Cause Of Joint Pain Research Articles

Síndrome do impacto do tornozelo na ressonância magnética: ensaio iconográfico

A síndrome do impacto do tornozelo é uma condição dolorosa causada por atrito de tecidos articulares, que é tanto causa quanto consequência de uma biomecânica alterada desta articulação. A sua principal causa são as lesões pós-traumáticas, principalmente lesões ligamentares, resultando em dor crônica no tornozelo. Do ponto de vista anatômico e clínico, estas síndromes são classificadas em: ântero-lateral, anterior, ântero-medial, póstero-medial e posterior. A ressonância magnética é um ótimo método diagnóstico para demonstrar as alterações ósseas e as partes moles dos vários tipos de impacto do tornozelo, fornecendo dados que auxiliam não só na comprovação desse diagnóstico, como na diferenciação com outras causas de dor articular. Os autores objetivam ilustrar os principais achados de ressonância magnética na síndrome do impacto do tornozelo.

Cartilage Degeneration is Associated with Augmented Chemically-induced Joint Pain in Rats: A Pilot Study

Osteoarthritis arising from cartilage degeneration is the most common cause of joint pain. However, the relationship between joint pain and cartilage degeneration is not well understood. We asked whether the inflammatory mediators participate in the joint pain in the presence of cartilage degeneration. We observed electromyographic responses of hindlimb flexors to four inflammatory mediators (bradykinin, ATP, acetylcholine, and serotonin) injected in normal rat knees and in those with monosodium iodoacetate (MIA)-induced arthritis. Joint cartilage of all the rats with MIA-induced arthritis histologically showed severe degeneration. We observed greater magnitude and longer duration responses in the MIA-induced arthritis than normal joints with all four mediators. The data suggested nociceptors in osteoarthritic joints are more sensitive to inflammatory mediators than in normal joints. Such nociceptive sensitization to inflammatory mediators may participate in the joint pain in osteoarthritis.

Calcific Tendinitis: A Pictorial Review

Calcific tendinitis is caused by the pathologic deposition of calcium hydroxyapatite crystals in tendons and is a common cause of joint pain. The disease typically affects the shoulder and hip, with characteristic imaging findings; however, any joint can be involved. Occasionally, calcific tendinitis can mimic aggressive disorders, such as infection and neoplasm, especially on magnetic resonance imaging. Radiologists should be familiar with the imaging findings to distinguish calcific tendinitis from more aggressive processes. Image-guided percutaneous needle aspiration and steroid injection of calcific tendinitis are useful techniques performed by the radiologist for the treatment of symptomatic cases. Familiarity with these procedures and their imaging appearance is an important aspect in the management of this common disease.

Rheumatologists’ recommendations on what to do in the dermatology office to evaluate and manage psoriasis patients’ joint symptoms

Background: Psoriasis patients presenting to the dermatologist for skin disease management may have joint symptoms related to psoriatic arthritis. Dermatologists should ask psoriasis patients about these, yet may not be sure about how to best collaborate with rheumatologists in the management of these patients. Objective: To describe how rheumatologists view the role of dermatologists in addressing and identifying signs and symptoms of psoriatic arthritis in psoriasis patients. Methods: A questionnaire was developed concerning the evaluation and management of joint complaints in a dermatology setting. The survey was sent to rheumatologists interested in psoriatic arthritis. Results: Rheumatologists recommended dermatologists ask psoriasis patients about joint pain, stiffness, swelling, and fatigue to evaluate for psoriatic arthritis. Rheumatology referral was recommended if patients had signs of inflammatory joint disease that were unrelieved by non-prescription non-steroidal anti-inflammatory drugs (NSAIDs). Patients with disabling joint symptoms, no improvement on (disease-modifying antirheumatic drug; DMARD) therapy, or with other causes of joint pain should be referred to rheumatology. Rheumatologists recommended that dermatologists only provide DMARD therapy for joint symptoms if concomitant skin disease warrants such treatment. Conclusions: Dermatologists play a pivotal role in preventing joint destruction in psoriasis patients by screening for signs of psoriatic arthritis, initiating treatment, and referring patients to a rheumatologist when appropriate.

Patterns and risk factors associated with aromatase inhibitor‐related arthralgia among breast cancer survivors

Arthralgia is common in postmenopausal breast cancer survivors (BCS) who are receiving aromatase inhibitors (AIs). The objective of this study was to evaluate the perceived onset, characteristics, and risk factors for AI-related arthralgia (AIA). In a cross-sectional survey of postmenopausal BCS who were receiving adjuvant AI therapy at a university-based oncology clinic, patient-reported attribution of AIs as a cause of joint pain was used as the primary outcome. Multivariate logistic regression analyses were performed to evaluate risk factors. Among 300 survey respondents, 139 (47%) attributed AI as a cause of their current arthralgia. Of those patients, 74% recognized the onset of AIA within 3 months of starting medication, and 67% rated joint pain as moderate or severe in the previous 7 days. In multivariate logistic regression analyses, the time since last menstrual period (LMP) was the only significant predictor of AIA. Controlling for covariates, the women who had their LMP within 5 years had the highest probability of reporting AIA (73%), whereas those who had their LMP > or =10 years previously had the lowest probability of reporting AIA (35%; adjusted odds radio, 3.39; 95% confidence interval, 1.21-9.44; P = .02). Wrists/hands, ankles/feet, elbows, and knees appeared to be associated more strongly with AI-related symptoms than non-AI-related joint symptoms (all P < .01). AIA was common, began within the first 3 months of therapy in most patients, and appeared to be related inversely to the length of time since cessation of menstrual function. These findings suggest that estrogen withdrawal may play a role in the mechanism of this disorder.

Managing joint pain in arthritis

Determining the cause of joint pain is essential but a focus on providing pain relief is also key, writes Susan Oliver.

912. Accelerated Chondrogenesis in Nanofiber Scaffolds Containing BMP-2 Genetically Engineered Chondrocytes

Articular cartilage injury and erosion is a common cause of joint pain often leading to osteoarthritis and permanent morbidity. This research sought to determine if genetically engineered chondrocytes can sustain chondrogenesis in a biodegradable nanofiber scaffold. We hypothesized that chondrocytes would adhere, seed, proliferate, and produce extracellular matrix proteins typical of articular cartilage within a polycaprolactone nanofiber scaffold and this would be accelerated and more robust with hBMP-2 genetically engineered cells.

Mutations in ANKH Cause Chondrocalcinosis

Chondrocalcinosis (CC) is a common cause of joint pain and arthritis that is caused by the deposition of calcium-containing crystals within articular cartilage. Although most cases are sporadic, rare familial forms have been linked to human chromosomes 8 (CCAL1) or 5p (CCAL2) (Baldwin et al. 1995; Hughes et al. 1995; Andrew et al. 1999). Here, we show that two previously described families with CCAL2 have mutations in the human homolog of the mouse progressive ankylosis gene (ANKH). One of the human mutations results in the substitution of a highly conserved amino acid residue within a predicted transmembrane segment. The other creates a new ATG start site that adds four additional residues to the ANKH protein. Both mutations segregate completely with disease status and are not found in control subjects. In addition, 1 of 95 U.K. patients with sporadic CC showed a deletion of a single codon in the ANKH gene. The same change was found in a sister who had bilateral knee replacement for osteoarthritis. Each of the three human mutations was reconstructed in a full-length ANK expression construct previously shown to regulate pyrophosphate levels in cultured cells in vitro. All three of the human mutations showed significantly more activity than a previously described nonsense mutation that causes severe hydroxyapatite mineral deposition and widespread joint ankylosis in mice. These results suggest that small sequence changes in ANKH are one cause of CC and joint disease in humans. Increased ANK activity may explain the different types of crystals commonly deposited in human CCAL2 families and mutant mice and may provide a useful pharmacological target for treating some forms of human CC.

Magnetic resonance imaging in patients with bone marrow disorders.

Magnetic resonance imaging (MRI) provides a non-invasive means to evaluate a large fraction of marrow in less than one hour. Marrow disorders produce non-specific changes in marrow signal intensities which primarily reflect changes in proportions of fat and cellular elements. The pattern of these signal changes narrows the differential diagnosis, and the combination of these features with the clinical context allows interpretations which are clinically useful in many ways. These include: 1) the diagnosis of avascular necrosis (and its distinction from other causes of joint pain), 2) detection of osteomyelitis, 3) differential diagnosis of hypoplastic disorders, 4) staging of lymphomas and myeloma, 5) selection of patients for autologous bone marrow transplant, 6) objective measures of marrow response to therapy, 7) detection of leukemic transformation, and 8) improved detection of marrow disease (primary or secondary) in patients with otherwise unexplained bone pain.

Subchondral avascular necrosis: a common cause of arthritis.

(1) Subchondral avascular necrosis is an important cause of joint pain and disability and accounts for upwards of 20% of total hip replacements done in our hospital. (2) Early diagnosis may be made with the aid of magnetic resonance imaging and radioactive isotope studies. (3) Although the signs and symptoms are similar to those of osteoarthritis, there are significant differences--namely, (a) a history of sudden onset of pain, present in more than half the patients; (b) a younger age group; (c) a shorter duration of symptoms at time of surgery; (d) clinically the limiting factor is pain rather than actual joint deformity to account for restriction of movement; (e) a high incidence of multiple sites of involvement. (4) The disease is commonly associated with steroid treatment or alcohol abuse. Although many other causes are recognised, they are rare in Western urban practice. (5) Patients with stage I-II subchondral avascular necrosis, especially of the knee, are better treated conservatively. (6) Surgical treatment gives less satisfactory results than the treatment of osteoarthritis by similar modalities.

Joint pain in children. When is it serious?

Diagnosis of the cause of joint pain in children depends on the physician's ability to distinguish benign from more serious joint conditions. Benign conditions include trauma, overuse syndromes, hypermobility syndrome, chondromalacia patellae, benign recurrent limb pains, and psychogenic rheumatism. Conditions that require further evaluation and ongoing therapy include Lyme disease, rheumatic fever, juvenile rheumatoid arthritis, neoplastic disease, various orthopedic conditions, infection, seronegative spondyloarthropathies, and the rarer connective tissue diseases. If diagnosed early and treated appropriately, most joint problems of childhood have a very good prognosis.

Leptin Inhibit the Effect of Pioglitazone in Reducing MMP-9 and MMP-13 of IL-1β-Induced Chondrocytes

Osteoarthritis (OA) is the most common cause of joint pain, but there’s still no satisfying treatment that can inhibit degradation of articular cartilage in OA. One approach that is being widely studied is through activation of PPAR-γ. Many studies have shown effect of PPAR-γ on OA either in vitro or in vivo in animal model. On the other hand, the main risk factor of OA is obesity. Obesity generally followed by increased of leptin level due to leptin resistance. The aim of this study is to examine the effect of pioglitazone as PPAR-γ agonist in reducing the level of MMP-9 and MMP-13 in OA chondrocyte with hyperleptinemia. MMP-9 and MMP-13 are key role enzymes that degrades cartilage in OA. This study use IL-1β-induced chondrocyte exposed to pioglitazone. Pioglitazone 0,1μM, 1μM, and 10μM reduce MMP-9 and MMP-13 level. Whereas pioglitazone together with leptin 10μg/ml reduce the decrease level of MMPs compared to the group without leptin. Leptin inhibit the effect of pioglitazone in reducing the level of MMPs.Keywords: OA, leptin, pioglitazone, MMP-9, MMP-13

THE SIGNIFICANCE OF JOINT PAINS CAUSED BY STERILE STREPTOCOCCUS TOXIN

Article1 July 1943THE SIGNIFICANCE OF JOINT PAINS CAUSED BY STERILE STREPTOCOCCUS TOXINPAUL S. RHOADS, M.D., F.A.C.P., MELVIN L. AFREMOW, M.D.PAUL S. RHOADS, M.D., F.A.C.P.Search for more papers by this author, MELVIN L. AFREMOW, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-19-1-60 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptIn 1937 Healey1reported that about 3 per cent of young adults being immunized against scarlet fever developed multiple joint pains as a reaction to one or more injections of the sterile filtrate of broth cultures of scarlet fever streptococci. She noted that the majority of persons who had this reaction gave a history of previous joint pains associated with rheumatic fever, or of streptococcus infections of the nose and throat. We had made similar observations. Healey showed that 74.6 per cent of a group of 63 such persons which she studied did not have joint pains when injected with...Bibliography1. HEALEY CE: The cause of joint pain occurring during immunization with scarlet fever streptococcus toxin, Jr. Am. Med. Assoc., 1937, cviii, 628. CrossrefGoogle Scholar2. COBURNPAULI AFRH: Studies in the immune response of the rheumatic subject and its relationship to activity of the rheumatic process. IV. Characteristics of strains of hemolytic streptococci effective and non-effective in initiating rheumatic activity, Jr. Clin. Invest., 1935, xiv, 766. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Evanston, Illinois*Delivered before the Regional Meeting of the American College of Physicians, Chicago, Ill., November 21, 1942.From the Department of Medicine, Northwestern University Medical School, and the Nurses' Infirmary of Cook County Hospital, Chicago. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byThe allergist's stake in collagen diseaseSerum electrophoretic pattern in experimental hypersensitivityRole of Dental Focal Infection in Etiology of DermatosisExperimental collagen disease from hypersensitization to streptococcus toxinThe Ætiology of Chronic RheumatismActive Immunization 1 July 1943Volume 19, Issue 1Page: 60-63KeywordsArthralgiaGroup A streptococciHospital medicinePharynxRheumatic feverScarlet feverStreptococcal infectionsStreptococcusToxinsYoung adults ePublished: 1 December 2008 Issue Published: 1 July 1943 PDF downloadLoading ...