Comparison of joint degeneration and pain in male and female mice in DMM model of osteoarthritis.

OBJECTIVE: While the prevalence of radiographic and symptomatic osteoarthritis (OA) is higher in women, male mice are more frequently used in animal experiments to explore its pathogenesis or drug efficacy. In this study, we examined whether sexual dimorphism affects pain and joint degeneration in destabilization of the medial meniscus (DMM) mouse model. METHODS: DMM or sham surgery was performed on the knee of male and female C57BL/6 mice. Joint damage was assessed by safranin O staining and scored using the Osteoarthritis Research Society International (OARSI) scoring system. Von Frey hair, incapacitance, and rotarod tests were conducted to measure joint pain. The analgesic effect of capsazepine (CPZ), a TRPV1 antagonist, was compared between male and female mice. RESULTS: Histology and OARSI scoring analysis showed that cartilage degeneration developed, and progressed in both male and female DMM groups, however, damage was less severe in females at the late stage of OA. Pain behavior, as measured by mechanical allodynia, was displayed for longer in male DMM mice compared to females. Incapacitance data showed that CPZ significantly reduced DMM-induced pain in male mice but not in female mice. Immunofluorescence microscopy analysis demonstrated that DMM surgery increased the expression of TRPV1 in both female and male dorsal root ganglion (DRG). Injection of CPZ significantly suppressed TRPV1 expression in the DRG of male mice only. CONCLUSION: Joint damage develops comparably in both female and male mice after DMM although it progresses less in females. There was a subtle sex difference in pain behaviors and analgesic efficacy of a TRPV1 antagonist, which was accompanied by a differential regulation of TPRV1.

Overexpression of secretory leukocyte peptidase inhibitor (SLPI) does not modulate experimental osteoarthritis but may be a biomarker for the disease.

OBJECTIVE: Osteoarthritic cartilage destruction can be regulated by the balance between proteases and anti-proteases. Here, we sought to identify novel cellular protease inhibitors associated with osteoarthritis (OA) pathogenesis. METHODS: Candidate molecules were screened from microarray data of chondrocytes treated with OA-associated catabolic factors. The functions of candidate molecules in OA pathogenesis were examined in primary-culture mouse articular chondrocytes and mouse models of OA, such as those stimulated by destabilization of the medial meniscus (DMM) or intra-articular (IA) injection of adenovirus expressing the candidate gene. The value of the selected candidate molecule as a biomarker of OA was examined by measuring its circulating levels in human and mouse blood. RESULTS: Bioinformatic analysis identified secretory leukocyte peptidase inhibitor (SLPI) as a highly upregulated cellular protease inhibitor in chondrocytes treated with pathogenic catabolic factors, including interleukin (IL)-1ß, hypoxia-inducible factor (HIF)-2α, and zinc importer ZIP8. The adenovirus-mediated overexpression of SLPI in joint tissues did not cause any OA-like change or modulate DMM- or HIF-2α-induced experimental OA in mice. SLPI also did not markedly modulate the expression of OA-associated catabolic or anabolic factors in chondrocytes. However, SLPI was specifically upregulated in OA cartilage, and the serum SLPI levels were significantly elevated in human OA patients and experimental OA mice, suggesting that SLPI may be a biomarker of OA. CONCLUSION: Although SLPI is upregulated in OA chondrocytes, it does not appear to per se modulate OA development in mice. However, it may be a potential biomarker of OA in humans and animal models.

Organothiol Monolayer Formation Directly on Muscovite Mica.

Organothiol monolayers on metal substrates (Au, Ag, Cu) and their use in a wide variety of applications have been extensively studied. Here, the growth of layers of organothiols directly onto muscovite mica is demonstrated using a simple procedure. Atomic force microscopy, surface X-ray diffraction, and vibrational sum-frequency generation IR spectroscopy studies revealed that organothiols with various functional endgroups could be self-assembled into (water) stable and adaptable ultra-flat organothiol monolayers over homogenous areas as large as 1 cm2 . The strength of the mica-organothiol interactions could be tuned by exchanging the potassium surface ions for copper ions. Several of these organothiol monolayers were subsequently used as a template for calcite growth.

Fibronectin fragment inhibits xylosyltransferase-1 expression by regulating Sp1/Sp3- dependent transcription in articular chondrocytes.

OBJECTIVE: We investigated the effects of 29-kDa amino-terminal fibronectin fragment (29-kDa FN-f) on xylosyltransferase-1 (XT-1), an essential anabolic enzyme that catalyzes the initial and rate-determining step in glycosaminoglycan chain synthesis, in human primary chondrocytes. METHODS: Proteoglycan and XT-1 expression in cartilage tissue was analyzed using safranin O staining and immunohistochemistry. The effects of 29-kDa FN-f on XT-1 expression and its relevant signaling pathway were analyzed by quantitative real-time-PCR, immunoblotting, chromatin immunoprecipitation, and immunoprecipitation assays. The receptors for 29-kDa FN-f were investigated using small interference RNA and blocking antibodies. RESULTS: The expression of XT-1 was significantly lower in human osteoarthritis cartilage than in normal cartilage. Intra-articular injection of 29-kDa FN-f reduced proteoglycan levels and XT-1 expression in murine cartilage. In addition, in 29-kDa FN-f-treated cells, XT-1 expression was significantly suppressed at both the mRNA and protein levels, modulated by the transcription factors specificity protein 1 (Sp1), Sp3, and activator protein 1 (AP-1). The 29-kDa FN-f suppressed the binding of Sp1 to the promoter region of XT-1 and enhanced the binding of Sp3 and AP-1. Inhibition of mitogen-activated protein kinase and nuclear factor kappa B signaling pathways restored the 29-kDa FN-f-inhibited XT-1 expression, along with the altered expression of Sp1 and Sp3. Blockading toll-like receptor 2 (TLR-2) and integrin α5ß1 via siRNA and blocking antibodies revealed that the effects of 29-kDa FN-f on XT-1 expression were mediated through the TLR-2 and integrin α5ß1 signaling pathways. CONCLUSION: These results demonstrate that 29-kDa FN-f negatively affects cartilage anabolism by regulating glycosaminoglycan formation through XT-1.

Polyamine patterns in plasma of patients with systemic lupus erythematosus and fever.

Systemic lupus erythematosus (SLE) is a systemic autoimmune disease with various clinical manifestations and serologic markers. In this study, we analyzed nine polyamine (PA) profiles of plasma from patients with SLE and healthy controls (HCs), and the relationship between the PA profiles and disease activity. PA alterations in plasma of 44 patients with SLE and fever were investigated using gas chromatography mass spectrometry (GC-MS) in selected ion monitoring mode using N-ethoxycarbonyl/ N-pentafluoropropionyl derivatives, and compared with those of 43 HCs. Patients with SLE and HCs showed differences in five of nine PA profiles. Among five changed PA levels, four PAs, namely N1-acetylcadaverine, spermidine, N1-acetylspermidine, and spermine, were dramatically decreased. However, the level of cadaverine was increased in patients with SLE. In the partial correlation with PA profiles and disease activity markers of SLE, several disease activity markers and nutritional markers were correlated with cadaverine, spermidine, and N 8-acetylspermidine. Thus, our results provide a comprehensive understanding of the relationship between PA metabolomics and disease activity markers in patients with SLE.

Mesenteric vasculitis after G-CSF administration in a severe neutropenic patient with systemic lupus erythematosus.

Granulocyte colony-stimulating factor (G-CSF) is commonly used with neutropenic patients to accelerate recovery. G-CSF is a hematopoietic cytokine that regulates the proliferation and differentiation of neutrophil precursors, and is known as a safe and effective treatment for chemotherapy-induced neutropenia. However, we encountered a case in which a patient with systemic lupus erythematosus (SLE) developed mesenteric vasculitis after G-CSF administration. The patient was a 36-year-old female admitted with fever, arthralgia, and generalized erythematous rash. Despite symptomatic improvement with a high-dose steroid, severe neutropenia persisted for three weeks, precipitating a decision to use G-CSF to enhance recovery. Mesenteric vasculitis developed 15 hours after administration of G-CSF injection. Because the response of immune cells such as neutrophils and T cells is uncontrolled and dysfunctional in patients with lupus, G-CSF therapy should be used with caution.

Concordance between the tuberculin skin test and interferon gamma release assay (IGRA) for diagnosing latent tuberculosis infection in patients with systemic lupus erythematosus and patient characteristics associated with an indeterminate IGRA.

OBJECTIVE: We investigated the agreement between the tuberculin skin test (TST) and the QuantiFERON-TB gold (QFT-G) assay in the diagnosis of latent tuberculosis infection (LTBI) in patients with systemic lupus erythematosus (SLE). Furthermore, we evaluated the factors associated with indeterminate results in the QFT-G assay in patients with SLE. METHODS: We enrolled 136 patients with SLE prospectively, and compared them to 66 patients with rheumatoid arthritis (RA). In addition to the TST, QFT-G assay, patients' medications, and Bacillus Calmette-Guérin (BCG) vaccination status were also investigated. A positive TST or QFT-G assay result without an active tuberculosis lesion on chest x-ray was considered to indicate a diagnosis of LTBI. RESULTS: The prevalence of LTBI was 26.5% in patients with SLE and 30.3% in patients with RA. The agreement between the TST and QFT-G assay was fair in SLE patients, but poor in RA patients. BCG vaccination was one factor associated with discordance between TST and QFT-G. Older age and higher SLE Disease Activity Index (SLEDAI) score were associated with a negative TST/positive QFT-G result in patients with SLE. Higher SLEDAI score and increased glucocorticoid dose were associated with an indeterminate result in the QFT-G assay for patients with SLE. CONCLUSIONS: Agreement between the QFT-G assay and TST in patients with SLE was found to be fair. However, BCG vaccination status, age, and SLEDAI score are all factors that could result in discordance between the two tests. Indeterminate results from the QFT-G assay may be caused by a higher SLEDAI score or increased glucocorticoid dose.

Pharmacist-involved care for patients with heart failure and acute coronary syndrome: a systematic review with qualitative and quantitative meta-analysis.

WHAT IS KNOWN AND OBJECTIVE: Many trials have indicated that interventions by pharmacists resulted in beneficial outcomes with positive effects on cardiovascular diseases. The interventions through pharmacist-involved pharmaceutical care in patients with heart failure (HF) and acute coronary syndrome (ACS) were reviewed systemically and examined. METHODS: A systematic literature search was conducted to identify relevant articles describing pharmacist interventions in HF and ACS. Most studies were evaluated qualitatively, and the strength of evidence was graded according to the Agency for Healthcare Research and Quality (AHRQ) guidelines. Some of the studies were also assessed by a meta-analysis. RESULTS: A total of 26 studies containing data on 9415 patients were identified. For all studies, the strength of the body of evidence was reviewed and graded, and 14 studies among them were meta-analysed. The evidence was not strong enough to determine the effects of pharmaceutical care on major and patient-centred outcomes, except the prescription rates of angiotensin-converting-enzyme inhibitors (ACEI) with a high strength of evidence. In the meta-analysis, all-cause hospitalization [odds ratio (OR), 0·74; 95% confidence interval (CI), 0·58-0·94] was reduced and the prescription rates of angiotensin-converting-enzyme inhibitors (ACEI; OR 1·43; 95% CI, 1·07-1·91) and beta-blockers (OR 1·92; 95% CI, 1·24-2·96) were significantly higher in the pharmaceutical care group compared with the usual care group. WHAT IS NEW AND CONCLUSIONS: All-cause hospitalization showed improvement in the pharmaceutical care group. However, the strength of evidence for the majority of outcomes with pharmaceutical care, except direct performance measures such as prescription rates, was either insufficient or low. This could be explained by the presence of imprecision and inconsistency derived from the diversity of pharmaceutical care, the heterogeneity of patient populations or clinical settings. Moreover, it may indicate the necessity for homogeneous applicable criteria for assessment. A standardized consensus of the guidelines for pharmaceutical care service should be considered to improve homogeneity.

Carotid subclinical atherosclerosis is associated with disease activity but not vitamin D in Korean systemic lupus erythematosus.

Atherosclerosis develops early in systemic lupus erythematosus (SLE) patients and is an important cause of mortality. Vitamin D deficiency is found to be associated with cardiovascular disease and autoimmunity. We evaluated the extent of carotid subclinical atherosclerosis and analyzed its correlation with vitamin D in SLE. One hundred and two female patients with SLE and 52 normal controls (NCs) were recruited. The mean carotid intima-media thickness (IMT) of SLE patients was 0.41 ± 0.08 mm, which was higher than that of NCs (0.32 ± 0.08 mm, p = 0.012). In addition, carotid plaques were more frequent and the plaque index was higher in SLE patients than in NCs (0.68 ± 1.39 vs. 0.26 ± 0.87, p = 0.026). Carotid IMT was correlated with age, body mass index, SLE disease activity index, and aspirin use in SLE patients. The plaque index was correlated with renal involvement. Vitamin 25(OH)D3 level was not correlated with carotid IMT, plaque index or disease activity markers. In SLE, the risk of cardiovascular disease is higher than that in NCs, which may be derived from systemic inflammation. It may be not suitable to assess vitamin D as a marker of disease activity or subclinical atherosclerosis in SLE patients.

MicroRNA-558 regulates the expression of cyclooxygenase-2 and IL-1ß-induced catabolic effects in human articular chondrocytes.

OBJECTIVE: Cyclooxygenase-2 (COX-2) is a major prostaglandin E2 (PGE2) synthetic enzyme and is involved in the pathogenesis of chronic inflammation and pain in osteoarthritis (OA). The objective of this study was to directly address whether microRNA (miR)-558 can control the interleukin (IL)-1ß-mediated induction of COX-2 and catabolic effects in human articular chondrocytes. MATERIALS AND METHODS: Total RNA was extracted from the cartilage tissues of normal and OA donors or cultured human articular chondrocytes. The expression of miR-558 was quantified by TaqMan assay. To investigate the repressive effect of miR-558 on COX-2 expression, human chondrocytes and chondrogenic SW1353 cells were transfected with mature miR-558 or an antisense inhibitor (anti-miR-558). The expression of COX-2 protein was determined by Western blot analysis and the involvement of miR-558 in IL-1ß-induced catabolic effects was examined by Western blot analysis and enzyme-linked immunosorbent assay (ELISA). Direct interaction between miR-558 and the putative site in the 3'-untranslated region (UTR) of COX-2 messenger RNA (mRNA) was validated by luciferase reporter assay. RESULTS: Normal human articular cartilage expressed miR-558, and its expression was significantly lower in OA cartilage. Stimulation with IL-1ß led to a significant reduction in miR-558 expression in normal and OA chondrocytes. IL-1ß-induced activation of MAP kinase (MAPK) and nuclear factor-κB (NF-κB) decreased miR-558 expression and induced COX-2 expression in chondrocytes. The overexpression of miR-558 directly suppressed the luciferase activity of a reporter construct containing the 3'-UTR of human COX-2 mRNA and significantly inhibited IL-1ß-induced upregulation of COX-2, while treatment with anti-miR-558 enhanced IL-1ß-induced COX-2 expression and reporter activity in chondrocytes. Interestingly, IL-1ß-induced activation of NF-κB and expression of matrix metalloproteinase (MMP)-1 and MMP-13 was significantly inhibited by miR-558 overexpression. CONCLUSION: These findings demonstrated that cartilage homeostasis is influenced by miR-558, which directly targets COX-2 and regulates IL-1ß-stimulated catabolic effects in human chondrocytes.

Association between bone marrow lesions detected by magnetic resonance imaging and knee pain in community residents in Korea.

OBJECTIVE: To describe the frequency of bone marrow lesions (BMLs) detected by magnetic resonance imaging (MRI), and to examine the association of BMLs with knee pain severity in community residents in Korea. METHODS: Participants were randomly chosen from the population-based Hallym Aging Study, irrespective of whether they had knee osteoarthritis (OA) or pain. Demographic and knee pain data were obtained by questionnaire. Radiographic evaluations consisted of weight-bearing knee anteroposterior radiographs and 1.5-T MRI scans. MRI was performed in the dominant knees of subjects without knee pain and in the more symptomatic knees of subjects with knee pain. BMLs were graded according to the whole-organ MRI score. RESULTS: The mean age of the 358 study subjects was 71.8 years, and 34.5% of subjects had radiographically detected knee OA. The prevalences of BMLs and large BMLs in the tibiofemoral compartments were 80.3% and 40.4%, respectively. After adjusting for age, sex, and body mass index, total and medial compartment BML scores were significantly associated with the presence of knee pain, and the association was stronger as the summary score for BML increased. In proportional regression analysis, knee pain severity increased with BML severity in any compartment and in the medial compartment. CONCLUSION: BMLs detected by MRI were highly prevalent in this elderly Asian population. BMLs were significantly linked to knee pain, and BML severity correlated with knee pain severity. BMLs may be important surrogate targets for monitoring pain and structure modification in OA therapeutics.

The interleukin 6 receptor alpha gene polymorphisms are associated with clinical manifestations of systemic lupus erythematosus in Koreans.

The human interleukin 6 receptor consists of two membrane-bound glycoproteins (IL-6Rα, IL-6RA and gp130/IL-6Rß, IL-6RB) interacting with IL-6, which is a multifunctional cytokine essential to the regulation of the immune response and acute-phase reactions. We have genotyped a single-nucleotide polymorphism (SNP) of the IL-6RA in Korean patients with systemic lupus erythematosus (SLE) (n = 300) and normal controls (NC, n = 299). Three SNPs were identified in the IL-6RA gene; -208 G ≥ A (NM_000565.3:c.-208G ≥ A, rs4845617) in the promoter region, 48841 T ≥ A (NM_000565.3:c.1067-17T ≥ A, rs4845374) in the intron 8 region and 48864 A ≥ C (NM_000565.3:c.1073A ≥ C, rs2228145) in the exon 9 region. There were no differences between the SLE and the NC in the genotype and haplotype frequencies. The 48864 A>C polymorphism was significantly associated with rash (P = 0.008). Also, the frequency of rash (P = 0.037), leucopenia (P = 0.033) and lymphopenia (P = 0.027) was significantly higher in patients with SLE having the haplotype HT2 [ATC]. These data suggest that genetic polymorphisms of IL-6RA gene may be associated with disease phenotypes of SLE in Korean.

Improved electrical and optical properties of ITO/Ag/ITO films by using electron beam irradiation and their application to ultraviolet light-emitting diode as highly transparent p-type electrodes.

We have investigated the effect of insertion of a Ag layer in ITO film as well as electron beam irradiation to the multilayer films on the electrical and optical properties of the ITO-based multilayer deposited by magnetron sputtering method at room temperature. Inserting a very thin Ag layer between ITO layers resulted in a significant decrease in sheet resistance and increased the optical band gap of the ITO/Ag/ITO multilayer to 4.35 eV, followed by a high transparency of approximately 80% at a wavelength of 375 nm. We have also fabricated ultraviolet light-emitting diodes (LED) by using the ITO/Ag/ITO p-type electrode with/without electron beam irradiation. The results show that the UV-LEDs having ITO/Ag/ITO p-electrode with electron beam irradiation produced 19% higher optical output power due to the low absorption of light in the p-type electrode.

The association between meniscal and cruciate ligament damage and knee pain in community residents.

OBJECTIVE: To describe the frequency of meniscal and cruciate ligament damage by magnetic resonance imaging (MRI) and to examine its association with knee pain in community residents in Korea. METHODS: Participants were randomly chosen regardless of knee osteoarthritis (OA) or pain from the population-based Hallym Aging Study. Demographic and knee pain data were obtained by questionnaire. Radiographic evaluations consisted of weight-bearing knee A-P radiographs and 1.5-T MRI scans. We assessed the integrities of the menisci and cruciate ligaments in the dominant knee of subjects without knee pain or in the more symptomatic knee among subjects with knee pain, and examined their association with knee pain using a logistic regression model. RESULTS: The mean age of the 358 study subjects was 71.8 years, and 51.4% were women. Meniscal and cruciate ligament damage were present in 49.7% and 8.0% of men and in 71.2% and 26.9% of women, respectively. The presence of meniscal damage was significantly associated with the presence of knee pain among subjects without radiographic knee OA (ROA), but not among subjects with ROA. The presence of cruciate ligament tear was associated with knee pain in subjects with or without ROA. The severity of knee pain was significantly correlated with medial meniscal damage grade but not with cruciate ligament tear. CONCLUSION: Incidental meniscal or cruciate findings on MRI were common in this elderly population. Among subjects without ROA, the presence of meniscal or cruciate damage was significantly associated with knee pain. The medial meniscal grade was significantly correlated with knee pain severity.

Association between variable number tandem repeats within the 3' flanking region of the interleukin-6 gene and systemic lupus erythematosus in Korean patients.

Variable number tandem repeat (VNTR) polymorphism located in the 3' flanking region of the interleukin-6 (IL-6) gene was examined in Koreans with systemic lupus erythematosus (SLE). We identified 15 VNTR alleles (K1 to K15) in the 3' flanking region by Genescan analysis. The VNTR K8 allele, a 648-base pair (bp) allele, was most commonly found in Koreans, being present in 74.8% of the SLE patients and 70.3% of the normal controls. The VNTR K9 (642 bp) allele was associated with susceptibility to SLE. In addition, the VNTR K9 was significantly associated with leukopenia (p = 0.048), thrombocytopenia (p = 0.020), and elevated C-reactive protein (p = 0.019). These data suggest that the VNTR K9 in the 3' flanking region of the IL-6 gene may be associated with disease susceptibility and the clinical phenotypes of SLE.

Leptin and ghrelin in Korean systemic lupus erythematosus.

Elevated serum leptin levels have been described in patients with systemic lupus erythematosus (SLE), however these studies have provided no information regarding the ghrelin levels. We investigated the clinical significance of serum leptin and ghrelin levels in SLE. The leptin levels of SLE patients were higher than those of normal healthy controls, while the ghrelin levels of the SLE were lower. In addition, the ghrelin levels were significantly lower in SLE patients with arthritis and hematologic disorder. Taken together, these findings suggest that leptin and ghrelin play a role in clinical manifestations observed in SLE.

Serum levels of soluble triggering receptor expressed on myeloid cells-1 (sTREM-1) and pentraxin 3 (PTX3) as markers of infection in febrile patients with systemic lupus erythematosus.

OBJECTIVE: To investigate the role of sTREM-1 and PTX3 as markers of infection in febrile patients with SLE. METHODS: In febrile (body temperature > or =38 degrees C) patients with SLE, blood samples of day 0, 1, 2, and 14 after presentation were drawn and relevant clinical data were collected. The patients were allocated to an infection group (n=19) or disease flare group (n=14). Serum levels of sTREM-1 and PTX3 were measured by ELISA using the serum samples of SLE patients and age- and sex-matched healthy controls (n=31). RESULTS: A total of 33 febrile episodes occurred in 32 SLE patients (19 infections, 14 flares) were studied. sTREM-1 levels on day 0 were significantly higher in the infection group than in the flare group (109.9 pg/ml (median) vs. 48.0 pg/ml, p=0.002), but PTX3 levels were similar in these two groups. The difference of sTREM-1 levels between infection group and flare group was persistent on day 1 and 2 (day 1, p=0.007; day 2, p=0.034). The highest diagnostic value (sensitivity=1.0, specificity=0.664) of sTREM-1 was obtained at the threshold value of 53.2 pg/mL. CONCLUSION: Serum sTREM-1 levels were significantly higher in the infection group than in the flare group of febrile SLE patients. Our findings suggest that serum sTREM-1 levels could be used to determine whether SLE patients have contracted an infection.

A developmentally regulated switch directs regenerative growth of Schwann cells through cyclin D1.

Sciatic nerve axons in cyclin D1 knockout mice develop normally, become properly ensheathed by Schwann cells, and appear to function normally. However, in the Wallerian degeneration model of nerve injury, the mitotic response of Schwann cells is completely inhibited. The mitotic block is Schwann cell autonomous and developmentally regulated. Rescue analysis (by "knockin" of cyclin E) indicates that D1 protein, rather than regulatory elements of the D1 gene, provides the essential Schwann cell function. Genetic inhibition of the Schwann cell cycle shows that neuronal responses to nerve injury are surprisingly independent of Schwann cell mitotic responses. Even axonal regrowth into the distal zone of a nerve crush injury is not markedly impaired in cyclin D1-/- mice.

Low rate of total hip replacement as reflected by a low prevalence of hip osteoarthritis in South Korea.

OBJECTIVE: We attempted to estimate the rate of total hip replacement (THR) using a national database and the prevalence of hip osteoarthritis (OA) from the reading of intravenous pyelograms (IVPs) in a Korean population. MATERIALS: Reimbursement records from all hospitals in South Korea were extracted from the Health Insurance Review Agency (HIRA) database. Records with both the procedure code corresponding to THR and containing the diagnosis code for hip OA were selected. We estimated the age- and sex-specific rates of THR from 2002 to 2006. Hip joints from 580 subjects older than 70 years old who underwent an IVP were assessed for the presence of OA. RESULTS: The rate of THR increased with age, reaching a peak over the age of 65-69 years, with the age-standardized risk ratios in women vs men of approximately 1.5. Although the rate of THR increased over the 5-year study period, it was significantly lower than that of total knee replacement (TKR) in Korean population (THR vs TKR 1:15.9). The prevalence of hip OA in the IVP cohort was 1.2% (1.7% for men and 0.7% for women). CONCLUSION: The rate of THR was significantly lower than that of TKR in Korean population. Hip OA prevalence among the IVP subjects was 1.2%. Further studies on factors that account for the low prevalence of hip OA among Asians need to be conducted.