Strength, Size, and Muscle Quality in the Upper Arm following Unilateral Training in Younger and Older Males and Females

Purpose To assess strength, size, and muscle quality differences between younger and older males and females in response to training. Methods The bicep and tricep of the non-dominant arm were trained for twelve weeks in younger and older males and females (n = 41). The bicep of both arms were assessed pre and post for muscle strength using one-repetition maximum (1 RM) testing, and size using magnetic resonance imaging (MRI). Results Strength (p < 0.05), mCSA (p < 0.05), and 1 RM MQ (p < 0.00) increased in response to training in all subjects regardless of age or gender. Younger and older subjects had similar increases in strength (45.49 ± 15.30% vs. 42.67 ± 26.67% respectively), mCSA (16.22 ± 7.98% vs. 19.17 ± 6.19% respectively), and 1RM MQ (25.73 ± 15.76 vs. 19.67 ± 20.66 respectively). Women increased their strength (55.59 ± 19.45% vs. 32.87 ± 15.66% p < 0.00 respectively), size (20.36 ± 6.29% vs. 14.72 ± 7.28% p < 0.02 respectively), and 1 RM MQ (29.74 ± 18.33% vs. 16.30 ± 15.59% p <.02) more than men. In comparing age and gender, younger females increased their strength more than older males (56.42 ± 12.92% vs. 29.17 ± 21.8% p <.02 respectively). Older females also increased their strength more than older males (54.68 ± 25.73 vs. 29.17 ± 21.80% respectively). Younger females increased their 1 RM MQ more than older males (.18 ± .08 kg/cm vs. .06 ± .08 kg/cm p <.02 respectively). Conclusion Strength and mCSA increases similarly in older and younger subjects. However, the overall strength and quality of the muscle seems to improve more in women than in men.

Barriers to Healthcare in a Multiethnic Cohort of Systemic Lupus Erythematosus (SLE) Patients: Patient and Physician Perceptions

Objective Barriers to medical care may influence health status. It is unclear whether problems with access can predict clinical outcomes in lupus. This study aimed to determine whether care barriers are associated with increased disease activity and damage in a multi-center, multiethnic SLE cohort. We also compared concordance between care barriers as reported by the patient and lupus specialist. Methods Data from SLE patients in 12 Canadian centers collected at annual visits, including demographics, treatment, disease activity and damage were analyzed. Results 654 patients were enrolled with ethnic groups being Caucasian [CC] (64%), Aboriginal [ABO] (9%), Asian [AS] (21%), and Black [BLK] (6%). 50.8% had at least one barrier to care including travel to a rheumatologist (32.0%), waiting to see a rheumatologist and cost of medications. Access to medication and costs were significantly associated with co-morbidity (p < 0.001, p = 0.04). There were significant associations between ethnicity and any physician perceived care barrier < p < 0.001), mostly in Aboriginal. Doctors identified half of patients who had access to medication problems (p = 0.003) and the relationship between doctors and patients identifying similar care barriers was weak (r = 0.09). A lower total household income significantly predicted the presence of any care barrier (p < 0.001). Conclusions Despite access to a lupus specialist many care barriers were identified, although we found few associations between care barriers and patient outcomes. The cost of medication was related to SLE disease activity; however, we cannot determine if this was cause or effect. Care barriers identified by lupus patients are significantly underestimated by physicians.

Serum Levels of Anti-Cyclic Citrullinated Peptide Antibodies in Patients with Sjögren Syndrome Accompanied by Rheumatoid Arthritis

A 47-year-old woman demonstrated bilateral wrist joint pain during 4 weeks. Her status did not fulfill the ACR classification criteria for RA, and her symptoms had almost disappeared 4 weeks later. After about 1 year, she again complained of tenderness and swelling in the bilateral wrist joints. The laboratory data were as follows: ESR:61 mm/hour, CRP: 1.0 mg/dl, RF: 172 IU/ml, MMP-3: 178.7 ng/ml, and anti-cyclic citrullinated peptide antibodies (aCCP): 488 U/ml. Based on these findings, we diagnosed the patient as having RA. She was treated with several anti-rheumatic drugs, and joint symptoms decreased. This case was regarded as undifferentiated arthritis at the first visit. We later found the high titers of aCCP using her frozen sera after she fulfilled with ACR critera for RA, although aCCP was not checked at first time because its analysis was not covered by national health insurance in Japan. Thus, it is possible that this patient should have been treated as having RA from the first visit. In general, aCCP shows excellent specificity for RA diagnosis although sensitivity is lower. In contrast, it has demonstrated that aCCP is positive in about 40% of patients 1 year before the onset of RA. The clinical outcomes of patients with joint symptoms and positive aCCP analysis, but do not fulfill the ACR criteria for RA, should be assessed in plural patients.

The Influence of Traditional Herbal Medicine (Kampo) on Anti-cyclic Citrullinated Peptide Antibody Levels

We present three rheumatoid arthritis (RA) patients successfully treated with traditional herbal medicine (THM: Kampo). The treatment with THM resulted in a decrease in RA disease activity such as DAS28, as well as in the serum levels of anti-cyclic citrullinated peptide antibodies (anti-CCP) in 3 cases. These observations suggest that disease progression may be retarded in patients who respond to THM since anti-CCP is important for the prediction of disease severity and radiographic joint damage. Additionally, serial mesurements of anti-CCP titers may be a useful indicator in assessing this kind of treatment efficacy.

A Comprehensive Clinicopathologic Analysis Suggests that Vascular Endothelial Growth Factor (VEGF) is the Most Likely Mediator of Periosteal New Bone Formation (PNBF) Associated with Diverse Etiologies

Periosteal new bone formation (PNBF) is the means by which appositional bone growth normally takes place on the surfaces of compact bone. Alterations in the periosteal microenvironment trigger complex interactions between osteoblasts and endothelial cells to promote PNBF. Physiologic processes like mechanical stress result in normal PNBF; but, a variety of pathologic processes result in excessive PNBF. The production of sufficient bone to be detectable by conventional radiography is a common feature of diverse etiologies, including infection; inflammation; prostaglandin E2 administration for ductal-dependent congenital heart disease; metabolic and hormonal abnormalities; neoplasms; fracture repair; systemic hypoxia; and hypertrophic osteoarthropathy. While the clinical settings and distribution of affected bone sites in these conditions are different, the histopathology of the PNBF is essentially identical; so, it seems logical that a common pathway might mediate them all. By combining the observations and insights gained from osseous research and studying the clinical pathology of these diverse conditions, we constructed a comprehensive pathway to explain PNBF. In doing so, it seems likely that Vascular Endothelial Growth Factor (VEGF) is the most likely common mediator of the pathways that lead to PNBF.

Skin Infection by Coagulase Negative Staphylococci as a Potential Triggering Factor for Cutaneous Leukocytoclastic Vasculitis

Introduction Leukocytoclastic vasculitis (LV) is a necrotising vasculitis of the small dermal blood vessels, clinically presented as palpable purpura. It is a heterogeneous disorder often limited to the skin but which may involve other organs. LV might be a serious drug reaction, caused by bacterial and viral infections, or less commonly a manifestation of systemic vasculitic syndromes. Case Reports Three patients were admitted to our institution with petechiae and palpable purpura. The cutanous lesions were affecting the lower limbs and in one patient also the upper extremities and the trunk. The diagnosis of leukocytoclastic vasculitis was made based on clinical and histopathological findings. Systemic involvement was excluded, as was connective tissue disease. Clinical examination revealed ulcers on the legs of each patient. Smears from those ulcers were taken and investigated for micro organisms. Culture results showed infection with coagulase negative staphylococci. Systemic signs of sepsis were absent; therefore the infections were treated locally. Two patients developed necrotic blisters during the first week of hospitalisation. To avoid further vasculitic complications steroids were administered parenterally and LV lesions diminished in all patients within ten days. Conclusion Drugs and connective tissue disease were ruled out as triggering factors of LV in the patients reported on. Therefore, it was concluded that superantigens produced by the coagulase negative staphylococci were responsible for LV.

Hypertrophic Synovitis of the Facet Joint Causing Root Pain

Osteoarthritic changes in the facet joints are common in the presence of degenerative disc disease. Changes in the joint capsule accompany changes in the articular surfaces. Intraspinal synovial cysts that cause radicular pain, cauda equina syndrome, and myelopathy have been reported; however, there have been few reports in orthopedic or neurosurgical literature regarding hypertrophic synovitis of the facet joint presenting as an incidental para-articular mass. Here, we report a case of hypertrophic synovitis causing root pain. We describe the case of a 65-year-old man suffering from right sciatica and right leg pain in the L5 nerve-root dermatome for 1 year; magnetic resonance imaging (MRI) revealed an enhanced mass around the L4–5 facet joint. We investigated this mass pathologically. After right medial facetectomy, the symptoms resolved. Pathological investigation revealed this mass was hypertrophic synovitis. Hypertrophic synovitis of the facet joint might cause root pain.

Cartilage-Specific Matrix and Integrin Expression in Three-Dimensional Articular Chondrocyte Cultures Overexpressing Human Interleukin-10

Interleukin (IL)-10 overexpression inhibits joint inflammation, however the effect of high local concentrations of IL-10 on chondrocyte homeostasis remains unclear. The aim of this study was to determine the effects of IL-10 overexpression on cartilage matrix production in three-dimensional (3D) chondrocyte cultures. Human articular chondrocytes were transduced with adenoviral vectors alone (adv/empty) or by vectors either overexpressing enhanced green fluorescence protein (adv/EGFP) or human IL-10 (adv/hIL-10) before their transfer to a 3D culture system. Non-transduced chondrocytes were used as controls. The expression of IL-10 or EGFP was confirmed using ELISA or flow cytometry. Chondrocytes synthesis of collagen types II and I, aggrecan, fibronectin and β1-integrin was determined over a period of 14 days post transduction using flow cytometry or immunohistochemistry. adv/EGFP or adv/IL-10 transduced chondrocytes expressed EGFP or secreted IL-10 detectable over the 2 weeks culture period. No suppression of collagen type II, aggrecan or β1-integrin synthesis by IL-10 overexpression was found and the deposition of collagen type I and fibronectin remained unaffected compared to the controls. IL-10 overexpression does not impair key features of chondrocytes differentiated phenotype (e.g. collagen type II and aggrecan expression) suggesting the potential use of IL-10 for gene therapeutic approaches in the joint.

Critical Involvement of Cytokines and Chemokines in the Pathogenesis of Rheumatoid Vasculitis

Vasculitis in rheumatoid arthritis (rheumatoid vasculitis) has a heterogeneous clinical presentation that includes skin disorders, neuropathy, eye symptoms and systemic inflammation. The molecular mechanisms underlying rheumatoid vasculitis are not fully understood; however, the importance of a chronic imbalance of the cytokines and chemokines involved in orchestrating inflammatory responses is well established in patients with rheumatoid arthritis, and similar dysregulation of these mediators has been suggested to occur in patients with rheumatoid vasculitis. In the present review, we discuss the involvement of cytokines and chemokines in the pathogenesis of rheumatoid vasculitis and evaluate their utility as laboratory parameters of active vasculitic disease. Also the involvement of adhesion molecules is discussed.

Radiological and Magnetic Resonance Imaging Findings in the Sacroiliac Joints in Patients with early Spondylarthropathy

Objective To compare the radiological (X-ray) and magnetic resonance imaging (MRI) findings in the sacroiliac (SI) joints in patients with early spondylarthropathy (SpA). Methods Forty consecutive HLA B27 antigen positive patients with early SpA and inflammatory low back pain (LBP) were studied. Their SI joints were investigated by posterior anterior plain X-ray and MRI. Results The X-ray and MRI examinations gave similar results in the SI joints in 24 patients, whereas they differed in 16, this difference being significant (p = 0.007). In those 16 patients, in whom the findings differed, the X-ray findings were normal but MRI showed sacroiliitis which was bilateral in 13 and unilateral in 3 patients. The kappa coefficient between these investigations was 0.346, showing poor agreement. Conclusion These results indicate that MRI may considerably improve the diagnosis of sacroiliitis in HLA B27 antigen positive patients with early SpA and inflammatory LBP.