The role of inhibition by phosphocitrate and its analogue in chondrocyte differentiation and subchondral bone advance in Hartley guinea pigs.

Phosphocitrate (PC) and its analogue, PC-ß ethyl ester, inhibit articular cartilage degeneration in Hartley guinea pigs. However, the underlying molecular mechanisms remain unclear. The present study aimed to investigate the hypothesis that PC exerted its disease-modifying effect on osteoarthritis (OA), in part, by inhibiting a molecular program similar to that in the endochondral pathway of ossification. The results demonstrated that severe proteoglycan loss occurred in the superficial and middle zones, as well as in the calcified zone of articular cartilage in the Hartley guinea pigs. Subchondral bone advance was greater in the control Hartley guinea pigs compared with PC- or PC analogue-treated guinea pigs. Resorption of cartilage bars or islands and vascular invasion in the growth plate were also greater in the control guinea pigs compared with the PC- or PC analogue-treated guinea pigs. The levels of matrix metalloproteinase-13 and type X collagen within the articular cartilage and growth plate were significantly increased in the control guinea pigs compared with PC-treated guinea pigs (P<0.05). These results indicated that articular chondrocytes in Hartley guinea pigs exhibited a hypertrophic phenotype and recapitulated a developmental molecular program similar to the endochondral pathway of ossification. Activation of this molecular program resulted in resorption of calcified articular cartilage and subchondral bone advance. This suggests that PC and PC analogues exerted their OA disease-modifying activity, in part, by inhibiting this molecular program.

Eight Hundred Twenty-Five Medial Mobile-Bearing Unicompartmental Knee Arthroplasties: The First 10-Year US Multi-Center Survival Analysis.

BACKGROUND: FDA approval for the Oxford phase III device was approved for use in the United States in 2004. This study seeks to provide the first long-term, large patient sample size, Oxford phase III multi-site survivorship study in the United States, investigating patient reported outcomes of pain and function, while also providing an in-depth analysis of causes for revision, and finally addressing recent advancements that can help aid the unicompartmental knee arthroplasty (UKA) process and further improve partial knee survivorship. METHODS: Between July 2004 and December 2006, 5 surgeons from around the United States performed medial UKA through the minimally invasive surgical approach, on 825 knees in 695 patients. This was a consecutive series of primary UKAs using the phase III mobile bearing; cemented Oxford Knee (Zimmer Biomet, Warsaw, IN), implanted utilizing phase III instrumentation. UKA survivorship considered all revisions as the end point. Implant survivorship eliminated revisions at which the original Oxford implant was determined to be well fixated and functional intra-operatively. RESULTS: A total of 93 knees were revised in this study. Mean follow-up was 9.7 years (6-12). Implant survivorship at year 10 was 90% (confidence interval 2.7%). UKA survivorship at year 10 was 85% (confidence interval 3.8%). Average preoperative American Knee Society Score (knee score) was 49 and rose to 90 postoperatively (standard deviations 16 and 18, respectively). Average preoperative American Knee Society Score (function score) was 55 and rose to 77 postoperatively (standard deviations 15 and 28, respectively). CONCLUSION: This was the first large-scale, 10-year, multi-site follow-up of the Oxford mobile-bearing medial UKA undertaken in the United States, displaying good survivorship and excellent patient outcomes.

Biological effects and osteoarthritic disease-modifying activity of small molecule CM-01.

Phosphocitrate inhibits cartilage degeneration, however, the prospect of phosphocitrate as an oral disease modifying drug might be limited. The purpose of this study was to investigate the biological effects and disease-modifying activity of a phosphocitrate "analog," CM-01 (Carolinas Molecule-01), and test the hypothesis that CM-01 is a disease modifying drug for osteoarthritis therapy. The effects of CM-01 on calcium crystal-induced expression of matrix metalloproteinase-1 and interleukin-1 beta, cell-mediated calcification and production of proteoglycan by chondrocytes were examined in cell cultures. Disease-modifying activity was examined using Hartley guinea pig model of posttraumatic osteoarthritis. Cartilage degeneration in untreated and CM-01 treated guinea pigs was examined with Indian ink and Safranin-O-fast green. Levels of matrix metalloproteinase-13, ADAM metallopeptidase with thrombospondin type 1 motif 5, chemokine (C-C motif) ligand 5, and cyclooxygenase 2 were examined with immunostaining. CM-01 inhibited crystal-induced expression of matrix metalloproteinase-1 and interleukin-1ß, reduced cell-mediated calcification, and stimulated the production of proteoglycan by chondrocytes. In Hartley guinea pigs, CM-01 not only reduced damages in articular surface but also reduced resorption of calcified zone cartilage. The reduction in cartilage degeneration was accompanied by decreased levels of matrix metalloproteinase-13, ADAM metallopeptidase with thrombospondin type 1 motif 5, chemokine (C-C motif) ligand 5 and cyclooxygenase 2. These findings confirmed that CM-01 is a promising candidate to be tested as an oral drug for human OA therapy. CM-01 exerted its disease-modifying activity on osteoarthritis, in part, by inhibiting the production of matrix-degrading enzymes and a molecular program resembling the endochondral pathway of ossification. © 2017 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 36:309-317, 2018.

Biological Effects of Phosphocitrate on Osteoarthritic Articular Chondrocytes.

BACKGROUND: Phosphocitrate (PC) inhibits osteoarthritis (OA) in Hartley guinea pigs. However, the underlying molecular mechanisms remain poorly understood. OBJECTIVE: This study sought to examine the biological effect of PC on OA chondrocytes and test the hypothesis that PC may exert its OA disease modifying effect, in part, by inhibiting the expression of genes implicated in OA disease process and stimulating the production of extracellular matrices. METHOD: OA chondrocytes were cultured in the absence or presence of PC. Total RNA was extracted and subjected to microarray analyses. The effect of PC on proliferation and chondrocyte-mediated calcification were examined in monolayer culture. The effect of PC on the production of extracellular matrices was examined in micromass culture. RESULTS: PC downregulated the expression of numerous genes classified in proliferation and apoptosis while upregulating the expression of many genes classified in transforming growth factor-ß (TGF-ß) receptor signaling pathway and ossification. PC also downregulated the expressions of many genes classified in inflammatory response and Wnt receptor signaling pathways. Consistent with its effect on the expression of genes classified in proliferation, ossification, and skeletal development, PC inhibited the proliferation of OA chondrocytes and chondrocyte-mediated calcification while stimulating the production of extracellular matrices. CONCLUSION: PC may exert its OA disease modifying effect, in part, through a crystal-independent mechanism or by inhibiting the expressions of many genes implicated in OA disease process, and at the same time, stimulating the expression of genes implicated in chondroprotection and production of extracellular matrices.

Patient-Directed Valgus Stress Radiograph of the Knee: A New and Novel Technique.

The radiographic investigation of patients with medial-compartment osteoarthritis of the knee is a critical element in the decision-making process of determining whether the patient is a candidate for unicompartmental or total knee arthroplasty. A valgus stress radiograph of the affected knee is an essential part of this radiographic investigation. Historically, this has been performed with manual stress applied by the surgeon or the radiologic technologist; thus, this examination requires 2 individuals to complete. In addition to being inefficient, 1 individual is exposed to radiation, which can be undesirable over many exposures and in a long career. For these reasons, we instituted a quality improvement project to develop a method of obtaining the valgus stress view with 1 technologist that would obviate these concerns. Of 78 examinations performed, 5 studies did not show complete correction of the varus deformity. Of these, 3 showed complete correction on a manual valgus stress radiograph, and 2 did not. Three patients displayed collapse of the lateral compartment, indicating a nonfunctional lateral compartment. The remaining 70 patients had identical radiographic results with both the manual and patient-directed valgus stress.

Disease-modifying effects of phosphocitrate and phosphocitrate-ß-ethyl ester on partial meniscectomy-induced osteoarthritis.

BACKGROUND: It is believed that phosphocitrate (PC) exerts its disease-modifying effects on osteoarthritis (OA) by inhibiting the formation of crystals. However, recent findings suggest that PC exerts its disease-modifying effect, at least in part, through a crystal-independent action. This study sought to examine the disease-modifying effects of PC and its analogue PC-ß-ethyl ester (PC-E) on partial meniscectomy-induced OA and the structure-activity relationship. METHODS: Calcification- and proliferation-inhibitory activities were examined in OA fibroblast-like synoviocytes (FLSs) culture. Disease-modifying effects were examined using Hartley guinea pigs undergoing partial meniscectomy. Cartilage degeneration was examined with Indian ink, safranin-O, and picrosirius red. Levels of matrix metalloproteinase-13 (MMP-13), ADAM metallopeptidase with thrombospondin type 1 motif 5 (ADAMTS5), chemokine (C-C motif) ligand 5 (CCL5), and cyclooxygenase-2 (Cox-2) were examined with immunostaining. The effects of PC-E and PC on gene expressions in OA FLSs were examined with microarray. Results are expressed as mean ± standard deviation and analyzed using Student's t test or Wilcoxon rank sum test. RESULTS: PC-E was slightly less powerful than PC as a calcification inhibitor but as powerful as PC in the inhibition of OA FLSs proliferation. PC significantly inhibited cartilage degeneration in the partial meniscectomied right knee. PC-E was less powerful than PC as a disease-modifying drug, especially in the inhibition of cartilage degeneration in the non-operated left knee. PC significantly reduced the levels of ADAMTS5, MMP-13 and CCL5, whereas PC-E reduced the levels of ADAMTS5 and CCL5. Microarray analyses revealed that PC-E failed to downregulate the expression of many PC-downregulated genes classified in angiogenesis and inflammatory response. CONCLUSIONS: PC is a disease-modifying drug for posttraumatic OA therapy. PC exerts its disease-modifying effect through two independent actions: inhibiting pathological calcification and modulating the expression of many genes implicated in OA. The ß-carboxyl group of PC plays an important role in the inhibition of cartilage degeneration, little role in the inhibition of FLSs proliferation, and a moderate role in the inhibition of FLSs-mediated calcification.

Cartilage Degeneration, Subchondral Mineral and Meniscal Mineral Densities in Hartley and Strain 13 Guinea Pigs.

Osteoarthritis is a joint disease involved in articular cartilage, subchondral bone, meniscus and synovial membrane. This study sought to examine cartilage degeneration, subchondral bone mineral density (BMD) and meniscal mineral density (MD) in male Hartley, female Hartley and female strain 13 guinea pigs to determine the association of cartilage degeneration with subchondral BMD and meniscal MD. Cartilage degeneration, subchondral BMD and meniscal MD in 12 months old guinea pigs were examined with histochemistry, X-ray densitometry and calcium analysis. We found that male Hartley guinea pigs had more severe cartilage degeneration, subchondral BMD and meniscal MD than female Hartley guinea pigs, but not female strain 13 guinea pigs. Female strain 13 guinea pigs had more severe cartilage degeneration and higher subchondral BMD, but not meniscal MD, than female Hartley guinea pigs. These findings indicate that higher subchondral BMD, not meniscal MD, is associated with more severe cartilage degeneration in the guinea pigs and suggest that abnormal subchondral BMD may be a therapeutic target for OA treatment. These findings also indicate that the pathogenesis of OA in the male guinea pigs and female guinea pigs are different. Female strain 13 guinea pig may be used to study female gender-specific pathogenesis of OA.

Early Fracture of a Vitamin-E-Infused, Highly Cross-Linked Polyethylene Liner After Total Hip Arthroplasty: A Case Report.

CASE: A vitamin-E-infused, highly cross-linked ultra-high molecular weight polyethylene (HXLPE) acetabular liner fractured without trauma less than twelve months after its implantation in a seventy-one-year-old woman. CONCLUSION: The remelting process utilized in the production of many commercially available HXLPE acetabular liners causes an immediate reduction in the fracture toughness of the material; however, it provides the benefit of oxidative stability, which prevents the loss of beneficial mechanical properties over time. Vitamin-E-infused HXLPE avoids the immediate decrease in fracture toughness by avoiding the remelting process. The case of our patient demonstrates that this material still can experience catastrophic failure despite acceptable component positioning.

Expression of phosphocitrate-targeted genes in osteoarthritis menisci.

Phosphocitrate (PC) inhibited calcium crystal-associated osteoarthritis (OA) in Hartley guinea pigs. However, the molecular mechanisms remain elusive. This study sought to determine PC targeted genes and the expression of select PC targeted genes in OA menisci to test hypothesis that PC exerts its disease modifying activity in part by reversing abnormal expressions of genes involved in OA. We found that PC downregulated the expression of numerous genes classified in immune response, inflammatory response, and angiogenesis, including chemokine (C-C motif) ligand 5, Fc fragment of IgG, low affinity IIIb receptor (FCGR3B), and leukocyte immunoglobulin-like receptor, subfamily B member 3 (LILRB3). In contrast, PC upregulated the expression of many genes classified in skeletal development, including collagen type II alpha1, fibroblast growth factor receptor 3 (FGFR3), and SRY- (sex determining region Y-) box 9 (SOX-9). Immunohistochemical examinations revealed higher levels of FCGR3B and LILRB3 and lower level of SOX-9 in OA menisci. These findings indicate that OA is a disease associated with immune system activation and decreased expression of SOX-9 gene in OA menisci. PC exerts its disease modifying activity on OA, at least in part, by targeting immune system activation and the production of extracellular matrix and selecting chondroprotective proteins.

Fibroblast-like synoviocytes induce calcium mineral formation and deposition.

Calcium crystals are present in the synovial fluid of 65%-100% patients with osteoarthritis (OA) and 20%-39% patients with rheumatoid arthritis (RA). This study sought to investigate the role of fibroblast-like synoviocytes (FLSs) in calcium mineral formation. We found that numerous genes classified in the biomineral formation process, including bone gamma-carboxyglutamate (gla) protein/osteocalcin, runt-related transcription factor 2, ankylosis progressive homolog, and parathyroid hormone-like hormone, were differentially expressed in the OA and RA FLSs. Calcium deposits were detected in FLSs cultured in regular medium in the presence of ATP and FLSs cultured in chondrogenesis medium in the absence of ATP. More calcium minerals were deposited in the cultures of OA FLSs than in the cultures of RA FLSs. Examination of the micromass stained with nonaqueous alcoholic eosin indicated the presence of birefringent crystals. Phosphocitrate inhibited the OA FLSs-mediated calcium mineral deposition. These findings together suggest that OA FLSs are not passive bystanders but are active players in the pathological calcification process occurring in OA and that potential calcification stimuli for OA FLSs-mediated calcium deposition include ATP and certain unidentified differentiation-inducing factor(s). The OA FLSs-mediated pathological calcification process is a valid target for the development of disease-modifying drug for OA therapy.

Biological activities of phosphocitrate: a potential meniscal protective agent.

Phosphocitrate (PC) inhibited meniscal calcification and the development of calcium crystal-associated osteoarthritis (OA) in Hartley guinea pigs. However, the mechanisms remain elusive. This study sought to examine the biological activities of PC in the absence of calcium crystals and test the hypothesis that PC is potentially a meniscal protective agent. We found that PC downregulated the expression of many genes classified in cell proliferation, ossification, prostaglandin metabolic process, and wound healing, including bloom syndrome RecQ helicase-like, cell division cycle 7 homolog, cell division cycle 25 homolog C, ankylosis progressive homolog, prostaglandin-endoperoxide synthases-1/cyclooxygenase-1, and plasminogen activator urokinase receptor. In contrast, PC stimulated the expression of many genes classified in fibroblast growth factor receptor signaling pathway, collagen fibril organization, and extracellular structure organization, including fibroblast growth factor 7, collagen type I, alpha 1, and collagen type XI, alpha 1. Consistent with its effect on the expression of genes classified in cell proliferation, collagen fibril organization, and ossification, PC inhibited the proliferation of OA meniscal cells and meniscal cell-mediated calcification while stimulating the production of collagens. These findings indicate that PC is potentially a meniscal-protective agent and a disease-modifying drug for arthritis associated with severe meniscal degeneration.

Phosphocitrate is potentially a disease-modifying drug for noncrystal-associated osteoarthritis.

Phosphocitrate (PC), a calcification inhibitor, inhibits the development of crystal-associated osteoarthritis (OA) in Hartley guinea pigs. However, the molecular mechanisms underlying its disease-modifying effect remain elusive. This study sought to test the hypothesis that PC has calcium crystal-independent biological activities which are, at least in part, responsible for its disease-modifying activity. We found that PC inhibited the proliferation of OA fibroblast-like synoviocytes in the absence of calcium crystals. Consistent with its effect on cell proliferation, PC downregulated the expression of numerous genes classified in cell proliferation. PC also downregulated the expression of many genes classified in angiogenesis and inflammatory response including prostaglandin-endoperoxide synthase 2, interleukin-1 receptor, type I, and chemokine (C-C motif) ligand 2. In contrast, PC upregulated the expression of many genes classified in musculoskeletal tissue development, including aggrecan, type I collagen, and insulin-like growth factor binding protein 5. These findings suggest that PC is not only a promising disease-modifying drug for crystal-associated OA but also for noncrystal-associated OA.

Histological examination of collagen and proteoglycan changes in osteoarthritic menisci.

This study sought to examine collagen and proteoglycan changes in the menisci of patients with osteoarthritis (OA). Collagens were examined using picrosirius red, and hematoxylin and eosin. Proteoglycans were examined using safranin-O and alcian blue. Types I and II collagens and aggrecan were examined using immunochemistry. Severe loss of collagens was observed to occur in OA menisci, particularly in the middle and deep zones and collagen networks were less organized than those of normal menisci. In contrast, proteoglycan staining in the middle and deep zones of OA meniscus increased compared to normal control menisci. Immunohistochemistry indicated that types I and II collagens were co-localized and the loss of types I collagen in OA menisci appeared more severe in the middle and deep zones than that in the surface zones. The loss of type II collagen however was severe across all three zones. Immunohistochemistry also indicated elevated aggrecan staining in OA menisci. These findings together indicate that severe loss of collagens and intrameniscal degeneration are hallmarks of OA menisci and that extracellular matrix degeneration occurred in OA menisci follows a pathway different from that occurred in OA articular cartilage. These findings are not only important for a better understanding of the disease process but also important for the development of novel structure-modifying drugs for OA therapy.

Meniscal calcification, pathogenesis and implications.

PURPOSE OF REVIEW: The purpose of this review is to discuss recent advances in the understanding of the nature of meniscal calcification and its relationships with meniscal degeneration and cartilage lesions in osteoarthritis. RECENT FINDINGS: Calcium crystals are universally present in hyaline articular cartilage, as well as the meniscus of the knee of end-stage osteoarthritis patients. Osteoarthritis meniscal cells display a distinct gene-expression profile different from normal meniscal cells, have elevated expression of ankylosis progressive analog (ANKH) and ectonucleotide pyrophosphatase/phosphodiesterase1 (ENPP1) and produce more calcium minerals than normal meniscal cells in vitro. Meniscal calcification is positively associated with meniscal degeneration, which is an early event in the development of osteoarthritis and correlates with cartilage lesions and clinical osteoarthritis scores. Phosphocitrate is a potent calcification inhibitor of osteoarthritis meniscal cell-mediated calcium deposition. Its effect on preventing meniscal degeneration and the molecular mechanisms underlying its disease-modifying activity in osteoarthritis remains elusive. SUMMARY: Recent findings support a pathogenic role of meniscal calcification in osteoarthritis. Meniscal calcification, similar to meniscal degeneration, is a predisposing factor for cartilage lesions. Meniscal calcification is a new target for the development of therapeutic disease-modifying drugs for osteoarthritis.

Calcium deposition in osteoarthritic meniscus and meniscal cell culture.

INTRODUCTION: Calcium crystals exist in the knee joint fluid of up to 65% of osteoarthritis (OA) patients and the presence of these calcium crystals correlates with the radiographic evidence of hyaline cartilaginous degeneration. This study sought to examine calcium deposition in OA meniscus and to investigate OA meniscal cell-mediated calcium deposition. The hypothesis was that OA meniscal cells may play a role in pathological meniscal calcification. METHODS: Studies were approved by our human subjects Institutional Review Board. Menisci were collected during joint replacement surgeries for OA patients and during limb amputation surgeries for osteosarcoma patients. Calcium deposits in menisci were examined by alizarin red staining. Expression of genes involved in biomineralization in OA meniscal cells was examined by microarray and real-time RT-PCR. Cell-mediated calcium deposition in monolayer culture of meniscal cells was examined using an ATP-induced (45)calcium deposition assay. RESULTS: Calcium depositions were detected in OA menisci but not in normal menisci. The expression of several genes involved in biomineralization including ENPP1 and ANKH was upregulated in OA meniscal cells. Consistently, ATP-induced calcium deposition in the monolayer culture of OA meniscal cells was much higher than that in the monolayer culture of control meniscal cells. CONCLUSIONS: Calcium deposition is common in OA menisci. OA meniscal cells calcify more readily than normal meniscal cells. Pathological meniscal calcification, which may alter the biomechanical properties of the knee meniscus, is potentially an important contributory factor to OA.

Analysis of meniscal degeneration and meniscal gene expression.

BACKGROUND: Menisci play a vital role in load transmission, shock absorption and joint stability. There is increasing evidence suggesting that OA menisci may not merely be bystanders in the disease process of OA. This study sought: 1) to determine the prevalence of meniscal degeneration in OA patients, and 2) to examine gene expression in OA meniscal cells compared to normal meniscal cells. METHODS: Studies were approved by our human subjects Institutional Review Board. Menisci and articular cartilage were collected during joint replacement surgery for OA patients and lower limb amputation surgery for osteosarcoma patients (normal control specimens), and graded. Meniscal cells were prepared from these meniscal tissues and expanded in monolayer culture. Differential gene expression in OA meniscal cells and normal meniscal cells was examined using Affymetrix microarray and real time RT-PCR. RESULTS: The grades of meniscal degeneration correlated with the grades of articular cartilage degeneration (r = 0.672; P < 0.0001). Many of the genes classified in the biological processes of immune response, inflammatory response, biomineral formation and cell proliferation, including major histocompatibility complex, class II, DP alpha 1 (HLA-DPA1), integrin, beta 2 (ITGB2), ectonucleotide pyrophosphatase/phosphodiesterase 1 (ENPP1), ankylosis, progressive homolog (ANKH) and fibroblast growth factor 7 (FGF7), were expressed at significantly higher levels in OA meniscal cells compared to normal meniscal cells. Importantly, many of the genes that have been shown to be differentially expressed in other OA cell types/tissues, including ADAM metallopeptidase with thrombospondin type 1 motif 5 (ADAMTS5) and prostaglandin E synthase (PTGES), were found to be expressed at significantly higher levels in OA meniscal cells. This consistency suggests that many of the genes detected in our study are disease-specific. CONCLUSION: Our findings suggest that OA is a whole joint disease. Meniscal cells may play an active role in the development of OA. Investigation of the gene expression profiles of OA meniscal cells may reveal new therapeutic targets for OA therapy and also may uncover novel disease markers for early diagnosis of OA.

Telomerase transduced osteoarthritis fibroblast-like synoviocytes display a distinct gene expression profile.

OBJECTIVE: To examine the differential gene expression in telomerase transduced osteoarthritis fibroblast-like synoviocytes (hTERT-OA 13A FLS) and telomerase transduced rheumatoid arthritis FLS (hTERT-RA 516 FLS) and test the hypothesis that longterm culture of hTERT-OA 13A FLS display a disease-specific gene expression profile. METHODS: Gene expression in passage 8 hTERT-OA 13A FLS and passage 8 hTERT-RA 516 FLS were compared using microarray assays. Differential expression of selected genes was further examined by reverse transcription-polymerase chain reaction (RT-PCR). After continuous expansion in culture for an additional 4 months, gene expression in the longterm cultures of hTERT-OA 13A FLS and hTERT-RA 516 FLS was again examined with microarray and real-time RT-PCR. RESULTS: hTERT-OA 13A FLS displayed a distinct gene expression profile. While hTERT-RA 516 FLS expressedADAMTS1, ADAMTS3, ADAMTS5, and several carboxypeptidases, hTERT-OA 13A FLS expressed matrix metalloproteinase (MMP)1, MMP3, and several cathepsins at higher levels. Numerous genes classified in the immune response, lipid transport/catabolism, and phosphate transport biological processes were also expressed at higher levels in hTERT-OA 13A FLS. In contrast, numerous genes classified in the positive regulation of cell proliferation, anti-apoptosis, and angiogenesis biological processes were expressed at higher levels in hTERT-RA 516 FLS. Further, of the recently proposed 21 candidate synovial biomarkers of OA, 12 (57%) were detected in our study. CONCLUSION: The findings indicate that OA FLS may not be a passive bystander in OA and that telomerase transduced OA FLS offer an alternative tool for the study of synovial disease markers and for the identification of new therapeutic targets for OA therapy.

Patient out-of-pocket expenses in major orthopedic procedures: total hip arthroplasty as a case study.

Total hip arthroplasty (THA) is a successful procedure for improving quality of life. There are few publications regarding out-of-pocket expenses incurred by individuals undergoing uncomplicated THA. Detailed billing and record reviews and patient phone surveys were conducted on 34 Medicare patients identifying charges and reimbursements recorded by the health care system and all out-of-pocket expenses incurred by patients undergoing uncomplicated THA (diagnostic related group [DRG] 209/current procedural terminology [CPT] 27130). Mean THA total billed charges were $46378, 89% of that from inpatient hospitalization and 5% incurred preoperatively and 7% postoperatively. Medicare reimbursement was $14647, supplemental reimbursement was $744, and patients paid a mean out-of-pocket expense of $758 (95% CI, 614-904; range, 102-1889). Our study supports the policy that THA remains an excellent value to both the patient and society.

Cementation of polyethylene liners into well-fixed metal shells at the time of revision total hip arthroplasty.

Cementing polyethylene liners into well-fixed metal shells at revision total hip arthroplasty is an accepted technique. Previous studies have tested the initial strength of this construct, but none have tested the construct under physiologic and abnormal loading conditions. The current study examines liner-shell performance under these conditions. In addition, this study quantitates whether hand-modified regular liners or liners designed for cementation with integrated cement spacers, which provide an even cement mantle, perform better. Cyclic loads of up to 4000 N for 500,000 cycles followed by 2000 N for 200,000 cycles of edge loading were used. The liners with integrated spacers demonstrated higher lever-out moments and statistically significant increase in tear-out loads.