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OBJECTIVE: For better management of rheumatoid arthritis (RA), new biomarkers are needed to predict the development of different disease courses. This study aims to identify autoantibodies against epitopes on proteins in the joints and to predict disease outcome in patients with new onset RA. METHODS: Sera from new onset RA patients from the Swedish BARFOT and TIRA-2 cohorts (n = 1986) were screened for autoantibodies to selected peptides (JointIDs) in a bead-based multiplex flow immunoassay. Disease outcomes included Boolean remission 1.0, swollen joint count and radiographic destruction. Multivariate logistic regression and zero-inflated negative binomial models that accounted for clinical factors were used to identify JointIDs with the strongest potential to predict prognosis. RESULTS: Boolean remission was predicted with 42% sensitivity and 75% specificity in male patients positive for antibodies to a non-modified collagen type II (COL2) peptide at 12 months. When antibodies to a specific citrullinated cartilage oligomeric protein (COMP) peptide were absent and the patient was in Boolean remission at 6 months, the sensitivity was 13% and the specificity 99%. Positivity for the non-modified COL2 peptide also reduced the frequency of swollen joints by 41% and 33% at 6 and 12 months, respectively. Antibodies to cyclic citrullinated peptides (aCCP) predicted joint destruction with low specificity (58%). Positivity for a COL2 and a glucose-6-phosphate dehydrogenase peptide in citrullinated forms increased specificity (86%) at the expense of sensitivity (39%). CONCLUSION: Autoantibodies against joint-related proteins at RA diagnosis predict remission with high specificity and, in combination with clinical factors, may guide future treatment decisions.

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Various diseases and conditions cause joint disorders. Osteoarthritis (OA) is characterized by the degeneration of articular cartilage, synovitis, and anabolic changes in surrounding bone tissues. In contrast, rheumatoid arthritis (RA) and hemophilic arthropathy (HA) display marked destruction of bone tissues caused by synovitis. RA is a representative autoimmune disease. The primary tissue of RA pathogenesis is the synovial membrane and involves various immune cells that produce catabolic cytokines and enzymes. Hemophilia is a genetic disorder caused by a deficiency in blood clotting factors. Recurrent intra-articular bleeding leads to chronic synovitis through excessive iron deposition and results in the destruction of affected joints. Although the triggers for these two joint diseases are completely different, many cytokines and enzymes are common in the pathogenesis of both RA and HA. This review focuses on the similarities between joint and bone destruction in RA and HA. The insights may be useful in developing better treatments for hemophilia patients with arthropathy and osteoporosis by leveraging advanced therapeutics for RA.

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OBJECTIVES: The treatments for rheumatoid arthritis (RA) have been greatly improved, and the tight control of disease activity yields superior clinical outcomes. This study aimed to elucidate the accompanying changes in hip destruction following the implementation of a treat-to-target strategy for patients with RA. METHODS: We extracted 190 hips over two periods, i.e. the early period (1998-2003) and the late period (2013-19), with 103 and 87 hips, respectively. The observed rheumatic changes, such as inward migration, upward migration, and femoral head collapse, were quantitatively evaluated, while osteoarthritic changes, such as the formation of a capital drop, were investigated from radiographs before primary total hip arthroplasty. RESULTS: A comparison of the two periods' data showed that the degree of inward migration (-3.44 vs. -7.45 mm; P < .001) and upward migration (+4.3 vs. +0.95 mm; P < .001) significantly decreased in the late-period group. The collapse of the femoral head was not significantly different. The incidence of capital drops was significantly higher in the late-period group (7.8% vs. 27.5%; P < .001). CONCLUSIONS: The degree of inward and upward migration representative of rheumatic changes reduced, whereas the frequency of capital drops as osteoarthritic changes increased during the late period.

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Advanced omarthritis or an irreparable lesion of the rotator cuff are indications for the implantation of a shoulder prosthesis. Several models are available and the choice of model depends on the specific pathology of the patient. Preoperative medication management must be taken into account in rheumatism patients. The correct aftercare is essential for the proper functioning of the prosthesis.

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As a chronic progressive autoimmune disease, rheumatoid arthritis (RA) is characterized by mainly damaging the synovium of peripheral joints and causing joint destruction and early disability. RA is also associated with a high incidence rate and mortality of cardiovascular disease. Recently, the relationship between lipid metabolism and RA has gradually attracted attention. Plasma lipid changes in RA patients are often detected in clinical tests, the systemic inflammatory status and drug treatment of RA patients can interact with the metabolic level of the body. With the development of lipid metabolomics, the changes of lipid small molecules and potential metabolic pathways have been gradually discovered, which makes the lipid metabolism of RA patients or the systemic changes of lipid metabolism after treatment more and more comprehensive. This article reviews the lipid level of RA patients, as well as the relationship between inflammation, joint destruction, cardiovascular disease, and lipid level. In addition, this review describes the effect of anti-rheumatic drugs or dietary intervention on the lipid profile of RA patients to better understand RA.

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OBJECTIVES: Since inflammation can cause joint destruction in patients with rheumatoid arthritis (RA), it is assumed that joints that are symptomatic at onset are at higher risk of joint destruction; however, this theory remains controversial. This study aimed to investigate whether the progression of joint destruction in hands and feet could be predicted from the clinical and radiographic findings at onset. METHODS: This study included 75 patients who visited our hospital within one year after the onset of RA with at least 12 months of follow-up. We examined the positive predictive value (PPV) and the sensitivity of the clinical findings (swelling, tenderness, and squeeze test) and joint destruction at onset for the progression of joint destruction. RESULTS: Sixty joints (45 metacarpophalangeal and proximal interphalangeal joints, 15 metatarsophalangeal joints) exhibited progressive structural destruction during the study course. Both the PPV and the sensitivity of the clinical findings for the progression of joint destruction were low; however, only the sensitivity of the squeeze test for the feet was high. The PPV of joint destruction at onset was higher than the clinical findings, and the sensitivity of joint destruction at onset was as high as the squeeze test for the feet.  Conclusions: Regular follow-up with imaging is necessary regardless of symptoms and joint destruction at the onset. Adding the squeeze test for feet to routine clinical practice may help predict the risk of joint destruction for the feet.

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OBJECTIVES: This study aimed to investigate the trend of joint destruction patterns on knee radiographs of patients with rheumatoid arthritis (RA) undergoing total knee arthroplasty (TKA) over the past 16 years. METHOD: Medial joint space, lateral joint space, medial spur area, lateral spur area (L-spur), and femoro-tibial angle were obtained from 831 preoperative knee radiographs of patients with RA who underwent TKA between 2006 and 2021 using software capable of automatic measurements. Non-hierarchical clustering was performed based on these five parameters. Trends in the five individual radiographic parameters and the ratio of each cluster were investigated during the target period. Moreover, clinical data from 244 cases were compared among clusters to identify factors associated with this trend. RESULTS: All parameters, except for L-spur, showed significant increasing trends from 2006 to 2021. The radiographs were clustered into groups according to the characteristic pattern of radiographic findings: cluster 1 (conventional RA type), with bicompartmental joint space narrowing (JSN), less spur formation, and valgus alignment; cluster 2 (osteoarthritis type), with medial JSN, medial osteophytes, and varus alignment; and cluster 3 (less destructive type), with mild bicompartmental JSN, less spur formation, and valgus alignment. The ratio of cluster 1 showed a significantly decreasing trend contrary to the significantly increasing trend in clusters 2 and 3. The DAS28-CRP of cluster 3 was higher than those of clusters 1 and 2. CONCLUSIONS: Radiographs of TKA recipients with RA are increasingly presenting osteoarthritic features in recent decades. Key Points • Using automated measurement software, morphological parameters were measured from radiographs of 831 patients with rheumatoid arthritis who had undergone TKA in the past 16 years. • Cluster analysis based on the radiographic parameters revealed that the radiographs of patients with end-stage knee arthritis requiring total knee arthroplasty were classified into three groups. • In patients with rheumatoid arthritis who have undergone total knee arthroplasty in the past 16 years, the proportion of clusters with features of osteoarthritis and difficult-to-treat rheumatoid arthritis has increased, while the proportion of conventional rheumatoid arthritis has decreased.

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Rheumatoid arthritis (RA), one of the most common autoimmune diseases, is characterized by multiple-joint synovitis with subsequent destruction of bone and cartilage. The excessive autoimmune responses cause an imbalance in bone metabolism, promoting bone resorption and inhibiting bone formation. Preliminary studies have revealed that receptor activator of NF-κB ligand (RANKL)-mediated osteoclast induction is an important component of bone destruction in RA. Synovial fibroblasts are the crucial producers of RANKL in the RA synovium; novel analytical techniques, primarily, single-cell RNA sequencing, have confirmed that synovial fibroblasts include heterogeneous subsets of both pro-inflammatory and tissue-destructive cell types. The heterogeneity of immune cells in the RA synovium and the interaction of synovial fibroblasts with immune cells have recently received considerable attention. The current review focused on the latest findings regarding the crosstalk between synovial fibroblasts and immune cells, and the pivotal role played by synovial fibroblasts in joint destruction in RA.

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Background Osteoarthritis (OA) is a chronic progressive disease that leads to the destruction of the articular cartilage inside the joint. OA is a common everyday musculoskeletal disorder worldwide, and it is believed that OA is triggered by genetics and environmental factors, including age, which is the most significant risk factor. This study aimed to investigate the general population's knowledge of OA and its related risk factors in Makkah, Saudi Arabia. Methodology This cross-sectional study was performed between December 2022 and January 2023 among the general population of Makkah, Saudi Arabia using an online survey using Google Forms. An appropriate statistical analysis was then conducted on the collected data. Results A total of 1,087 participants enrolled in this study. According to the multivariate logistic regression analysis, 48% (n = 789) of the participants reported that OA occurs due to joint cartilage age and use. In total, 69.7% of the participants knew that OA is a chronic problem, 84.4% knew it is a common disease, and 39.3% thought that all types of joints can suffer from OA. Over half (53.1%) of the participants knew that joint stiffness is a sign of OA, and 63.4% thought that OA may lead to the loss of joint motion. Over four-fifths (82.5%) thought that advancing age is a risk factor for OA, and 27.5% incorrectly thought that the incidence of OA is equal between men and women. Overall, 62.9% of the participants knew about clinical examinations and X-rays. Moreover, 78% thought that physiotherapy can improve the symptoms of OA, and 65.3% thought that some types of exercise can help. Finally, 35.8% of the participants had an overall awareness of OA, while 64.2% had poor awareness. Conclusions The general public of Makkah showed low knowledge of OA and its associated risk factors. Many misunderstandings about the causes, risk factors, and treatment of OA were acknowledged. Awareness campaigns with brochures and flyers can be used to raise the population's knowledge.

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Irreversible destruction of joints is the hallmark of rheumatoid arthritis (RA). Osteoclasts are the only bone-resorbing cells and play an important role in joint rebuilding. BML-111 (5(S),6(R),7-trihydroxyheptanoic acid methyl ester, C8 H16 O5 ) is a synthetic lipoxin A4 agonist with antioxidant and anti-inflammatory properties. The present study aimed to investigate the effect of BML-111 on osteoclasts in vivo and in vitro, to investigate its therapeutic effect on joint destruction in RA. Cell Counting Kit-8 assay and flow cytometry were used to exclude cytotoxic effects of BML-111 to bone marrow-derived macrophages (BMMs). Then, osteoclasts were differentiated in vitro from BMMs by used macrophage colony-stimulating factor and receptor activator of nuclear factor-κB ligand, and osteoclasts were observed following tartrate-resistant acid phosphatase staining with or without BML-111 treatment. Meanwhile, absorption pit assay and immunofluorescence staining of the fibrous actin ring were used to observe osteoclast function. Moreover, we examined mitogen-activated protein kinase (MAPK) and nuclear factor-κB (NF-κB) activation. We established collagen-induced arthritis in a rat model and, after treatment with BML-111, joint swelling was measured and the knee joints were processed for histology. We also examined serum and tissue for osteoclastogenesis-related markers. BML-111 inhibited osteoclast formation and differentiation in a time- and concentration-dependent manner, and downregulated the expression levels of MAPK and NF-κB in vitro. Meanwhile, BML-111 effectively alleviated joint structural damage and inhibited osteoclast formation in vivo. BML-111 inhibited osteoclast formation and differentiation in vitro and in vivo, and delayed the progression of joint destruction.

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OBJECTIVE: To determine the efficacy of peficitinib in reducing joint damage and predictive factors affecting treatment response in Japanese patients with rheumatoid arthritis. METHODS: This post hoc analysis used data from a placebo-controlled, phase 3 trial (RAJ4) of peficitinib in patients with rheumatoid arthritis and inadequate response to methotrexate. Erosion and joint space narrowing (JSN) were assessed at baseline and at Week 28/early termination of treatment using the van der Heijde-modified Sharp method. A univariate logistic regression analysis of change from baseline in a modified total Sharp score identified predictive factors with significant treatment interaction; the effects of these factors on treatment response were further evaluated using a multivariate model. RESULTS: The analyses included 481 patients. For most joint groups, peficitinib demonstrated a reduced change from baseline at Week 28/early termination in erosion and JSN scores versus placebo; a numerically greater effect was observed with peficitinib 150 mg versus 100 mg. Baseline C-reactive protein (CRP) and prednisolone dose were identified as clinically significant negative predictive factors: the treatment effect decreased as CRP or prednisolone dose increased for both peficitinib doses. CONCLUSIONS: Peficitinib 100 mg and 150 mg reduced joint damage versus placebo, across almost all joint groups. Higher baseline CRP and/or prednisolone dose were associated with reduced peficitinib efficacy. CLINICALTRIALS.GOV IDENTIFIER: NCT02305849.

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Background: Associations between rheumatoid arthritis (RA) and reduced skeletal muscle have been studied, and we firstly reported myopenia independently predict one-year radiographic progression in RA. Myokine myostatin can negatively regulate skeletal muscle mass and promote osteoclast differentiation. However, there is no report about their relationships in RA patients. We firstly explored the relationship of serum myostatin and disease characteristics, as well as aggravated joint destruction during one-year follow-up. Methods: Consecutive RA patients were recruited from a real-world prospective cohort and completed at least one-year follow-up. Baseline serum level of myostatin was measured by enzyme-linked immunosorbent assay. Clinical data in RA patients as well as muscle index in both RA patients and healthy controls were collected. One-year radiographic progression as primary outcome was defined by a change in the total Sharp/van der Heijde modified score ≥0.5 units. Results: Totally 344 RA patients (age 47.9 ± 12.5 years, 84.0% female) and 118 healthy control subjects (age 42.8 ± 11.3 years, 74.6% female) were recruited. Compared with healthy controls, RA patients showed a higher level of serum myostatin at baseline (3.241 ± 1.679 ng/ml vs. 1.717 ± 0.872 ng/ml, P<0.001), although lower appendicular skeletal muscle mass index (ASMI, 6.0 ± 0.9 kg/m2 vs. 6.5 ± 1.0 kg/m2, P<0.001). In RA patients, those with high myostatin level showed a higher rate of radiographic progression than low myostatin group (45.3% vs. 18.6%, P<0.001). Furtherly, RA patients were stratified into four subgroups according to serum myostatin and myopenia. Compared with other three subgroups, RA patients with high myostatin overlapping myopenia had the highest rate of radiographic progression (67.2% vs. 10.3%-31.4%, P<0.001), as well as the lowest proportion of remission and the highest rate of physical dysfunction during one-year follow-up. After adjustment for confounding factors, high serum myostatin (AOR=3.451, 95%CI: 2.016-5.905) and myopenia (AOR=2.387, 95%CI: 1.416-4.022) at baseline were risk factors for one-year radiographic progression, especially for those with high myostatin overlapping myopenia (AOR=10.425, 95%CI: 3.959-27.450) as the highest-risk individuals among four subgroups. Significant synergistic interaction effect was observed between high myostatin and myopenia on one-year radiographic progression (AP=66.3%, 95%CI: 43.2%-89.3%). Conclusion: Myostatin is a novel predictor of aggravated joint destruction in RA patients which has synergistic interaction with myopenia for predicting value.

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Rheumatoid arthritis (RA) is a systemic autoimmune disease accompanied with joint destruction. Serious joint destruction will eventually lead to disability and the decline of life quality in RA patients. At present, the therapeutic effect of drugs to alleviate joint destruction in RA is limited. Recently, accumulating evidences have shown that long non-coding RNAs (lncRNAs) play an important role in the pathogenesis of joint diseases. Therefore, this paper reviews the expression change and the action mechanism of lncRNAs in joint destruction of RA in recent years. A more comprehensive understanding of the role of lncRNAs in joint destruction will help the treatment of RA.

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The Authors describe a case of rapid right hip destructive septic arthritis in a 50-year-old male patient with no previous noteworthy medical history. Patient arrived to our attention following a one week history of right hip pain. Laboratory markers and imaging at presentation were negative. However, on a follow-up examination significant joint effusion was noted and joint tap was performed. Despite wide spectrum antibiotic therapy institution, significant joint damage was observed. This required surgical femoral head excision with antibiotic loaded spacer, followed by hip arthroplasty surgery 12 weeks afterwards. Complete healing of the infection and recovery of pain-free joint motion was noted at 1 year follow-up.

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Activated fibroblast-like synoviocytes (FLS) play a pivotal role in synovial inflammation and joint destruction of rheumatoid arthritis (RA). The mechanisms by which sonic hedgehog (SHH) signaling promotes RA FLS-mediated chronic inflammation and tissue damage are not fully understood. The present study aims to determine the role of SHH signaling in the pathogenesis of RA and to explore the potential mechanism(s). We found that the components of SHH signaling were highly expressed in FLS and synovial tissue from patients with RA and in the joint tissue of collagen-induced arthritis (CIA) mice. Overexpression of SHH aggravated the synovial inflammation and joint destruction of CIA and exacerbated cartilage degradation in the cartilage and RA FLS-engrafted severe combined immunodeficiency (SCID) model. Conversely, inhibition of SHH signaling significantly alleviated arthritis severity and reduced cartilage destruction caused by the invasion of RA FLS in vivo. Moreover, we found that p38 mitogen-activated protein kinase (MAPK) cascade was regulated by SHH signaling in RA FLS and the level of phospho-p38 in the joint tissue of CIA was decreased after blockade of SHH signaling. Inhibition of p38 MAPK abolished the effect of SHH overexpression on synovial inflammation and articular destruction of CIA and suppressed the aggressive properties of RA FLS, which were promoted by SHH agonist. In conclusion, our study suggests that SHH signaling aggravates synovial inflammation and joint destruction of experimental arthritis and promotes the abnormal behavior of RA FLS in a p38-dependent manner. SHH-p38 MAPK signaling could be a potential target for the treatment of RA.

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AIMS: To explore the synovial expression of mucin 1 (MUC1) and its role in rheumatoid arthritis (RA), as well as the possible downstream mechanisms. METHODS: Patients with qualified synovium samples were recruited from a RA cohort. Synovium from patients diagnosed as non-inflammatory orthopaedic arthropathies was obtained as control. The expression and localization of MUC1 in synovium and fibroblast-like synoviocytes were assessed by immunohistochemistry and immunofluorescence. Small interfering RNA and MUC1 inhibitor GO-203 were adopted for inhibition of MUC1. Lysophosphatidic acid (LPA) was used as an activator of Rho-associated pathway. Expression of inflammatory cytokines, cell migration, and invasion were evaluated using quantitative real-time polymerase chain reaction (PCR) and Transwell chamber assay. RESULTS: A total of 63 RA patients and ten controls were included. Expression of MUC1 was observed in both the synovial lining and sublining layer. The percentage of MUC1+ cells in the lining layer of synovium was significantly higher in RA than that in control, and positively correlated to joint destruction scores of RA. Meanwhile, MUC1+ cells in the sublining layer were positively correlated to the Krenn subscore of inflammatory infiltration. Knockdown of MUC1, rather than GO-203 treatment, ameliorated the expression of proinflammatory cytokines, cell migration, and invasion of rheumatoid synoviocytes. Knockdown of MUC1 decreased expression of RhoA, Cdc42, and Rac1. Treatment with LPA compromised the inhibition of migration and invasion, but not inflammation, of synoviocytes by MUC1 knockdown. CONCLUSION: Upregulated MUC1 promotes the aggression of rheumatoid synoviocytes via Rho guanosine triphosphatases (GTPases), thereby facilitating synovitis and joint destruction during the pathological process of RA.Cite this article: Bone Joint Res 2022;11(9):639-651.

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Rheumatoid arthritis (RA) is a systemic autoimmune disease during which fibroblast-like synoviocytes (FLS) contribute to both joint inflammation and destruction. FLS represent the core component of the synovial membrane. Following inflammation of this membrane, an effusion of cell-rich synovial fluid (SF) fills the joint cavity. Unlikely, SF has been shown to contain fibroblasts with some shared phenotypic traits with the synovial membrane FLS. These cells are called SF-FLS and their origin is still unclear. They are either brought into the synovium via migration through blood vessels, or they could originate within the synovium and exist in projections of the synovial membrane. SF-FLS function and phenotype are poorly documented compared to recently well-characterized synovial membrane FLS subsets. Furthermore, no study has yet reported a SF-FLS single-cell profiling analysis. This review will discuss the origin and cellular characteristics of SF-FLS in patients with RA. In addition, recent advances on the involvement of SF-FLS in the pathogenesis of RA will be summarized. Current knowledge on possible relationships between SF-FLS and other types of fibroblasts, including synovial membrane FLS, circulating fibrocytes, and pre- inflammatory mesenchymal (PRIME) cells will also be addressed. Finally, recent therapeutic strategies employed to specifically target SF-FLS in RA will be discussed.

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BACKGROUND: Rheumatoid arthritis (RA) is a disease that can cause joint destruction and multiple arthritis. We retrospectively investigated bone and joint destruction during the perinatal period in adult patients with RA and juvenile idiopathic arthritis (JIA) in our hospitals in the last decade. METHODS: The study included 15 women, with 20 pregnancies, 19 childbirths, and one fetal death recorded between 2009 and 2018. We analyzed patient characteristics, disease activity, the modified total Sharp score (mTSS), and ΔmTSS from prepregnancy to delivery and from delivery to one year after delivery in the biologics (BIO) group (biologics used before pregnancy) and non-BIO group (not using biologics). RESULTS: There were five preterm births and seven low-birth-weight infants. The Clinical Disease Activity Index (CDAI) before pregnancy and postdelivery worsened from 12±1.8 to 19.9±2.7 (p<0.05). The mTSS at prepregnancy and postdelivery was 47.7±12.2 and 57.3±11.1 in the BIO group, respectively, and 58.9±11.9 and 75.0±13.1 in the non-BIO group, respectively. In addition, the ΔmTSS value from prepregnancy to delivery and from delivery to one year after delivery was 14.5±4.8 and 9.2±1.7 in the BIO group, respectively (p<0.05), and 16.1±5.2 and 8.3±4.0 in the non-BIO group, respectively. CONCLUSION: The disease activity worsened, and bone and joint destruction progressed in both the BIO and non-BIO groups during the perinatal period in adult patients with RA and JIA in the last decade.

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Osteoarthritis (OA) is a degenerative disease resulting from progressive joint destruction caused by many factors. Its pathogenesis is complex and has not been elucidated to date. Advanced glycation end products (AGEs) are a series of irreversible and stable macromolecular complexes formed by reducing sugar with protein, lipid, and nucleic acid through a non-enzymatic glycosylation reaction (Maillard reaction). They are an important indicator of the degree of ageing. Currently, it is considered that AGEs accumulation in vivo is a molecular basis of age-induced OA, and AGEs production and accumulation in vivo is one of the important reasons for the induction and acceleration of the pathological changes of OA. In recent years, it has been found that AGEs are involved in a variety of pathological processes of OA, including extracellular matrix degradation, chondrocyte apoptosis, and autophagy. Clearly, AGEs play an important role in regulating the expression of OA-related genes and maintaining the chondrocyte phenotype and the stability of the intra-articular environment. This article reviews the latest research results of AGEs in a variety of pathological processes of OA, to provide a new direction for the study of OA pathogenesis and a new target for prevention and treatment. Cite this article: Bone Joint Res 2022;11(5):292-300.

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AIMS: This study aimed to answer two questions: what are the best diagnostic methods for diagnosing bacterial arthritis of a native joint?; and what are the most commonly used definitions for bacterial arthritis of a native joint? METHODS: We performed a search of PubMed, Embase, and Cochrane libraries for relevant studies published between January 1980 and April 2020. Of 3,209 identified studies, we included 27 after full screening. Sensitivity, specificity, area under the curve, and Youden index of diagnostic tests were extracted from included studies. We grouped test characteristics per diagnostic modality. We extracted the definitions used to establish a definitive diagnosis of bacterial arthritis of a native joint per study. RESULTS: Overall, 28 unique diagnostic tests for diagnosing bacterial arthritis of a native joint were identified. The following five tests were deemed most useful: serum ESR (sensitivity: 34% to 100%, specificity: 23% to 93%), serum CRP (sensitivity: 58% to 100%, specificity: 0% to 96%), serum procalcitonin (sensitivity: 0% to 100%, specificity: 68% to 100%), the proportion of synovial polymorphonuclear cells (sensitivity: 42% to 100%, specificity: 54% to 94%), and the gram stain of synovial fluid (sensitivity: 27% to 81%, specificity: 99% to 100%). CONCLUSION: Diagnostic methods with relatively high sensitivities, such as serum CRP, ESR, and synovial polymorphonuclear cells, are useful for screening. Diagnostic methods with a relatively high specificity, such as serum procalcitonin and synovial fluid gram stain, are useful for establishing a diagnosis of bacterial arthritis. This review helps to interpret the value of various diagnostic tests for diagnosing bacterial arthritis of a native joint in clinical practice. Cite this article: Bone Joint J 2021;103-B(12):1745-1753.

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