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ID PMID Title PublicationDate abstract
16436492 The effect of infliximab on bone metabolism markers in patients with rheumatoid arthritis. 2006 Jun OBJECTIVE: The aim of this study was to evaluate urinary excretion of N-telopeptide of type I collagen (NTX) and deoxypyridinoline (DPD), markers of bone resorption, and serum bone alkaline phosphatase (BAP) level, a marker of bone formation and an early marker of osteoblast differentiation, in patients with rheumatoid arthritis (RA) treated with infliximab. METHODS: Seventeen male and female patients (age 60.7+/-2.53 yr; mean disease duration 12.9+/-3.01 yr; Steinbrocker's class II-IV) with RA, diagnosed according to the criteria of the American College of Rheumatology (ACR), took part in the study between March 2003 and January 2005. None of the patients had a history of oestrogen replacement therapy. All patients were treated with infliximab combined with methotrexate. Infliximab was infused intravenously at 3 mg/kg at baseline, 2 and 6 weeks, then every 8 weeks. To evaluate disease activity, ESR, CRP, the numbers of swollen and tender joints, modified Stanford Health Assessment Questionnaire (mHAQ) score and ACR score were measured. Levels of NTX and DPD in urine and BAP in serum were measured in all patients. RESULTS: ESR, CRP, the number of swollen joints and tender joints, and mHAQ score had decreased significantly 6 weeks after initial treatment and were still low 6 months after initial treatment. NTX levels had decreased significantly 6 weeks after the initial treatment and were still low 6 months after initial treatment. DPD levels had decreased 6 months after initial infusion. Mean serum BAP level did not differ significantly among the three time points. NTX levels were statistically corresponding with the number of swollen joints and mHAQ scores. DPD levels were statistically lower corresponding with ESR. CONCLUSION: Infliximab therapy may inhibit generalized bone loss in patients with RA. NTX is a more sensitive marker than DPD.
16386446 Clinical evaluation of a cohort of patients with rheumatoid arthritis treated with anti-TN 2006 Jan OBJECTIVES: TNF-alpha inhibitors have been effective in randomized controlled studies for the treatment of RA. The purpose of this study was to evaluate the clinical, laboratory, and radiological responses in a cohort of unselected patients with RA treated with TNF-alpha inhibitors in the community. METHODS: Using the Swiss Clinical Quality Management in Rheumatoid Arthritis, a centralized system of data gathering for RA patients, we obtained the following information regarding patients treated with a TNF-alpha inhibitor in the Geneva Canton before 02/2003: demographics; clinical data (disease activity, functional status, treatments received and type of TNF-alpha inhibitor used); laboratory and radiographic data. RESULTS: A total of 66 patients (mean age = 60.5 years) with long-standing disease (mean duration = 12.5 years) were analyzed. Sixteen patients (24%) discontinued anti-TNF-alpha, half within the first 6 months of the study. Mean DAS score decreased from 4.8+ /- 0.4 to 3.8 +/- 0.4 (P < 0.01); HAQ scores (mean = 1.35) remained unchanged; pain, evaluated on a 10-point scale, decreased from 5.0 at baseline to 3.3 (P < 0.001). CRP values decreased steadily from 17.9 at baseline to 5.6 at 20 months or later. The progression of radiographic damage decelerated in 30 patients, accelerated in 12, and remained unchanged in one. CONCLUSIONS: The responses of this community-based group of patients with severe, long-standing RA to TNF-alpha inhibitors revealed a reassuring similarity to those of patients enrolled in controlled clinical trials.
18046754 Summary of contributions to GAW15 Group 13: candidate gene association studies. 2007 Here we summarize the contributions to Group 13 of the Genetic Analysis Workshop 15 held in St. Pete Beach, Florida, on November 12-14, 2006. The focus of this group was to identify candidate genes associated with rheumatoid arthritis or surrogate outcomes. The association methods proposed in this group were diverse, from better known approaches, such as logistic regression for single nucleotide polymorphism (SNP) analysis and haplotype sharing tests to methods less familiar to genetic epidemiologists, such as machine learning and visualization methods. The majority of papers analyzed Genetic Analysis Workshop 15 Problems 2 (rheumatoid arthritis data) and 3 (simulated data). The highlighted points of this group analyses were: (1) haplotype-based statistics can be more powerful than single SNP analysis for risk-locus localization; (2) considering linkage disequilibrium block structure in haplotype analysis may reduce the likelihood of false-positive results; and (3) visual representation of genetic models for continuous covariates may help identify SNPs associated with the underlying quantitative trait loci.
16861538 Periarticular bone findings in rheumatoid arthritis: T2-weighted versus contrast-enhanced 2006 Aug OBJECTIVE: The purpose of this study was to establish the relative predictive value of T2-weighted and contrast-enhanced T1-weighted MRI techniques for bone erosions that are evident on CT. Because it is known that MRI depicts abnormalities in the periarticular bone of patients with rheumatoid arthritis, we wanted to compare the outcomes of T2-weighted versus contrast-enhanced T1-weighted MRI techniques. MATERIALS AND METHODS: Eleven patients with rheumatoid arthritis underwent CT imaging of their most affected wrist. Fast spin-echo T2-weighted MR images were then acquired with spectral fat saturation. Enhanced T1-weighted spin-echo images acquired before and after IV administration of gadopentetate dimeglumine were used to determine the percent enhancement. Imaging examinations were scored for 15 anatomic zones. The CT score was based on cortical bone erosion. The MR score was based on periarticular bone marrow signal alteration. RESULTS: Both T2-weighted MR images with spectral fat saturation and enhanced T1-weighted images were concordant for the presence or absence of bone abnormalities in 122 of 165 zones (74%). Of the 43 zones that were discordant for an abnormality by the two MR techniques, the T2-weighted images were positive in five zones, and enhanced T1-weighted images were positive in 38 zones (p < 0.001). Of the 43 zones that were discordant by the two MR techniques, enhanced T1-weighted images were concordant with CT in 20 zones, whereas the T2-weighted images were concordant with CT in 23 zones (p = 0.76). A greater proportion of lesions detected by the T2-weighted images were "edema-like" signal patterns. CONCLUSION: In rheumatoid arthritis, contrast-enhanced T1-weighted MRI depicts more periarticular bone abnormalities than fat-suppressed T2-weighted MRI. These MR techniques are equally predictive of frank, erosive disease that is evident on CT.
18537958 Approaches to the treatment of early rheumatoid arthritis with disease-modifying antirheum 2008 Aug This paper reviews recent approaches to treatment of early rheumatoid arthritis (RA) with disease-modifying antirheumatic drugs (DMARDs). The literature on treatment the early RA published between 1995 and 2007 was accessed through the PubMed database from the National Library of Medicine. Keywords were 'early rheumatoid arthritis', 'disease-modifying antirheumatic drugs', 'biologic agents' and 'combination therapy'. Only results of trials on human subjects that directly measured the effects of DMARDs or biological agents on clinical, laboratory parameters and radiological progression of early RA were selected. Combination therapy suppresses RA activity and radiological progression more effectively than monotherapy. If better control of RA is evident after 3-6 months of treatment with the combination of DMARDs, one must still decide whether to stop the first DMARD, stop the second, or continue with the combination. Combination therapy biological agents (infliximab, adalimumab) with methotrexate and etanercept therapy alone may induce remission in many patients with early RA. It is a method of choice in patients with an adverse prognosis. The main indications for combination therapy 'standard' DMARDs or combination 1 DMARDs with a biological agent are such variables as detection of a shared epitope, increase of concentration of anticyclic citrullinated peptide antibodies, rheumatoid factor, C-reactive protein, 28-joint disease activity score, Sharp score and presence of erosion in joints. The majority of rheumatologists believe that patients with RA should be treated with DMARDs earlier rather than later in the disease process. Further trials should establish the optimal approaches to early RA therapy.
16980215 Chemokine inhibition in inflammatory arthritis. 2006 Oct Synovial inflammation in rheumatoid arthritis (RA) and other arthritides is, in part, dependent on migration of inflammatory cells as well as retention of these cells at the site of inflammation. Chemokines play a critical role in these processes and represent an attractive target for therapeutic intervention. Animal models of RA have shown that it is possible to induce clinical improvement by specifically targeting chemokines or their receptors. Although at present only very limited data exist, initial data suggest that it may be possible to reduce synovial inflammation in patients with RA by specific chemokine blockade. Innovative trial design may help to screen for potentially interesting chemokine antagonists in an early stage of development.
17661914 The MHC2TA-168A/G and +1614G/C polymorphisms and risk for multiple sclerosis or chronic in 2007 Sep The -168A-G polymorphism has been shown to influence transcription of the MHC2TA gene and has been implicated in several inflammatory/autoimmune disorders. Attempts to reproduce these findings have been inconclusive. We investigated the role of this promoter single nucleotide polymorphism (SNP) in 440 multiple sclerosis (MS), 293 rheumatoid arthritis (RA), 74 juvenile idiopathic arthritis (JIA) patients and 316 healthy controls from Northern Ireland. We also genotyped a non-synonymous SNP in exon 11, +1614G/C. There was no significant difference in the -168G allele frequencies and carriage rates in the separate RA, JIA, or MS collections compared with the control group [odds ratio (OR) = 1.1, 95% confidence intervals (CI) = 0.86-1.44; OR = 1.1, 95% CI = 0.75-1.68; OR = 1.1, 95% CI = 0.84-1.35, respectively]. Assessment of the common phenotype (chronic inflammatory disease; n = 807 vs 316 controls) was negative as well. Carriage of +1614C was protective against JIA (OR = 0.6, 95% CI = 0.3-1.0) and showed a similar trend in RA and MS (OR = 0.7, 95% CI = 0.5-1.0; OR = 0.8, 95% CI = 0.6-1.0, respectively). The common phenotype (chronic inflammatory disease) was also significant (OR = 0.7, 95% CI = 0.6-1.0).
18234712 Signalling, inflammation and arthritis: NF-kappaB and its relevance to arthritis and infla 2008 May In the synovial cells of patients with RA, activation of the nuclear factor-kappaB (NF-kappaB) pathway results in the transactivation of a multitude of responsive genes that contribute to the inflammatory phenotype, including TNF-alpha from macrophages, matrix metalloproteinases from synovial fibroblasts and chemokines that recruit immune cells to the inflamed pannus. This is largely a consequence of activation of the 'canonical' NF-kappaB pathway that involves heterodimers of p50/p65. Whilst much information on the role of NF-kappaB in inflammation has been gleaned from genetic deficiency of the respective genes in mice, important differences exist in the signalling networks between human and murine immune cells and immortalized cell lines. Despite these differences at the molecular level, the importance of NF-kappaB in inflammation is undisputed and inhibition of the pathway is widely believed to have great potential as a therapeutic target in RA. Commercial effort has gone into developing inhibitors of NF-kappaB activation. However, inhibition of the NF-kappaB activation can result in an exacerbation of inflammation if TNF-alpha production by macrophages is not controlled. It will be important that such inhibitors are carefully monitored before their long-term use in chronic inflammatory conditions such as RA.
17893996 Citrullination by peptidylarginine deiminase in rheumatoid arthritis. 2007 Jun Rheumatoid arthritis (RA) is a complex, multifactorial disease with genetic and immunological aspects. Because RA is an autoimmune condition, dysregulation of the immune system is implied. Many linkage and association studies have also indicated that multiple genetic factors are associated with RA. Although the contribution of each genetic factor is small, the combination of these factors affects RA development. Previous studies have suggested that genetic changes affect the internal immunological environment, which results in autoimmune diseases. More recent genetic studies indicate that the HLA-DRB gene is the predominant cause of RA and that other non-HLA genes are also involved. We reported that peptidylarginine deiminase (gene name abbreviated to PADI, protein name abbreviated to PAD) type 4 is the one of the non-HLA genetic factors involved in RA via citrullination. Antibodies against citrullinated proteins/peptides are highly specific to RA, but the physiological roles of PADI gene, PAD proteins as their products and citrullinated proteins/peptides are obscure. However, levels of anticitrullinated protein antibodies are apparently also increased and were involved in the pathogenesis of autoimmune arthritis in mice with collagen-induced arthritis (CIA). These data suggested that citrullinated protein and anticitrullinated protein antibodies play important roles in the development of RA. This review summarizes the relationship between RA and citrullination, as well as the role of PADI4 genetics.
16511920 Loss of cortical bone from the metacarpal diaphysis in patients with rheumatoid arthritis: 2006 Mar OBJECTIVE: To identify factors associated with the loss of cortical diaphyseal bone over time in patients with rheumatoid arthritis (RA). METHODS: We measured the combined cortical thickness (CCT) of the second metacarpal bone from digitized hand radiographs in an RA cohort. We estimated the rate of loss of CCT, and tested the effect of factors that could accelerate the rate. RESULTS: We studied 649 patients, who had 2990 hand radiographs. The median interval between the first and last followup radiograph was 2 years (range 0 to 23 yrs). The mean CCT at baseline was 4.04 mm (standard deviation 1.18). CCT loss was greatest during the earliest observation stages, following a square-root function of time at a rate of 0.393 mm/year(1/2) (95% CI 0.360, 0.423). Patients with a mean erythrocyte sedimentation rate (ESR) < 30 mm/h lost CCT at a rate of 0.303 mm/year(1/2) (95% CI 0.247, 0.358); those with a mean ESR > 30 and < or = 60 mm/h lost CCT at 0.395 mm/year(1/2) (95% CI 0.345, 0.446); and those with ESR > 60 mm/h lost CCT at 0.554 mm/year(1/2) (95% CI 0.480, 0.628). Patients who received a cumulative dose of glucocorticoids > or = 11.7 g lost CCT at 0.659 mm/year(1/2) (95% CI 0.577, 0.742), compared to 0.361 mm/year(1/2) (0.323, 0.401) in patients who did not receive glucocorticoids. In a multivariable model, the effect of the ESR and cumulative glucocorticoids was independent of age at RA onset, RA duration, sex, ethnic group, body mass index, presence of rheumatoid nodules, rheumatoid factor, and the HLA-DRB1 shared epitope. CONCLUSION: Early rapid loss of cortical diaphyseal bone occurs in patients with RA, followed by gradual slowing. Systemic inflammation and glucocorticoids seem to accelerate bone loss independently of other risk factors. Cortical diaphyseal bone may be an important target of the disease process in RA.
17643937 B cells in rheumatoid arthritis. 2007 Aug Though its etiology remains unknown thus far, the role that autoimmune processes play in rheumatoid arthritis (RA) pathogenesis has been widely proven. Given the easier accessibility of humoral components, the first feature of this contribution to be recognized has been the occurrence of the so-called rheumatoid factor in a large proportion of RA patients. This antibody recognizes the Fc portion of human IgG. By investigating RA pathologic processes and also through experimental models where immune complexes play a fundamental role, many other autoantibodies have then come to our knowledge to be associated with the disease. Their presence and persistence implies that clones of autoreactive B cells survive and proliferate in RA patients under a continuous stimulation. Whether this is a mechanism of disease initiation or just an epiphenomenon is still unclear but no doubt exists that autoantibodies represent a very useful tool in both diagnostic and prognostic terms. Being much more than simple autoantibody producers, B cells are able to secrete many important cytokines and to efficiently present antigens to T lymphocytes in the synovial environment. All of these functions are essential in the development of RA, and lately have claimed attention as B cell depletion has become a common and effective strategy of treatment in RA.
18687584 Rituximab and abatacept for rheumatoid arthritis. 2008 Aug Estimates from the UK indicate that around 0.5-1.0% of the population have rheumatoid arthritis. Here we assess the place of rituximab (MabThera--Roche Products Ltd) and abatacept (Orencia--Bristol-Myers-Squibb), drugs in two new classes, which are licensed for certain adults with the condition.
16490755 Effects of PTPN22 C1858T polymorphism on susceptibility and clinical characteristics of Br 2006 Aug OBJECTIVES: To confirm the association of a functional single-nucleotide polymorphism (SNP), C1858T (rs2476601), in the PTPN22 gene of British Caucasian rheumatoid arthritis (RA) patients and to evaluate its influence on the RA phenotype. METHODS: A total of 686 RA patients and 566 healthy volunteers, all of British Caucasian origin, were genotyped for C1858T polymorphism by PCR-restriction fragment length polymorphism assay. Data were analysed using SPSS software and the chi 2 test as applicable. RESULTS: The PTPN22 1858T risk allele was more prevalent in the RA patients (13.9%) compared with the healthy controls (10.3%) (P = 0.008, odds ratio 1.4, 95% confidence interval 1.09-1.79). The association of the T allele was restricted to those with rheumatoid factor (RF)-positive disease (n = 524, 76.4%) (P = 0.004, odds ratio 1.5, 95% confidence interval 1.1-1.9). We found no association between PTPN22 and the presence of the HLA-DRB1 shared epitope or clinical characteristics. CONCLUSIONS: We confirmed the previously reported association of PTPN22 with RF-positive RA, which was independent from the HLA-DRB1 genotype.
18328158 Determination of anti-cyclic citrullinated peptide antibodies in the sera of patients with 2008 Jan OBJECTIVE: To determine the frequency of anti-cyclic citrullinated peptide (anti-CCP) antibodies in patients with HCV infection, primary biliary cirrhosis (PBC) and type-I autoimmune hepatitis (AIH) to assess the specificity of anti-CCP antibodies. METHODS: Rheumatoid factor (RF) and anti-CCP antibodies were measured in the sera from patients with HCV infection (n=45), PBC (n=73), AIH (n=55) and rheumatoid arthritis (n=48), and also from the sera of healthy subjects (n=23). Anti-CCP antibodies were measured using a second generation enzyme-linked immunosorbent assay (ELISA). RESULTS: No sera with elevated anti-CCP were found in the patients with HCV infection. Two PBC patients (2.7%) and six AIH patients (10.5%) had anti-CCP antibodies. The seropositivity for anti-CCP in these autoimmune disease patients was associated with a high frequency of RA association [PBC; 100% (2/2), AIH; 86.4% (5/6)]. CONCLUSIONS: Although anti-CCP antibodies may be present in patients with autoimmune liver diseases, almost seropositive patients had concomitant RA. As a result, the measurement of anti-CCP antibodies may therefore be helpful for accurately diagnosing RA in patients with these liver diseases.
17265487 A novel DNA vaccine targeting macrophage migration inhibitory factor protects joints from 2007 Feb OBJECTIVE: Previous studies have demonstrated that neutralization of macrophage migration inhibitory factor (MIF) by anti-MIF antibodies decreases joint inflammation and destruction in a type II collagen-induced arthritis model in mice. The aim of this study was to develop and describe a simple and effective method of active immunization that induces anti-MIF autoantibodies, which may neutralize MIF bioactivity. METHODS: We developed a MIF DNA vaccine by introducing oligonucleotides encoding a tetanus toxoid (TTX) Th cell epitope into the complementary DNA sequence of murine MIF. Mice were injected with this construct in conjunction with electroporation. The ability of this immunization to inhibit the development of collagen antibody-induced arthritis (CAIA) in BALB/c mice and spontaneous autoimmune arthritis in interleukin-1 receptor antagonist (IL-1Ra)-deficient mice was then evaluated. RESULTS: Mice that received the MIF/TTX DNA vaccine developed high titers of autoantibodies that reacted to native MIF. Compared with unvaccinated mice, vaccinated mice also produced less serum tumor necrosis factor alpha after receiving an intravenous injection of lipopolysaccharide. In addition, vaccination with MIF/TTX DNA resulted in significant amelioration of both CAIA in BALB/c mice and symptoms of autoimmune arthritis in IL-1Ra-knockout mice. CONCLUSION: These results suggest that MIF/TTX DNA vaccination may be useful for ameliorating the symptoms of rheumatoid arthritis.
18720714 [Some proteins of acute phase of inflammation in differential diagnostics of rheumatoid ar 2008 Levels of lactoferrin (LF), antithrombin-III (AT-III) and beta2-macroglobulin (MG) in blood of patients with rheumatoid arthritis (RA), reactive arthritis (ReA) and systemic lupus erythematosus (SLE) were examined for assessment their importance in differential diagnostics of the diseases. It was shown that on the average, LF and AT-III levels were increased at RA, while MG level was practically unchanged. At the same time LF level was stable high regardless of RA activity and duration degree, but its concentration was significantly increased also in ReA patients (33% patients). AT-III, on the contrary, depended on process activity and duration, was more specific to RA, than LF, but its sensitivity at RA was not enough high (from 25 to 44% patients with increased levels subject to disease duration and activity). Coefficient LFE/AT-III, obtained by multiplication of these proteins concentration, had the greatest diagnostic value. Its sensitivity at RA is on the average 85%, and specificity at differential diagnostics of RA--80% vs. ReA and 92% vs. SLE. We consider that coefficient LFbetaAT-III can be used as an additional criterion at differential diagnostics at RA early stages, while other specific antibodies cannot be detected yet.
17854748 What is the role of rituximab in the treatment of rheumatoid arthritis? 2007 Sep Rituximab is a monoclonal antibody against CD20 that was developed for the treatment of relapsed or refractory B-cell non-Hodgkin's lymphoma (NHL). Recent controlled trials have shown that B cell-targeted therapy with rituximab is effective in RA (which suggest that B lymphocytes may be critical in its pathogenesis of RA) and early exposure data suggest that the tolerability and safety profile of rituximab may be even better in RA than in NHL patients. Rituximab is generally well tolerated, with a low incidence of serious adverse events, including serious infections. Available evidence suggests that its clinical benefits depend on effective B cell depletion, and the fact that its novel mode of action leads to the depletion of B cells makes it distinct from other biological therapies for RA that target T cells and their related cytokines. Although complete peripheral B cell depletion is regularly seen in RA and other autoimmune diseases, especially systemic lupus erythematosus (SLE), incomplete depletion has been reported in a subset of patients, even after full dosing with rituximab.
18205826 The MMP2 rs243865-T allele is not a major genetic factor for rheumatoid arthritis in the F 2008 Apr The MMP2 rs243865-T allele was recently suggested to be associated with rheumatoid arthritis (RA) in a case-control study. MMP2 is a positional RA candidate gene. Our aim was to test rs243865 in a French family based study. No significant result was shown. The MMP2 rs243865-T allele is not a major rheumatoid arthritis genetic factor in this population.
16471244 [Evaluation of the degree of clinical rheumatoid arthritis activity based on the concentra 2006 Jan BACKGROUND/AIM: Experimental in vitro and in vivo investigations in a mouse model have proved that TNF-alpha, IL12, IL-15 and IL18 participate in the pathogenesis of erosive inflammatory arthritis. The aim of this research was to determine the clinical significance of cytokines in the evaluation of the activity of rheumatoid arthritis (RA). METHODS: Inside a 4-year period we followed-up 64 patients with RA as newly ocurred or in the phase of worsening. We observed the clinical manifestation of the disease upon which we divided the patients in to 3 groups: the patients with low active RA, patients with moderate active RA, and the patients with wild active RA. The control group (n=25 patients) included the patients with osteoarthrosis (OA), and arthritis of the knee. In the samples of serum of all of the patients the concentratin of cytokines TNF-alpha, IL-12, IL-15, and IL-18 were determined using the immunoenzymatic methods in mice for human interleukines. By comparing the concentrations in 30 patients with the high, 14 patiens with moderate, and 20 patiens with the mild activity of RA it was determined that the patients with the high degree of the disease activity, had significantly high (p < 0.01; p < 0.05) concentrations of the examined cytokines in blood and synovial fluid as compared to the patients with the moderate and mild active disease. There was a relationship (p < 0.01) between the concentrations of cytokines in blood and synovial fluid with the quantity of the Disease Activity Score in 28 joints. CONCLUSIONS: Cytokines concentrations could be good indicators of the degree of the general activity of RA. This research could contribute to the interpretation of insufficiently well known views of the pathogenesis role and significance of citokines in an active disease.
16567783 Interobserver variation in the measurement of patellar height after total knee arthroplast 2006 Apr We assessed the reproducibility and accuracy of four ratios used to measure patellar height, namely the Blackburne-Peel, Caton-Deschamps, Insall-Salvati and modified Insall-Salvati, before and after total knee arthroplasty. The patellar height was measured, by means of the four ratios, on the pre- and post-operative lateral radiographs of 44 patients (45 knees) who had undergone total knee arthroplasty. Two independent observers measured the films sequentially, in identical conditions, totalling 720 measurements per observer. Statistical analysis, comparing both observers and ratios, was carried out using the intraclass correlation coefficient. Before operation there was greater interobserver variation using either the Insall-Salvati or modified Insall-Salvati ratios than when using the Caton-Deschamps or Blackburne-Peel methods. This was because of difficulty in identifying the insertion of the patellar tendon. Before operation, there was a minimal difference in reliability between these methods. After operation the interobserver difference was greatly reduced using both the Caton-Deschamps and Blackburne-Peel methods, which use the prosthetic joint line, compared with the Insall-Salvati and modified Insall-Salvati, which reference from the insertion of the patellar tendon. The theoretical advantage of using the Insall-Salvati and modified Insall-Salvati ratios in measuring true patellar height after total knee arthroplasty needs to be balanced against their significant interobserver variability and inferior reliability when compared with other ratios.