replacement, Tampere, Finland. We will compare the short-term functional outcome of TKR performed with a novel personalized TKR design (Persona CR, Zimmer, Warsaw, IN, USA) against TKRs performed with two conventional designs (PFC CR, DePuy, Warsaw, IN, USA and Nexgen CR, Zimmer, Warsaw, IN, USA). In total, 80 patients will be randomized in each of the three study arms. The primary outcome in this study is the Oxford Knee Score (OKS), which is a validated patient-reported outcome measure (PROM). Secondary outcome measures include the Forgotten Joint Score, the 15D, the UCLA activity score, and the VAS pain scale. The results will be analyzed after 2-year follow-up. DISCUSSION: This paper presents a prospective, randomized, single-center trial study protocol. It provides details of patient randomization, PROMs, follow-up, methods of analysis of the material, and publication plan. An important aspect that will be considered in the study will be the economic effects of the novel designs as they are substantially more expensive, and the benefits of the added costs remain unknown. In addition, it is especially important to carry out evaluative studies in independent centers that are not biased by the interests of the manufacturers. TRIAL REGISTRATION: Retrospectively registered, November, 2017, ClinicalTrials.gov Identifier: NCT03339557 .

Outcome of knee arthroplasty in patients aged 65 years or less: a prospective study of 232 patients with 2-year follow-up.

BACKGROUND AND AIMS: Previous studies have reported lower implant survival rates, residual pain, and higher patient dissatisfaction rates following knee arthroplasty in younger knee arthroplasty patients. We aimed to assess the real-world effectiveness of knee arthroplasty in a prospective non-selected cohort of patients aged 65 years or less with 2-year follow-up. MATERIAL AND METHODS: In total, 250 patients (272 knees) aged 65 years or less were enrolled into this prospective cohort study. Patient-reported outcome measures were used to assess the outcome. RESULTS: The mean Oxford Knee Score and all Knee Injury and Osteoarthritis Outcome Score subscales increased significantly (p < 0.001) from preoperative situation to the 2-year follow-up. Significant increase (p < 0.001) in physical activity was detected in High-Activity Arthroplasty Score and RAND-36 Physical Component Score (PCS). Pain was also significantly (p < 0.001) relieved during the follow-up. Total disappearance of pain was rare at 2 years. Patients with milder (Kellgren-Lawrence grade 2) osteoarthritis were less satisfied and reported poorer patient-reported outcome measure than those with advanced osteoarthritis (Kellgren-Lawrence grade 3-4). There was no difference in the outcome (any patient-reported outcome measure) between patients who underwent total knee arthroplasty and those who received unicondylar knee arthroplasty. CONCLUSION: We found that measured with a wide set of patient-reported outcome measures, both total knee arthroplasty and unicondylar knee arthroplasty resulted in significant pain relief, as well as improvement in physical performance and quality of life in patients aged 65 years or less. Real-world effectiveness of these procedures seems to be excellent. 15% of patients still had residual symptoms and were dissatisfied with the outcome at 2 years after the operation.

Effects of FGF-2 and FGF receptor antagonists on MMP enzymes, aggrecan, and type II collagen in primary human OA chondrocytes.

OBJECTIVES: Fibroblast growth factor (FGF)-2 is a member of the FGF family and is found in the synovial fluid of patients with osteoarthritis (OA). The aim of this study was to investigate the effects of FGF-2 on human OA cartilage/chondrocytes by examining the association between FGF-2 and the cartilage degrading enzymes matrix metalloproteinase (MMP)-1 and MMP-13 and the major cartilage matrix components aggrecan and collagen II. METHOD: Cartilage samples were obtained from 97 OA patients undergoing total knee replacement surgery. Cartilage tissue cultures were conducted and levels of FGF-2, MMP-1, and MMP-13 released into the culture medium were measured by immunoassay. The effects of FGF-2 on the expression of MMP-1, MMP-13, aggrecan, and collagen II were further investigated in cultures of primary human OA chondrocytes. RESULTS: FGF-2, MMP-1, and MMP-13 were released into the culture medium from cartilage samples obtained from patients with OA. FGF-2 concentrations correlated positively with the concentrations of MMP-1 (r = 0.414, p < 0.001) and MMP-13 (r = 0.362, p < 0.001). FGF-2 also up-regulated the production of MMP-1 and MMP-13, and down-regulated the expression of aggrecan and collagen II, in human OA chondrocyte cultures. Furthermore, FGF receptor antagonists AZD4547 and NVP-BGJ398 down-regulated the expression of MMP-1 and MMP-13 and up-regulated aggrecan and collagen II both in the absence and in the presence of exogenous FGF-2. CONCLUSIONS: Our results suggest that, in contrast to its growth factor-like effects in some other tissues, FGF-2 induces catabolic effects in human OA cartilage. Moreover, FGF receptor antagonists showed promising beneficial effects on the balance of catabolic and anabolic factors within OA cartilage.

Aurothiomalate inhibits the expression of mPGES-1 in primary human chondrocytes.

OBJECTIVES: Microsomal prostaglandin E synthase-1 (mPGES-1) is a terminal enzyme in the production of prostaglandin E2 (PGE2) and its expression is upregulated during inflammation. mPGES-1 is considered as a potential drug target for the treatment of arthritis to reduce adverse effects related to the current non-steroidal anti-inflammatory drugs (NSAIDs). Our aim was to study the expression of mPGES-1 in primary human chondrocytes and whether the expression is affected by clinically used antirheumatic drugs. METHOD: Primary human chondrocytes were isolated from cartilage samples obtained from patients undergoing total knee replacement surgery. Expression of mPGES-1 was studied by quantitative real-time polymerase chain reaction (PCR) and Western blot analysis. PGE2 levels were measured by enzyme-linked immunosorbent assay (ELISA). RESULTS: mPGES-1 expression in primary human chondrocytes was enhanced when the cells were exposed to interleukin-1ß (IL-1ß) and mPGES-1 protein levels continued to increase up to the 96-h follow-up. Aurothiomalate inhibited mPGES-1 expression and PGE2 production in a dose-dependent manner, as did the anti-inflammatory steroid dexamethasone. Other disease-modifying antirheumatic drugs (DMARDs) studied (sulfasalazine, methotrexate, and hydroxychloroquine) did not alter mPGES-1 expression. CONCLUSIONS: The results introduce aurothiomalate as the first, and so far the only, DMARD found to be able to inhibit mPGES-1 expression. The effect is likely involved in the mechanisms of action of this gold-containing DMARD in rheumatic diseases. The results are implicated in the regulatory mechanisms of mPGES-1 expression, which are under intensive research.

Adverse reaction to metal debris is more common in patients following MoM total hip replacement with a 36 mm femoral head than previously thought: results from a modern MoM follow-up programme.

We conducted a retrospective study to assess the prevalence of adverse reactions to metal debris (ARMD) in patients operated on at our institution with metal-on-metal (MoM) total hip replacements with 36 mm heads using a Pinnacle acetabular shell. A total of 326 patients (150 males, 175 hips; 176 females, 203 hips) with a mean age of 62.7 years (28 to 85) and mean follow-up of 7.5 years (0.1 to 10.8) participating in our in-depth modern MoM follow-up programme were included in the study, which involved recording whole blood cobalt and chromium ion measurements, Oxford hip scores (OHS) and plain radiographs of the hip and targeted cross-sectional imaging. Elevated blood metal ion levels (> 5 parts per billion) were seen in 32 (16.1%) of the 199 patients who underwent unilateral replacement. At 23 months after the start of our modern MoM follow-up programme, 29 new cases of ARMD had been revealed. Hence, the nine-year survival of this cohort declined from 96% (95% CI 95 to 98) with the old surveillance routine to 86% (95% CI 82 to 90) following the new protocol. Although ARMD may not be as common in 36 mm MoM THRs as in those with larger heads, these results support the Medicines and Healthcare Products Regulatory Agency guidelines on regular reviews and further investigations, and emphasise the need for specific a follow-up programme for patients with MoM THRs.

Resistin as a factor in osteoarthritis: synovial fluid resistin concentrations correlate positively with interleukin 6 and matrix metalloproteinases MMP-1 and MMP-3.

OBJECTIVES: Resistin is an adipocytokine that has been related to inflammation and insulin resistance. Following knee injury, elevated levels of resistin have been found in synovial fluid (SF) while very little is known about the role of resistin in osteoarthritis (OA). The aim of the present study was to investigate resistin levels in OA joints and to determine if it is associated with inflammatory and catabolic factors in the joints. METHOD: SF, plasma, and cartilage samples were collected from 88 OA patients undergoing knee replacement surgery. Resistin levels were measured by enzyme-linked immunosorbent assay (ELISA) in SF, plasma, and cartilage culture media. RESULTS: Significant levels of resistin [0.75 (0.67) ng/mL; median (IQR)] were found in SF from OA patients. Resistin correlated positively with interleukin (IL)-6 (r = 0.39, p < 0.001) and with matrix metalloproteinases MMP-1 (r = 0.31, p = 0.004) and MMP-3 (r = 0.24, p = 0.024) in SF. Resistin was also released from cultured OA cartilage and it correlated with resistin levels in SF (r = 0.39, p < 0.001). In addition, resistin levels in plasma correlated positively with those in SF (r = 0.44, p < 0.001). There were no differences in SF or plasma resistin concentrations between females and males or between non-diabetic and diabetic patients, and resistin did not correlate with body mass index (BMI). CONCLUSIONS: Resistin is present in OA joints and is released from OA cartilage. Levels of resistin in SF are associated with inflammatory and catabolic factors, suggesting that resistin has a role to play in the pathogenesis of, and as a possible drug target in, OA.

Expression of IL-10 family cytokines in rheumatoid arthritis: elevated levels of IL-19 in the joints.

OBJECTIVES: Interleukin (IL)-10 functions as an anti-inflammatory cytokine in rheumatoid arthritis (RA). New IL-10 family cytokines IL-19, IL-20, IL-22, IL-24, and IL-26 have recently been discovered. Information concerning the expression and function of these cytokines in autoimmune diseases is currently limited. The aim of this study was to investigate their expression in RA. METHODS: mRNA levels of the cytokines were studied using quantitative reverse transcriptase polymerase chain reaction (RT-PCR). Peripheral blood (PB) and synovial fluid (SF) mononuclear cells (MCs), purified T cells, and monocytes/macrophages from RA patients and healthy volunteers, and synovial tissues from patients with RA or osteoarthritis (OA), were examined. The expression of IL-19 protein in T cells and monocytes/macrophages was studied by flow cytometry. RESULTS: IL-10 and IL-19 mRNA levels were significantly elevated in SFMCs from patients with RA compared with PBMCs from RA patients or healthy volunteers. IL-20 and IL-22 mRNA levels were also upregulated in RA SFMCs but their level of expression was lower than that of IL-10 or IL-19. Importantly, synovial tissue IL-19 levels in RA were increased when compared with OA. IL-19 expression was upregulated in both T cells and macrophages derived from patients with RA. IL-1beta increased IL-19 levels in PBMCs, suggesting that elevated levels of IL-1 in RA joints may contribute to upregulated IL-19 expression. CONCLUSIONS: The majority of the IL-10 family cytokines are expressed in RA. IL-19 demonstrated the highest expression in rheumatoid joints, and could thus be involved in the regulation of synovial inflammation in RA.

Selective iNOS inhibitor 1400W enhances anti-catabolic IL-10 and reduces destructive MMP-10 in OA cartilage. Survey of the effects of 1400W on inflammatory mediators produced by OA cartilage as detected by protein antibody array.

OBJECTIVES: In osteoarthritis (OA), the balance between catabolic and anabolic mediators and their regulators in cartilage is disturbed. Proinflammatory cytokine interleukin-1 (IL-1) plays a central role in cartilage destruction and nitric oxide (NO) mediates many of its destructive effects. In the present study, we investigated the secretion of 40 mediators related to inflammation or cartilage degradation by OA cartilage samples with a protein antibody array. The effects of IL-1 and a selective iNOS-inhibitor 1400W on the mediator release were also studied. METHODS: Cartilage tissue was obtained from the leftover pieces of total knee replacement surgery from OA patients. Protein antibody array was used to measure production of 40 mediators in the culture medium. ELISA was used to confirm the antibody array results. RESULTS: OA cartilage secreted spontaneously 15 out of the 40 measured mediators. IL-1Beta enhanced production of 11 of these inflammatory mediators in OA cartilage along with increased NO production. Treatment with a selective iNOS inhibitor 1400W enhanced the production of IL-10, while the levels of MMP-10 were reduced in IL-1 -treated OA cartilage. CONCLUSION: OA cartilage produces many of the mediators involved in the pathogenesis of OA. The ability of 1400W to enhance levels of anti-catabolic IL-10 and to reduce levels of destructive MMP-10 points to the anti-inflammatory mechanisms that iNOS-inhibitors may have.

The role of nitric oxide in osteoarthritis.

Elevated levels of markers of nitric oxide (NO) production are found in osteoarthritic joints suggesting that NO is involved in the pathogenesis of osteoarthritis (OA). In OA, NO mediates many of the destructive effects of interleukin-1 (IL-1) and tumour necrosis factor-alpha (TNF-alpha) in the cartilage, and inhibitors of NO synthesis have demonstrated retardation of clinical and histological signs and symptoms in experimentally induced OA and other forms of arthritis. As an important factor in cartilage, the regulation of inducible nitric oxide synthase (iNOS) expression and activity, and the effects of NO are reviewed, especially in relation to the pathogenesis of OA.

The expression of SOCS is altered in rheumatoid arthritis.

OBJECTIVES: Cytokines play a key pathogenic role in rheumatoid arthritis (RA). Several cytokines signal through the JAK-STAT pathway, which is negatively regulated by the suppressors of cytokine signalling (SOCS) proteins. Since SOCS protein levels can profoundly modulate cellular responses to cytokines, we have investigated their expression in chronic RA. METHODS: The levels of SOCS1-3 and CIS1 mRNA in peripheral blood (PB) and synovial fluid (SF) mononuclear cells (MCs), purified T cells and monocytes from RA patients and healthy volunteers were studied using quantitative reverse transcriptase polymerase chain reaction (RT-PCR). SOCS mRNA and protein expression in synovial tissues were examined by RT-PCR and immunohistochemistry. RESULTS: The levels of SOCS1 and SOCS3 were significantly increased in PBMCs from RA patients when compared with healthy volunteers. These differences were mainly due to up-regulation of SOCS1 in PB T cells and of SOCS3 in PB monocytes. In addition, SOCS2 was up-regulated in PB T cells. Interestingly, SF T cells expressed lower and SF macrophages higher levels of SOCS molecules than their PB counterparts. Similarly, while a significant portion of macrophages in synovial tissues expressed SOCS1 and SOCS3 proteins, the majority of T cells remained SOCS negative. Finally, SOCS1 was up-regulated in the synovial membranes from patients with RA when compared with osteoarthritis. CONCLUSIONS: SOCS expression levels are profoundly altered in RA, and the profile of SOCS expression is dependent on both the cell type as well as the cellular compartment.

Spacer prostheses in two-stage revision of infected knee arthroplasty.

At present, no consensus exists on the best spacer alternative for the management of two-stage exchange arthroplasty of infected knee arthroplasties. In this retrospective study, patient records of 24 patients, who had undergone two-stage revisions in which resterilised prosthetic components were used as spacers, were reviewed. The outcome was compared to that of operations performed during the same period (1993-2003) using cement spacers (n=10). With an average follow-up of 32 months, control of infection was achieved in 26 cases (76%), with good or excellent clinical outcome in 19 cases (56%). Treatment failed and resulted in amputation at the level of the thigh before reimplantation in one case. Three patients did not undergo reimplantation. In four cases (12%) infection relapsed. The reinfection rate did not differ between the two spacer groups. Patients treated with resterilised components had a superior range of motion during the period between the two stages. Operative time was shorter and there was less blood loss in the reimplantation arthroplasty when a prosthetic spacer was used. We consider resterilised prosthetic components a safe and effective alternative to cement spacers in the management of infected knee arthroplasties.

TGFbeta inhibits IL-1 -induced iNOS expression and NO production in immortalized chondrocytes.

OBJECTIVE: The balance between anti-inflammatory (e.g. TGFbeta) and proinflammatory cytokines (e.g. IL-1 and TNFalpha), regulates destructive processes in OA cartilage. IL-1 and TNFalpha enhance nitric oxide (NO) production in OA cartilage through the inducible nitric oxide synthase (iNOS) pathway and NO mediates many of the destructive effects of these cytokines. The aim of the present study was to investigate the effects of TGFbeta on NO production in immortalized H4 chondrocytes exposed to IL-1. RESULTS: IL-1 induced NO production in chondrocytes through nuclear factor kappa B (NF-kappaB) sensitive and dexamethasone insensitive expression of iNOS. TGFbeta inhibited IL-1 -induced iNOS expression and NO production in chondrocytes, but it did not have any effect on iNOS mRNA levels. iNOS protein levels were similar in cells treated with IL-1 or IL-1+TGFbeta when measured after 8 h incubation, whereas when measured after 12 h and 24 h incubations, iNOS protein levels were 50% and 80% lower in cells treated with IL-1+TGFbeta than in cells treated with IL-1 alone. CONCLUSION: TGFbeta suppressed IL-1-induced iNOS expression and NO production in chondrocytes, probably by enhancing iNOS protein degradation. This finding suggests an additional mechanism for TGFbeta to counteract the destructive effects of IL-1 in OA.

Aurothiomalate and hydroxychloroquine inhibit nitric oxide production in chondrocytes and in human osteoarthritic cartilage.

OBJECTIVES: Nitric oxide (NO) is a destructive mediator produced by activated chondrocytes. The aim of the present study was to investigate the effect of disease-modifying anti-rheumatic drugs (DMARDs) on interleukin-1beta (IL-1beta)-induced NO production in chondrocyte cultures, and in human osteoarthritic cartilage. RESULTS: Aurothiomalate, hydroxychloroquine, methotrexate and leflunomide inhibited IL-1beta-induced inducible NO synthase (iNOS) expression and NO production in immortalized H4 chondrocytes, while penicillamine and sulfasalazine had no effect. This can be explained by the fact that the four effective DMARDs also suppressed IL-1beta-induced activation of nuclear factor kappa B (NF-kappaB), which is a crucial transcription factor for iNOS. Aurothiomalate and hydroxychloroquine also inhibited IL-1beta-induced NO production in OA cartilage whereas methotrexate and leflunomide had no effect. CONCLUSION: Aurothiomalate and hydroxychloroquine suppressed IL-1beta-induced NO production in chondrocyte cultures and in OA cartilage. The results suggest an additional anti-inflammatory mechanism for aurothiomalate and hydroxychloroquine and indicates their possible therapeutic value in the treatment of osteoarthritis (OA).

Effects of TNFalpha-antagonists on nitric oxide production in human cartilage.

OBJECTIVE: Nitric oxide (NO) produced by cartilage and synovial membrane is implicated in the pathogenesis of osteoarthritis (OA) and rheumatoid arthritis (RA). In inflamed joints NO is synthesized in response to proinflammatory cytokines and it is involved in the joint destruction. The aim of the present study was to investigate the effects of TNFalpha-antagonists infliximab and etanercept on NO production in human cartilage. DESIGN: Cartilage specimen obtained from OA patients undergoing knee replacement surgery were studied for iNOS expression and NO production in organ culture to allow intact chondrocyte-matrix interactions. TNFalpha and soluble TNFalpha receptor release was measured by ELISA. RESULTS: Osteoarthritic cartilage produced NO spontaneously and its production was enhanced by proinflammatory cytokines TNFalpha (tumor necrosis factor alpha), IL-1beta (interleukin-1beta), IL-17 (interleukin-17) and by bacterial lipopolysaccharide (LPS). TNFalpha-antagonists infliximab and etanercept inhibited TNFalpha-induced NO production in a dose dependent manner but they had no effect on IL-1beta-, IL-17- and LPS-stimulated NO synthesis. TNFalpha and soluble TNFalpha receptors (sTNFRI and sTNFRII) were produced by human osteoarthritic cartilage. A neutralizing antibody against soluble TNFRI enhanced spontaneous NO production whereas an antibody against soluble TNFRII had no effect. CONCLUSIONS: TNFalpha-antagonists infliximab and etanercept suppressed TNFalpha-induced NO production. This effect was not seen on IL-1-, IL-17- or LPS-induced NO production suggesting that TNFalpha is not an autacoid mediator in these processes. The studies with neutralizing antibodies against soluble TNFRI suggest that endogenous cartilage-derived TNFalpha-antagonists modulate NO production in osteoarthritic cartilage.

Regulation of the nitric oxide production resulting from the glucocorticoid-insensitive expression of iNOS in human osteoarthritic cartilage.

OBJECTIVE: Nitric oxide (NO) produced by cartilage and synovial membranes is implicated in the pathogenesis of osteoarthritis (OA) and inhibitors of NO synthesis may have indications in the treatment or prevention of joint destruction in OA. Because the signaling mechanisms as well as the NOS isoform involved in induction of NO production in human cartilage remain in many parts unclear, the present study was designed to investigate the regulation of inducible NO synthesis in human intact OA cartilage. METHODS: Cartilage specimens were collected from OA patients undergoing knee replacement surgery and studied for iNOS expression and NO production in organ culture to allow intact chondrocyte-matrix interactions. J774 macrophages were used for comparison as a well-documented source of iNOS. RESULTS: OA cartilage expressed iNOS and produced NO in the absence of exogenous cytokines. Addition of interleukin-1 beta (IL-1 beta), tumor necrosis factor alpha (TNF alpha) or lipopolysaccharide (LPS) into the culture medium enhanced NO production in a dose-and time-dependent manner. Various NOS inhibitors suppressed NO production in the following order of potency: 1400W (novel selective iNOS inhibitor)=L-NIO>L-NMMA>L-NAME. Cycloheximide (an inhibitor of protein synthesis), pyrrolidine dithiocarbamate (PDTC; an NF-kappa B inhibitor) and genistein (an inhibitor of tyrosine protein kinases) inhibited cytokine-induced NO production, while dexamethasone, diaminohydroxypyrimidine (DAHP; an inhibitor of tetrahydrobiopterin synthesis) and PD 98059 (p42/44 MAP kinase inhibitor) had no effect. CONCLUSIONS: The results suggest that NO synthesis in human osteoarthritic cartilage derives from the glucocorticoid-insensitive expression of iNOS. Very similar mechanisms appear to regulate inducible NO synthesis in human osteoarthritic cartilage and J774 macrophages with the exception that dexamethasone inhibited NO production in J774 cells but not in osteoarthritic cartilage.

The femoral canal fill of two different cementless stem designs. The accuracy of radiographs compared to computed tomographic scanning.

In 19 cadaver femora we compared the fill of two types of femoral stems (plastic replica) using computed tomographic (CT) scan with a border detecting computer program and conventional radiographs. In the metaphyseal area the fill of the two types was surprisingly similar. In the diaphysis the straight stem filled significantly more than the proximally anatomic and distally over-reamed stem. Using conventional radiographs the fill measures were from 1.2 to 2.1 times higher than the values of CT scan, depending on the method of calculation. When both anteroposterior and lateral views were used, the fill as measured by radiographs correlated well with the fill as measured using CT scan. When conventional radiographs are used for evaluation of the canal fill, the calculation based on hypothetical rectangular areas at each level seemed to provide the most accurate results.

Alarming wear of the first-generation polyethylene liner of the cementless porous-coated Biomet Universal cup: 107 hips followed for mean 6 years.

Wear of the socket liner and resulting osteolysis are the major causes of failure in cementless hip arthroplasties. We report alarming wear of the first-generation polyethylene liner of the cementless porous-coated Biomet Universal cup. Radiographs of 107 primary hip arthroplasties were analyzed retrospectively. The mean follow-up time was 74 (47-91) months. The linear wear of the polyethylene liners was assessed using a modification of the Livermore method. The median linear wear was 1.0 (0-6.2) and the median linear wear rate was 0.17 mm/year. There was a statistically significant difference between the 28 mm and 32 mm femoral head groups both in the volumetric wear and in the volumetric wear rate. The median linear wear was 0.28 mm/year and 0.14 mm/year for the 32 mm and 28 mm heads, respectively. So far, 14 revisions have been performed or have been scheduled because of excessive wear of the polyethylene liner. In regression analysis, the factors related to the wear rate were the 32 mm size of the femoral head and screw fixation of acetabular shell. We found that the cases with calcar rounding were associated with significantly greater wear. Possible reasons for increased wear of the Hexloc liner may be the cylindrical design, thin polyethylene, and poor quality of the polyethylene. Regular clinical and radiographic follow-ups are recommended especially for hips with 32 mm femoral heads or with screw fixation. If progressive wear of the liner is observed, revision must be considered.

The effects of cementless femoral stem shape and proximal surface texture on 'fit-and-fill' characteristics and on bone remodeling.

We measured the post-operative radiological "fit and fill" of two different femoral stem designs, one with a straight proximally porous-coated (Bi-Metric, n=50) and the other with a proximally anatomic, hydroxyapatite-coated and distally over-reamed stem (ABG, n=26). A comparison was then made between the clinical and radiological 5-year follow-up data of these two series and also of the bone remodeling changes around the stems. The observed differences in "fit and fill" parameters in the metaphyseal region were minute. However, in the diaphyseal bone the straight stem had substantially more cortical contact. The clinical results were excellent for both groups. Subsidence (>2 mm) was more frequent with the anatomical ABG stems, although the ABG stems had better bone ingrowth in the lower metaphyseal area. The present results indicate that the anatomical design may improve the fit and fill of a femoral stem in the metaphysis. On the other hand, a looser fill of the diaphyseal bone made the stems of this type more susceptible to subsidence. The straight stem with tight diaphyseal fit showed excellent stability, but the good bone ingrowth and remodeling around the distal part of the stem indicates stress transfer through this region and increased stress shielding of the proximal metaphyseal femur.

Diversity of proximal femoral medullary canal.

To analyze the endosteal dimensions of the proximal femoral medullary canal, we studied 50 cadaver femora using computed tomography and a border detection method from 20 mm above the lesser trochanter, the osteotomy level, down to the isthmus. We documented the presence of a dense calcar septum in 96% of femora studied. In addition to mediolateral, anteroposterior, and neck-oriented dimensions, we calculated canal flare indices (CFIs) between the osteotomy level and the isthmus and metaphyseal canal flare indices (MCFIs) between the osteotomy level and the level 20 mm below the lesser trochanter midpoint to describe the shape of the endosteal cavity. With respect to the canal opening, the anteroposterior and mediolateral planes parallelled each other over the entire region as indicated by the high correlation (r = .7, P < .001) between the CFIs in these directions. The prediction of one dimension from another was unreliable in the metaphyseal region, where bone ingrowth is supposed to occur in a femoral prosthesis. The MCFI seemed to be the best parameter to distinguish the various types of proximal femoral canal shapes. We have described the variability of the proximal femoral endosteal dimensions in detail and find that the wide variation in the shape and size of the proximal femoral medullary canal means that it is almost impossible to achieve 100% cortical contact with the stem, especially in the metaphysis.