Aim. Septic arthritis (SA) is considered a medical emergency. The most common etiological agents are glucose consuming bacteria, so we evaluated the clinical utility of synovial fluid (SF) glucose levels and other biochemical parameters for supporting the diagnosis of the disease and their association with a positive bacteria culture and joint destruction. Methods. Adult patients with SA diagnose were enrolled prospectively between July 2018 and October 2019. As control group, adults with knee osteoarthritis, meniscus and/or knee ligaments lesions were enrolled. SF samples were obtained from the joints by arthrocentesis/arthrotomy. Microbiological analyses of SF were performed using Brucella broth blood culture flasks, samples were incubated at 37°C with 5% CO. 2. for 24 hours. Gram stain, chocolate and blood agar were used for the identification and growth of the bacteria. SF glucose levels, pH and leukocyte esterase were measured as biochemical parameters using a glucometer and colorimetric test strips. The Outerbridge classification was used for grading the osteochondral injury. Furthermore, blood samples were collected from patients and control subjects for determining glucose levels. Results. We included 8 subjects with knee ligaments lesions, 6 with meniscus lesions and 5 with osteoarthritis as control group, as well as 20 patients with SA diagnose. The mean age of the patients was 57.8 years with a 65% of male predominance. The most common affected joint was the knee (85%). SF culture was positive in 60% of the cases and the most common etiological agent was Staphylococcus aureus (58.3%). SF glucose levels from patients were lower than the controls (P=0.0018) and showed the lowest concentration in patients with a positive culture (P=0.0004). There was also a difference between blood and SF glucose concentration from the positive culture patients (P<0.0001). Leucocyte esterase presented the highest values in positive culture patients (P=<0.0001) and a more acidic pH was found compared to the control group (P<0.0001). Regarding the osteochondral injury, the lowest concentrations of SF glucose were found in patients with a higher grade in the classification (P = 0.0046). Conclusions. SF glucose and leukocyte esterase concentrations might be a quick and cheap useful parameter for the physician for distinguishing between bacterial infection and not infected joint. In addition, the lowest SF glucose levels might give information about the joint damage due to the disease

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

Rheumatoid arthritis (RA) is an autoimmune disease characterized by symmetrical and chronic polyarthritis. Fibroblast-like synoviocytes are mainly involved in joint inflammation and cartilage and bone destruction by inflammatory cytokines and matrix-degrading enzymes in RA. Approaches that induce various cellular growth alterations of synoviocytes are considered as potential strategies for treating RA. However, since synoviocytes play a critical role in RA, the mechanism and hyperplastic modulation of synoviocytes and their motility need to be addressed. In this review, we focus on the alteration of synoviocyte signalling and cell fate provided by signalling proteins, various antioxidant molecules, enzymes, compounds, clinical candidates, to understand the pathology of the synoviocytes, and finally to achieve developed therapeutic strategies of RA.

Cite this article: Bone Joint Res 2021;10(4):285–297.

Acetabulum fractures caused by civilian firearms represent a unique challenge for orthopaedic surgeons. Treatment strategies should include the assessment of infection risk due to frequently associated abdominal injuries and maintenance of joint function. Still, internationally accepted treatment algorithms are not available. The aim of the study was to increase knowledge about civilian gunshot fractures of the acetabulum by describing their characteristics and management at a high-volume tertiary hospital. All adult patients admitted to our hospital between January 2009 and December 2022 with civilian gunshot fractures of the acetabulum were included in this descriptive retrospective study. In total our institution treated 301 patients with civilian gunshot fractures of the hip joint and pelvis during the observation period, of which 54 involved the acetabulum. Most patients were young males (88,9%) with a mean age of 29 years. Thirty patients (55,6%) had associated intraabdominal or urological injuries. Fracture patterns were mostly stable fractures with minor joint destruction amenable to conservative fracture treatment (n=48, 88,9%). Orthopaedic surgical interventions were performed in 21 patients (38,9%) with removal of bullets in contact with the hip joint via arthrotomy or surgical hip dislocation as most frequent procedures. Most patients received antibiotics on admission (n=49, 90,7%). Fracture related infections of the acetabulum were noted in six patients (11,1%) while the mortality in the study population was low with one demised patient (1,9%) due to the trauma burden. Most civilian acetabulum gunshot fractures are associated with intraabdominal or urological injuries. In comparison to the literature on extremity gunshot fractures, there is an increased risk of infection in our study population. The decision for surgical wash-out and bullet removal should be based on contamination and anticipated joint destruction, while osteosynthesis or primary arthroplasty are rarely necessary for these injuries

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

Abstract. Aim. End-stage arthropathy is a well-known complication of haemophilia, with recurrent haemarthroses leading to joint destruction, deformity, pain, and stiffness. In the knee, this is often treated with total knee arthroplasty (TKA), which can be more challenging in patients with haemophilia (PwH) and associated with poorer outcomes. We conducted a systematic literature review and meta-analysis to determine implant survivorship, functional outcomes and complication rates. Method. A systematic review was conducted using MEDLINE, EMBASE, and PubMed for studies reporting TKA outcomes with Kaplan-Meier survivorship in PwH (PROSPERO registered). Meta-analysis was performed for survivorship and outcomes, and the results were compared to outcomes from the National Joint Registry (NJR). Results. 19 studies, totalling 1187 TKAs (average age 39 years) were reviewed. In PwH, implant survivorship at 5, 10, and 15 years was 94%, 86%, and 76% respectively, whereas NJR reported survivorship for males <55 years was 94%, 90%, and 86%. Survivorship generally improved over the time period studied (1973–2017), but was inversely correlated with HIV infection (common in PwH). Range of motion improved by 10–20° post-operatively, and there were large improvements in Patient Reported Outcome Measures (PROMS). The prosthetic joint infection rate (PJI) was 6% compared to 0.5-1% in non-PwH, but the reporting of other complications, especially haematological, was inconsistent. Conclusions. TKA in PwH has similar 5-year survivorship to non-PwH, but a six-fold higher infection rate. There were marked improvements in range of motion and PROMS, but complications were poorly reported. There remains a need for larger, long-term studies with standardised reporting

Abstract. OBJECTIVE. Knee varus malalignment increases medial knee compartment loading and is associated with knee osteoarthritis (OA) progression and severity. 1. Altered biomechanical loading and dysregulation of joint tissue biology drive OA progression, but mechanistic links between these factors are lacking. Subchondral bone structural changes are biomechanically driven, involve bone resorption, immune cell influx, angiogenesis, and sensory nerve invasion, and contribute to joint destruction and pain. 2. We have investigated mechanisms underlying this involving RANKL and alkaline phosphatase (ALP), which reflect bone resorption and mineralisation respectively. 3. and the axonal guidance factor Sema3A. Sema3A is osteotropic, expressed by mechanically sensitive osteocytes, and an inhibitor of sensory nerve, blood vessel and immune cell invasion. 4. Sema3A is also differentially expressed in human OA bone. 5. HYPOTHESIS: Medial knee compartment overloading in varus knee malalignment patients causes dysregulation of bone derived Sema3A signalling directly linking joint biomechanics to pathology and pain. METHODS. Synovial fluid obtained from 30 subjects with medial knee OA (KL grade II-IV) undergoing high tibial osteotomy surgery (HTO) was analysed by mesoscale discovery and ELISA analysis for inflammatory, neural and bone turnover markers. 11 of these patients had been previously analysed in a published patient-specific musculoskeletal model. 6. of gait estimating joint contact location, pressure, forces, and medial-lateral condyle load distribution in a published data set included in analyses. Data analysis was performed using Pearson's correlation matrices and principal component analyses. Principal Components (PCs) with eigenvalues greater than 1 were analysed. RESULTS. PC1 (32.94% of variation) and PC2 (25.79% of variation) from PCA analysis and correlation matrices separated patients according to correlated clusters of established inflammatory markers of OA pain and progression (IL6/IL8, r=0.754, p<0.001) and anti-inflammatory mediators (IL4/IL10, r=0.469, p=0.005). Bone turnover marker ALP was positively associated with KL grade (r=0.815, p=0.002) and negatively associated with IL10 (r=−0.402, p=0.018) and first peak knee loading pressures (r=−0.688, p=0.019). RANKL was positively associated with IL4 (r=0.489, p=0.003). Synovial fluid Sema3A concentrations showed separate clustering from all OA progression markers and was inversely correlated with TNF-α (r=−0.423, p=0.022) in HTO patients. Sema3A was significantly inversely correlated with total predicted force in the medial joint compartment (r=−0.621, p=0.041), mean (r=−0.63, p=0.038) and maximum (r=−0.613, p=0.045) calculated medial compartment joint pressures during the first phase and mean (r=−0.618, p=0.043) and maximum (r=−0.641, p=0.034) medial compartment joint pressures during midstance outputs of patient-specific musculoskeletal model. CONCLUSIONS. This study shows joint inflammatory status and mechanical overloading influence subchondral bone-remodelling. Synovial Sema3A concentrations are inversely correlated to patient-specific musculoskeletal model estimations of pathological medial overloading. This study reveals Sema3A as a biological mediator with capacity to induce OA pain and disease progression that is directly regulated by gait mechanical loading. Declaration of Interest. (b) declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research reported:I declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project

Abstract. Cranial cruciate ligament (CrCL) disease/rupture is a highly prevalent orthopaedic disease in dogs and common cause of pain, lameness, and secondary joint osteoarthritis (OA). Previous experiments investigating the role of glutamate receptors (GluR) in arthritic degeneration and pain revealed that OA biomarkers assessing early bone turnover and inflammation, including osteoprotegerin (OPG) and the receptor activator of nuclear factor kappa-B ligand (RANKL) are more likely to be influenced by glutamate signalling. Moreover, interleukin-6 (IL-6) has a complex and potentially bi directional (beneficial and detrimental) effect, and it is a critical mediator of arthritic pain, OA progression and joint destruction. Objectives. 1) to recruit dogs undergoing CrCL disease/rupture surgery and obtain discarded synovial fluid (SF) and serum/plasma (ethics approval, RCVS:2017/14/Alves); 2) to quantify the biomarkers listed above in the SF and serum/plasma by enzyme linked immunosorbent assay (ELISA); 3) to assess radiographic OA at the time of surgery and correlate it with the biomarkers and clinical findings. Methods. Abnova, Abcam and AMSBIO ELISA kits were tested using a validation protocol relating the standard curve to a dilution series of SF and serum/plasma (1× to 1/50×), with and without SF hyaluronidase treatment to evaluate linearity, specificity and optimal dilutions. Validated ELISA kits were used to measure [IL-6], glutamate [glu], [RANKL] and [OPG] in SF and serum/plasma. For each dog, CrCL disease pre-operative lameness scores were graded as: (1) mild, (2) moderate (easily visible), (3) marked (encumbered), (4) non-weightbearing lameness. Blinded OA scoring was performed on radiographs [15–60, normal-severe OA]. Results. canine population (n=14) was of various breeds, aged between 2–10 years and weighing 17.1–45.5Kg; 42.86% male; 57.14% female; 83.33% males and 62.5% females were neutered. Lameness scores varied from 1 and 4 (average 2.07±1.12) and radiographic OA scores from 18 and 36 (average 27.86±5.11). Individual correlations in concentrations with respect to age, weight, lameness score (1–4) and OA scores (15–60) were tested. SF [glu] and lameness score were inversely correlated with higher levels of lameness corresponding to lower SF [glu] (P=0.0141). SF [RANKL] inversely correlated with weight (P=0.0045) and lameness score (P=0.0135), and serum [RANKL] inversely correlated with weight (P=0.0437). There was also a negative correlation between SF and serum [OPG] and weight (P=0.0165 and P=0.0208, respectively). No other significant correlations were detected. Overall, [glu] and [IL-6] are increased in SF compared to serum/plasma, by 12.84 and 1.28, respectively, whereas all the remaining biomarkers are higher (2–3 times) in the serum/plasma compared to SF. Principal component analysis (PCA) and Pearson correlation coefficient matrix [IL-6/glu/RANKL/OPG] (n=7) showed SF [IL-6] correlates with SF [glu] (rs=0.64) and strong positive correlations between SF/serum [RANKL] and SF/serum [OPG] (rs 0.68–0.96). Conclusions. Dogs with CrCL disease show an association between the bone remodelling markers RANKL and OPG, and the inflammatory cytokine IL-6, and to a lesser extent SF [glu]. Therapeutics targeting bone remodelling, IL-6 or GluR/[glu] may be of interest for the management of OA in dogs. Declaration of Interest. (b) declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research reported:I declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project

Osteoarthritis (OA), one of the most common motor system disorders, is a degenerative disease involving progressive joint destruction caused by a variety of factors. At present, OA has become the fourth most common cause of disability in the world. However, the pathogenesis of OA is complex and has not yet been clarified. Long non-coding RNA (lncRNA) refers to a group of RNAs more than 200 nucleotides in length with limited protein-coding potential, which have a wide range of biological functions including regulating transcriptional patterns and protein activity, as well as binding to form endogenous small interference RNAs (siRNAs) and natural microRNA (miRNA) molecular sponges. In recent years, a large number of lncRNAs have been found to be differentially expressed in a variety of pathological processes of OA, including extracellular matrix (ECM) degradation, synovial inflammation, chondrocyte apoptosis, and angiogenesis. Obviously, lncRNAs play important roles in regulating gene expression, maintaining the phenotype of cartilage and synovial cells, and the stability of the intra-articular environment. This article reviews the results of the latest research into the role of lncRNAs in a variety of pathological processes of OA, in order 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 2021;10(2):122–133

Aim. Septic arthritis is a painful infection of articular joints that is typically treated by irrigation & debridement along with antibiotic therapy. There is debate amongst the medical community whether antibiotic administration should be delayed until fluid cultures have been taken to improve culture yield. However, delaying antibiotics can also have negative consequences, including joint destruction and sepsis. Therefore, the purposes of this study were to determine: 1) whether delayed antibiotic treatment affects culture yield and prognosis and 2) if the culture yield of patients treated for septic arthritis differs for hip, knee, and shoulder based on timing of antibiotic administration. Method. A retrospective analysis was conducted on 111 patients with septic arthritis of the hip, knee, or shoulder admitted from 3/2016 to 11/2018. In patients with multiple septic joints, each joint was analyzed individually (n=122). Diagnosis was determined by the treatment of irrigation & debridement and/or a positive culture. Patients without all intervention times recorded or with periprosthetic joint infection were excluded. Demographics, laboratory tests, culture results, and intervention times were obtained through chart review. Patients were grouped based on antibiotic therapy timing: >24 hours prior to arthrocentesis (Group 1), between 24 hours and 1 hour prior (Group 2), and 1 hour prior to post-arthrocentesis (Group 3). Analysis was conducted using chi-squared tests. Results. The mean age of each group were similar: Group 1 (n=38) 55.7 years, Group 2 (n=20) 57.2 years, and Group 3 (n=64) 54.8 years. No difference was observed in culture sensitivity between groups (p=0.825) with 71.1% (27/38) positive cultures in Group 1, 75% (15/20) in Group 2, and 76.6% (49/64) in Group 3. Similarly, frequency of related readmissions within 90 days (p=0.863) did not significantly vary: 26.3% (10/38) in Group 1, 20% (4/20) in Group 2, and 25% (16/64) in Group 3. Additionally, there were no significant differences in culture sensitivity in the knee (p=0.618; Groups: 87.5%, 75%, 70.6%), shoulder (p=0.517; Groups: 77.8%, 66.7%, 90%), and hip (p=0.362; Groups: 61.9%, 80%, 80%). Conclusions. Culture sensitivities and rates of readmission were similar for all patients regardless of antibiotic administration timing. These results suggest that antibiotic administration should not be delayed in septic arthritis to improve culture yield. However, the data does not suggest that early antibiotic administration will result in better clinical outcomes by lowering readmission rates. Further research is needed to better determine the clinical benefits that early administration of antibiotics may have on patient outcomes

Our approach to reconstructing forefoot deformities in patients with rheumatoid arthritis was as follows. In the lateral toes with mild or moderate joint destruction, shortening oblique osteotomy of the metatarsals is performed. With severe joint destruction, metatarsal head is resected. Arthrodesis of the first MTP joint is performed as a rule with resection arthroplasty in the lateral toes. When shortening oblique osteotomy in the lateral toes is indicated, the great toe is managed as follows: in young patients with mild joint destruction in the great toe (Larsen grades I and II) and who are able to ambulate well, Mitchell’s osteotomy is done. In older patients, or in patients with moderate or severe joint destruction (Larsen grades III to V), flexible hinge toe prosthesis is implanted. Between 1987 and 2000, Mitchell’s osteotomy was performed on 47 feet in 31 patients, whose mean age was 53 years, Larsen grade was 2.5 and hallux valgus angle (HVA) was 35.0 (SD11.9). Arthroplasty with flexible hinge toe prosthesis was performed on 31 feet in 23 patients, 58 years, Larsen grade was 3.7 and HVA was 45.3 (SD12.9). After 1995, grommets were used in 17 feet. In 2002, we studied clinical results of them. 40 feet of Mitchell’s osteotomy had no pain and 7 feet had some pain. 26 feet of arthroplasty with flexible hinge toe prosthesis had no pain and 5 feet had some pain. Radiologically, HVA was 17.2 (SD10.3) in Mitchell’s osteotomy and 12.1 (SD6.3) in arthroplasty with flexible hinge toe prosthesis. Maintenance of correction by arthroplasty with flexible hinge toe prosthesis was better than Mitchell’s osteotomy significantly, especially more than 30 degrees of HVA. Without grommets, grade 0 was 8 feet, grade I was 3, and grade II was 3 feet judged by Granberry’s grade. But no revision surgery was performed by silicone synovitis or fracture of implant. With grommets, there were no fractures. We added degree of HVA to management of operation after 2002. More than 40 degrees of HVA was considered flexible hinge toe prosthesis. After 2002, Mitchell’s osteotomy was performed on 7 feet in 6 patients, 53.7 years, Larsen grade was 2.4 and HVA was 32.3 (SD6.8). Arthroplasty with flexible hinge toe prosthesis was performed on 14 feet in 10 patients, 60.7 years, Larsen grade was 3.9 and HVA was 42.5 (SD7.5). Radiological result in these patients at 2005, HVA was 14.6 (SD4.9) in Mitchell’s osteotomy and 14.9 (SD2.5) in arthroplasty with flexible hinge toe prosthesis

Introduction. A staging system has been developed to revise the 1994 ARCO classification for ONFH. The final consensus resulted in the following 4-staged system: stage I—X-ray is normal, but either magnetic resonance imaging or bone scan is positive; stage II—X-ray is abnormal (subtle signs of osteosclerosis, focal osteoporosis, or cystic change in the femoral head) but without any evidence of subchondral fracture, fracture in the necrotic portion, or flattening of the femoral head; stage III—fracture in the subchondral or necrotic zone as seen on X-ray or computed tomography scans. This stage is further divided into stage IIIA (early, femoral head depression ≤2 mm) and stage IIIB (late, femoral head depression >2 mm); and stage IV—X-ray evidence of osteoarthritis with accompanying joint space narrowing, acetabular changes, and/or joint destruction. Radiographs, magnetic resonance imaging (MRI), and computed tomography (CT) scans may all be involved in diagnosing ONFH; however, the optimal diagnostic modality remains unclear. The purpose of this study was to identify: 1) how ONFH is diagnosed at a single academic medical center, and 2) if CT is a necessary modality for diagnosing/staging OFNH. Methods. The EMR was queried for the diagnosis of ONFH between 1/1/2008–12/31/2018 at a single academic medical center. CT and MRI scans were reviewed by the senior author and other contributors. The timing and staging quality of the diagnosis of ONFH were compared between MRI and CT to determine if CT was a necessary component of the ONFH work-up. Results. There were 803 patients with ONFH over the 10 years of study. 382 had CT only, 166 had MRI only, and 255 had both a CT and MRI. Of the 255 patients who had both CT and MRI, 228 actually had ONFH after inspection. A diagnosis of ONFH was made by MRI only in 57% (129/228) while another 21% (48/228) used MRI and CT simultaneously. 22% (51/228) of cases were diagnosed by CT scan first. 94% (48/51) of these cases involved a cancer (CA) diagnoses, the CT scans were used for CA staging and were not helpful with ARCO staging of ONFH. The other 3 cases identified asymptomatic ONFH. MRI scans performed after diagnosis with CT in symptomatic patients were then utilized for staging. Conclusion. Although CT scan was a useful adjunct for diagnosing ONFH during a staging workup for CA, it was not useful for ARCO staging of ONFH and treatment decisions. Based on this retrospective study, CT scan is not necessary when using the Revised ARCO Staging System

The aim of this abstract is to show that acute osteomyelitis is one of the most feared complication of orthopedic surgery. A rapid and aggressive treatment is mandatory in order to avoid significant bone loss, joint destruction and, in most cases, salvage of the limb. After apparent cure of the infection, sequelae must be addressed. In this case, the joint destruction was important, so reconstruction procedures where impossible. In a superficial and relatively small joint such as the elbow, it is preferred to do an arthrodesis than an arthroplasty because the risk of reactivation of the infection with implant involvement is very important. We present a case report of a 69 years old woman, who had a supra-intra-condylar fracture (AO 13-C1) of the right humerus. She was treated with open reduction and internal fixation with 2 internal lag screws and 2 external lag screws. After 6 weeks, she was admitted with a dislocated elbow associated with pain, loss of limb function, cubita nerve palsy and a purulent discharge from the surgical wound. She started vancomycin and was submitted to surgery with debriment, hardware removal and fixation with an external fixator was used. The local signs of infection disappeared progressively. After normalization of the laboratory parameters of infection, the patient was submitted to an elbow arthrodesis using a posterior contour plate. The elbow achieved solid fixation and infection was eradicated, at least for the time being, allowing the patient to use the upper limb in her daily live activities. The treatment of post operative acute osteomyilits is challenging, In this case, after apparent solution of the infection, a solid fixation of the elbow was achieved, allowing the use of the upper limb in the patient daily activities

Purpose: Operative wounds are commonly washed with a more or less diluted antiseptic solution to prevent infection or to treated overt infection. Chlorhexidine is widely used. We report the cases of nine patients who developed joint destruction attributed to peroperative irrigation with a chlorhexidine solution. Material and methods: Nine patients (three men and six women) who had undergone surgery in another facility were referred to our unit for unexplained postoperative chondrolysis. The joint localisations were: wrists (n=7) after surgery for a dorsal arthrosynovial cyst (mean age 37 years); elbow (n=1) after surgery for epicondylalgia (age 49 years); shoulder (n=1) after arthroscopy for sub-acromial impingement (age 51 years). The time between surgery and the first consultation in our unit varied from three to nine years (mean five years four months). Persistent stiffness had been noted in the postoperative period with pain at joint mobilisation which worsened progressively. For the patients with chondrolysis of the wrist: the x-rays demonstrated destruction of the radius-first ray joint in one, the medio-carpal joint in four and overall destruction in two. Overall joint destruction was also observed in the elbow and shoulder patients. Search for other causes of joint destruction was negative; infection and inflammatory rheumatoid disease were ruled out. The common feature identified in all patients was joint irrigation with a chlorhexidine solution (Biseptine®). Results: Four of the nine patients underwent surgical treatment: a four-bone arthrodesis with scaphoidectomy was used for the three patients with mediocarpal involvement and a shoulder arthrodesis was performed in one patient. The pathology study demonstrated cartilage defects filled with dense strongly hyalinised acellular tissue. Bacteriological specimens were all negative. Discussion: The chondrolytic effect of chlorhexidine, a member of the biguanide family, was first reported in 1986 with a few cases described with knee involvement. Experimentally, there would be a dose-dependent effect. The mechanism involves a disorganisation of the cell membrane with cartilaginous necrosis and ostocartilaginous resorption. Individual predisposition cannot be ruled out. Conclusion: In light of these observations, it would be advisable to avoid peroperative joint irrigation with chlorhexidine solution

Aetiology and pathogenesis: The pathogenesis of boutonnière deformity, in the rheumatoid patient is usually quite clear, and is due to either a central slip failure or volar subluxation of the middle phalanx. This subluxation is seen more commonly in the patients with psoriatic arthropathy. The most common cause is a chronic synovitis of the proximal interphalangeal joint leading to attenuation of the sagital fibres between the central slip and the lateral bands and at a later stage disruption or attenuation of the central slip itself. Synovitis of the pip joint with separation of the lateral bands from the central slip allows the lateral bands to sublux forwards to lie anterior to the axis of rotation thus the intrinsics which extend the proximal and distal joints of the finger come to act as flexors of the proximal joint and continue to act as extensors to the distal joint. The patient will use the intrinsic muscles and they now have a flexion force upon the PIP joint and hyperextension force on the DIP joint, causing a boutonnière deformity. Volar subluxation of the middle phalanx draws forwards the lateral bands and defunctions the central slip creating the same imbalance. Scarring of the volar plate as is seen in volar plate injuries with the production of a pseudo-boutonnière deformity is sometimes seen in psoriatic arthropathy. In a boutonnière deformity the PIP joint is flexed and the DIP joint is extended. With the joints in this position, the origin and insertion of the intrinsic muscles are closer together, and as a consequence, with the passing of time, the muscles fibres will remodel in a shortened position, creating a lateral band tightness. Classification: Boutonnière deformity can be classified into four stages. Type I. The deformity is totally correctable passively, and there is full flexion of the DIP joint when the PIP joint is fully extended. The patient has a passively correctable flexion deformity of the PIP joint, and can actively flex the distal interphalangeal joint. The anatomical alterations are the following: elongation of the sagital fibres and volar displacement of the lateral bands but no secondary shortening of musculo-tendinous system. Type II. Flexion of the DIP joint is limited when the PIP joint is passively corrected. The patient cannot actively or passively flex the distal interphalangeal joint, when the PIP joint is passively corrected. Secondary shortening of the intrinsic/lateral band system because the intrinsics have remodelled in a shortened position. Type III. Stiffness of the PIP joint without joint destruction. There is no passive correction of the deformity but the joint surfaces are sound. The patient can not passively extend the PIP joint nor flex the DIP joint. Type IV. Stiffness of the PIP joint with joint destruction. In these cases, stiffness of the PIP joint is not only due to soft tissue remodelling but mainly to joint destruction. In this type, destruction of the joint cartilage should be added to the previously described anatomical deformities. X-ray examination is needed to confirm the diagnosis. Treatment: Boutonnière deformities, are both aesthetically and functionally less disabling than swan neck deformities because there is usually little loss of active PIP joint flexion. Some therapeutic options exist, and choosing the most appropriate surgical procedure will depend on the severity of the anatomical deformities which need to be corrected. Correction of PIP joint flexion. Mobilisation of the lateral bands and transposition of the lateral bands posterior to the axis of rotation of the PIP joint. Release of the volar plate of the PIP joint is often necessary because of secondary contracture. Improving active DIP joint flexion. The only way to restore loss of active DIP joint flexion is by performing a Dolphin tenotomy or formal lengthening of the conjoined lateral bands over the middle phalanx. Improving passive PIP joint extension. Passive extension of the PIP joint can usually be obtained by gentle manipulation and serial application of plaster of paris casts, as well as the use of a Capner (or armchair splint)the dorsal structures are usually quite thin and lax. If the joint can not be passively extended, a surgical release of the lateral bands is indicated,. Y-V plasty shortening of the central slip and extensor mechanism is usually necessary. A longitudinal incision at both sides of the central slip, allowing the lateral bands to displace dorsally during PIP joint extension with reefing of the lateral bands to the remnants of the central slip is needed in most cases. PIP joint arthroplasty. A PIP joint arthroplasty should be considered when the joint is destroyed. A radiological examination is essential in making the diagnosis, as many stiff PIP joints in flexion do not have their joint surfaces preserved because boutonnière deformities are often secondary to PIP joint synovitis. A full soft tissue procedure must be performed at the same time. DIP joint arthrodesis. Arthrodesis is only indicated for the treatment of uncorrectable deformity of the DIP joint with or without joint destruction, confirmed by radiological examination. The functional results of an arthroplasty are far superior for the treatment of a swan neck than a boutonnière deformity, because of the integrity of the extensor apparatus in the former, allowing for immediate postoperative motion. 7. PIP joint arthrodesis will be the treatment of choice if the finger presents a gross deformity with deteriorating function or failed surgery

Arthrosis of the hip joint can be a significant source of pain and dysfunction. While hip replacement surgery has emerged as the gold standard for the treatment of end stage coxarthrosis, there are several non-arthroplasty management options that can help patients with mild and moderate hip arthritis. Therefore, the purpose of this paper is to review early prophylactic interventions that may help defer or avoid hip arthroplasty. Nonoperative management for the symptomatic hip involves minimizing joint inflammation and maximizing joint mobility through intra-articular joint injections and exercise therapy. While weight loss, activity modifications, and low impact exercises is generally recommended for patients with arthritis, the effects of these modalities on joint strength and mobility are highly variable. Intra-articular steroid injections tended to offer reliable short-term pain relief (3–4 weeks) but provided unreliable long-term efficacy. Additionally, injections of hyaluronic acid do not appear to provide improved pain relief compared to other modalities. Finally, platelet rich plasma injections do not perform better than HA injections for patients with moderate hip joint arthrosis. Primary hip joint arthrosis is rare, and therefore treatment such as peri-acetabular osteotomies, surgical dislocations, and hip arthroscopy and related procedures are aimed to minimise symptoms but potentially aim to alter the natural history of hip diseases. The state of the articular cartilage at the time of surgery is critical to the success or failure of any joint preservation procedures. Lech et al. reported in a series of dysplastic patients undergoing periacetabular osteotomies that one third of hips survived 30 years without progression of arthritis or conversion to THA. Similarly, surgical dislocation of the hip, while effective for treatment of femoroacetabular impingement, carries a high re-operation rate at 7 years follow up. Finally, as the prevalence of hip arthroscopic procedures continues to rise, it is important to recognise that failure to address the underlying structural pathologies can lead to failure and rapid joint destruction. In summary, several treatment modalities are available for the management of hip pain and dysfunction in patients with a preserved joint space. While joint preservation procedures can help improve pain and function, they rarely alter the natural history of hip disease. The status of the articular cartilage at the time of surgery is the most important predictor of treatment success or failure

Inflammatory changes in synovial tissues occur commonly in knee osteoarthritis (OA) and are termed “inflammatory OA”. The pathogenic significance of this inflammatory OA is uncertain. It is also not known whether inflammatory changes in the synovial membrane are reflected in the synovial fluid (SF) and whether the SF contains a similar inflammatory cell infiltrate. This study examined 34 cases of knee joint OA and cytologically and immunohistochemically characterised inflammatory cells in the synovial membrane and SF. Specimens of SF and synovial membrane were taken at the time of knee arthroplasty. All cases of inflammatory OA synovium contained (CD68+) macrophages; several cases also contained a scattered, focally heavy (CD3+) lymphocytic infiltrate and occasional lymphoid aggregates. Inflammatory changes in OA SF reflected this cell composition with numerous CD68+ macrophages and CD3+ lymphocytes being noted in inflammatory OA cases. The SF volume was greater (> 5ml) in cases of inflammatory OA. Non-inflammatory OA knee joints contained very few inflammatory cells, which were mainly macrophages, in both the synovial membrane and SF. Our findings indicate that inflammatory changes in the synovial membrane of OA knee joints are reflected in the SF and that the volume of SF is commonly increased in cases of inflammatory OA. Both macrophages and lymphocytes in the inflammatory infiltrate of knee joint SF may contribute to joint destruction in OA by providing mononuclear phagocyte osteoclast precursors and the production of inflammatory cytokines and growth factors that promote osteoclastogenesis. In conclusion, the cytology of SF and synovitic membrane are similar in inflammatory OA. With knee effusions of greater than 5mls and inflammatory synovitic membrane consideration of total knee arthoplasty in the presence of single compartment disease should be considered because of the risk of further joint destruction

We distinguish three phases of rheumatoid arthritis:. the phase of hypertrophic synovitis;. the phase of joint disorganization;. the phase of joint destruction. During the synovitis phase, expansion of the synovial membrane leads to changes in the neighboring tissues with distension of the joint capsule and ligaments and destruction of the cartilage tissue. Tumefaction and increased volume of the tenosynovial membrane interferes with tendon gliding, giving rise to limited motion and pain. As the phase advances, tendon tears may appear because of invasiveness of the tenosynovial tissue. Surgical treatment during the synovitis phase can include synovectomy or tenosynovectomy. During the phase of joint disorganization, capsule and ligament distension induce the deviations and instabilities characteristic of rheumatoid arthritis. The basic objective of surgery is to realign the joints and restore the anatomic relations. Cartilage is lost during the phase of joint destruction and surgical reconstruction is the only option (arthroplasty, arthrodesis) but with inevitable loss of function. Wrist lesions should be treated before more distal joints. The principle of repairing the most proximal joint first applies for the entire upper limb. For the dorsal aspect of the fingers, injury to the extensor system gives rise to three characteristic deformities: mallet finger, swan-neck finger, and button hole finger. A detailed knowledge of the extensor system is needed to better understand the origin of these deformations. Briefly, the extensor system is composed of three tendon elements: the lateral bands, the median bands and the common tendon, and two retinacular elements: Landsmeer’s oblique retinacular ligament and Cleland’s transverse retinacular ligament. The objectives of surgery are:. achieve pain relief;. improve function (motion, stability);. prevent disease progression; and. improve the aesthetic aspect

Femoral head aseptic necrosis is a common complication after HSCT. In allogeneic HSCT recipients, hip tuberculosis on top of aseptic necrosis is infrequent and the mortality is high. We present a case of hip joint tuberculosis in a 57-year-old man with acute myelomonocytic leukemia (M4) treated with HSCT. The patient developed extensive chronic graft versus host disease (cGVHD) five months after transplantation and was treated with cyclosporine and corticosteroids. Eight months after the transplantation because of low-grade fever, elevated ESR and abnormal chest CT scan findings, empirical anti-TB treatment started despite negative tuberculin skin test. Three weeks later anti-TB treatment was stopped because of hepatic enzyme elevation. One year after the transplantation he complained about bilateral hip pain. MRI revealed bilateral femoral head aseptic necrosis. One year later, the right femoral head collapsed, and suddenly, rapid hip joint destruction occurred. He was planned to have total right hip arthroplasty. During the operation an abscess was evacuated and biopsy showed tuberculosis. Necrotic tissues and bone were removed and suction drainage was applied. Diagnosis was confirmed by acid-fast stain, PCR and cultures. In BACTEC MGIT 960 culture system and on Löwenstein-Jensen Mycobacterium tuberculosis was isolated, which was sensitive to all first line anti-TB drugs. After one year of anti-TB treatment (HRZE for 2 months followed by HRE for 10 months), synovial fluid samples were negative for tuberculosis. The patient was submitted to cementless total left hip replacement. Three months later, the right hip was allografted on the acetabular side and a reinforcement ring was used in order to perform a successful total hybrid arthroplasty. Nine months postoperatively the patient is symptom free and able to walk. Tuberculosis should be considered in the differential diagnosis when rapid joint destruction occurs. Early diagnosis improves response to anti-TB therapy and surgery

Introduction and Aims: Unilateral joint destruction in small joints of the hand presents a difficult challenge, particularly in younger patients. Pyrocarbon has a number of properties which may render it more suitable than metal for hemiarthroplasty in selected circumstances. We reviewed the results of our experience with PIP and MCP hemiarthroplasty utilising pyrocarbon implants to evaluate the clinical outcome in each case. Method: Since December 2001, 10 pyrocarbon hemiarthroplasties were implanted in 10 patients. Eight were implanted into the PIP joint and two into the MCP joint. The average patient age was 34.5 years (range 19–65). Nine procedures were for trauma and one for arthrosis. The decision to implant was taken when other reconstructive options were not considered possible and the patient would otherwise have been offered arthrodesis or amputation or total joint arthroplasty. The patients were reviewed clinically to establish their range of motion, pain control and satisfaction with surgery. Radiographic review was undertaken. Results: After an average follow-up of 13 months (range three to 23 months) all joints remain in-situ. The average arc of motion is 50.5 degrees. Average extension was minus eight degrees (range 0–20) and average flexion was 58.5 (range 15–90). There was no evidence of loosening. Erosion of the intact side of the joint was noted in only one patient. One patient was not satisfied with the final outcome. Conclusion: The short-term results of PIP and MCP hemiarthroplasty with a pyrocarbon prosthesis show reasonable promise and this procedure merits further evaluation of its role in the treatment of unilateral joint destruction. It may be preferable to either total joint arthroplasty or fusion, particularly in the younger patient