Bacterial arthritis and osteitis in adults.
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Arthritis, Infectious↗
Biomedical subjects
M L Mahowald
Publications and source records attributed to M L Mahowald.
Sleep fragmentation in rheumatoid arthritis.
Fatigue is commonly reported by patients with rheumatoid arthritis (RA), and it is frequently used to evaluate disease activity and response to therapy. We theorized that the feeling of fatigue in patients with RA may be a manifestation of disturbance of sleep. Sixteen patients with chronic, active RA, who were selected for early onset of fatigue (less than 6 hours after morning awakening), were extensively evaluated by formal all-night polysomnographic recording and multiple sleep latency testing (MSLT). Although no sleep deprivation was found, all patients had some type of marked disturbances of sleep, including unanticipated sleep apnea (2 patients), frequent movement of extremities (all 16 patients), and frequent arousal (all 16 patients). The alpha-delta sleep pattern was present in 13 patients, and 7 were found by MSLT to be hypersomnolent. None of the patients accurately recognized the degree of their sleep disruption. Our findings from the MSLT indicate that fatigue in patients with RA may be a manifestation of sleep fragmentation, rather than a nonspecific constitutional symptom.
Aged↗
Progressive ankylosis (ank/ank) in mice: an animal model of spondyloarthropathy. II. Light and electron microscopic findings.
Murine progressive ankylosis was studied by light and electron microscopy (EM). By light microscopy, the earliest synovial lesion was inflammatory followed by synovial proliferation and cartilage erosions. Later changes included progressive joint ankylosis by fibrosis and ossification of articular and periarticular tissues and new bone proliferation. By EM, synovial cell proliferation and hypertrophy with collagen deposition was seen before the appearance of intracellular and extracellular hydroxyapatite crystals. These pathologic changes are the same as those found in the human spondyloarthropathies. Our EM findings demonstrate that hydroxyapatite crystals appear in the joints of ank/ank mice after the initial inflammatory phase.
Animals↗
Progressive ankylosis (ank/ank) in mice: an animal model of spondyloarthropathy. III. Proliferative spleen cell response to T cell mitogens.
Murine progressive ankylosis is a spontaneous disorder of mice resulting from a homozygous recessive genetic defect (ank/ank) which produces an inflammatory arthritis of peripheral and axial joints eventually resulting in ankylosis of these joints. This disorder resembles the human spondyloarthropathies clinically, radiographically and histologically. Various studies in humans with spondyloarthropathies have described defects of cellular immunity but these results are conflicting. We measured the spleen cell response to mitogen in ank/ank mice and in normal littermates. The spleen cell response to the T cell mitogens phytohaemagglutinin and concanavalin A was decreased in ank/ank mice compared with their normal littermates. The response to the B cell mitogen lypopolysaccharide was normal in both ank/ank mice and normal littermates. Serum from ank/ank mice did not inhibit spleen cell responses to mitogen. Ank/ank spleen cells were not inhibitory of normal spleen cell responses to mitogens. Addition of irradiated normal spleen cells to ank/ank spleen cells did not restore the mitogen responses to normal. It is possible that the ank/ank gene results in the phenotypic expression of an abnormal or decreased cell product involved in T cell proliferation. Several recently described cytokines could be potential candidates for this product.
Animals↗
Progressive ankylosis in mice. An animal model of spondylarthropathy. I. Clinical and radiographic findings.
To determine its similarity to human spondylarthropathies, we studied murine progressive ankylosis, a spontaneously occurring disorder of joints in mice. Clinically, peripheral joints were inflamed initially, then became ankylosed in a predictable sequence from distal to proximal. Forefeet were involved before hindfeet. Axial joint involvement produced severe spinal ankylosis. Extraarticular manifestations included balanitis and crusting skin lesions. Radiographically, bony erosions and calcification of articular and periarticular tissues were extensive, and vertebral syndesmophytes produced a "bamboo" spine. We conclude that progressive ankylosis is a systemic disease with many clinical and radiographic similarities to human spondylarthropathies, and it may represent a useful animal model for the study of the human diseases.
Animals↗
The Minnesota Arthritis Training Program: emphasis on self-management, not compliance.
Based on a needs assessment of our ambulatory patients and review of available arthritis education programs, we developed an innovative education and exercise program, the Minnesota Arthritis Training Program (MATP). Patients are taught self-management skills including how to: (1) interpret changing physical symptoms and limitations caused by joint inflammation and apply modifications to their individualized exercise program; (2) recognize common drug toxicites and use a decision analysis schema to manage side effects to decrease the risk of serious toxicity and decrease dependency on professionals safely; (3) develop strategies to modify activity schedules to make the most of limited stamina; (4) recognize and understand psychological problems produced by rheumatoid arthritis (RA) including sexual dysfunction, depression and breakdown of communication; and (5) reconstitute social support systems.
Arthritis, Rheumatoid↗
T cells are required for coxsackievirus B1 induced murine polymyositis.
Murine polymyositis (PM) induced by coxsackievirus B1 (CVB1) has been used as a model of human PM. Our study was undertaken to investigate the role of T cells in CVB1 induced PM by examining disease development in neonatally thymectomized mice. Clinical weakness and histological inflammatory myositis occurred in 42.7% of sham operated animals but only 7.7% of thymectomized mice. These experiments demonstrate the importance of T cells in the pathogenesis of this virus induced autoimmune disorder.
Animals↗
Coxsackievirus B 1-induced polymyositis. Lack of disease expression in nu/nu mice.
Chronic inflammatory myositis similar to human polymyositis occurs in mice after infection with a strain of Coxsackievirus B 1 (CVB 1). To investigate the role of T cells in the pathogenesis of this disorder, we compared disease expression in T cell-deficient athymic nude (nu/nu) mice and heterozygotes (nu/+) with normal T cell function. Acute infectious myositis occurred in nu/nu and nu/+ mice. Chronic (greater than 21 d postinfection) weakness and myositis, however, developed only in nu/+. Resistance to disease in nu/nu mice was not explained by insusceptibility to infection; the amount of virus lethal for 50% of mice and virus replication were comparable in both groups. Additionally, anti-CVB 1 antibody production was similar in both groups. Reconstitution of infected nu/nu mice with spleen cells from normal mice resulted in disease. These results demonstrate that chronic weakness after infection with this virus is not simply a sequela of acute myonecrosis and suggest that T cells play a pivotal role in the pathogenesis of chronic myositis.
Animals↗
Examination of the foot in rheumatic disease.
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Foot↗
Antigen-induced experimental septic arthritis in rabbits after intraarticular injection of Staphylococcus aureus.
With the Dumonde-Glynn model of antigen-induced arthritis, a rabbit model was developed to examine the histopathologic differences between normal and arthritic joints in the same animal infected by intraarticular injections of Staphylococcus aureus. Microscopic examination of whole joint sections and a quantitative histopathologic scale were used to compare changes in all the articular components of 17 normal and 17 arthritic joints infected for less than two weeks. The histological changes were more severe in infected arthritic joints than in infected normal joints (mean +/- SD total histology score, 13.8 +/- 2.4 and 9.3 +/- 4.0, respectively; P less than .001). In infected arthritic joints, subsynovial abscesses extended into subchondral bone via the pannus of chronic synovitis at articular margins and intraarticular attachments of cruciate ligaments, rather than by initial cartilage destruction and direct extension into subchondral bone.
Abscess↗
Use of technetium-99m methylene diphosphonate and gallium-67 citrate scans after intraarticular injection of Staphylococcus aureus into knee joints of rabbits with chronic antigen-induced arthritis.
Numerous clinical studies have questioned the ability of radionuclide scans to differentiate septic from aseptic joint inflammation. A clinical study may not be able to document an underlying disease process or duration of infection and, thus, may make conclusions about the accuracy of scan interpretations open to debate. In this study, the Dumonde-Glynn model of antigen-induced arthritis in rabbits was used as the experimental model to study technetium and gallium scans in Staphylococcus aureus infection of arthritic and normal joints. Gallium scans were negative in normal rabbits, usually negative in antigen-induced arthritis, but positive in septic arthritis. The bone scan was usually negative in early infection but positive in late septic arthritis, a finding reflecting greater penetration of bacteria into subchondral bone because of the underlying inflammatory process.
Animals↗
Preparation of whole rabbit knee joints for microscopic examination.
A paraffin embedding method to prepare whole rabbit knee joints for histological examination is described. This method provides good quality microscopic sections thin enough for the study of cellular detail and does not require prolonged processing. When examining pathologic changes in experimental arthritis, it is advantageous to be able to examine the intact joint with the structural relations of the joint components preserved. Sections of the whole joint provide numerous areas where bone, cartilage and synovium are contiguous for examination. Having obtained poor results using methods recommended for small bony specimens, we modified several existing procedures to obtain a reliable method for preparing excellent microscopic sections of the whole rabbit knee joint.
Animals↗
Animal models of infectious arthritis.
The results from animal studies of bacterial joint infection have demonstrated pathogenic changes in synovium, cartilage, and bone which lead to joint destruction. Mechanisms responsible for the changes in these articular components remain to be more completely defined in order to develop methods to prevent articular destruction. Eradication of the active infectious process with early institution of antibiotics and adequate drainage is required but is not sufficient to prevent chronic destructive processes initiated by the acute bacterial infection. Biochemical effects of changes in the anabolic and catabolic functions of the cells in bone, cartilage, and synovium and the control mechanisms for these functions undoubtedly hold the key to prevention of destruction in infectious arthritis. Much less is understood about the pathogenic changes and mechanisms in infections caused by anaerobic bacteria, mycobacteria, fungi or viruses. Application of advances in immunological, morphological and biochemical techniques to animal models of infectious arthritis provides the opportunity to increase understanding of pathogenic mechanisms and to develop innovative methods of treatment.
Animals↗
Synergy between adjuvant arthritis and collagen-induced arthritis in rats.
Adjuvant arthritis (AA) in rats is susceptible to cell-mediated passive transfer. Collagen-induced arthritis (CIA) in rats is susceptible to passive transfer with antibody to type II collagen. We report here the development of strikingly severe arthritis in Lewis rats as the result of synergy between passively transferred antibody to type II collagen from rats with CIA and concanavalin A (Con A)-stimulated lymph node or spleen cells from syngeneic rats with AA. Similar synergy was seen in rats with AA given anticollagen antibody, in rats with CIA given Con A-stimulated adjuvant spleen cells, and in rats actively immunized with CII and complete Freund's adjuvant. The synergistic process caused a very severe polyarthritis, characterized by marked swelling and erythema in all the joints of the distal extremities, with histologic and radiographic evidence of early, extensive erosion of articular cartilage. Synergy was apparent if the lymphoid cells from AA rats were given up to 1 mo after a single injection of anticollagen antibody. No synergy was seen when normal rat immunoglobulin or anti-ovalbumin antibody was substituted for anticollagen antibody, when Con A-stimulated lymphoid cells from normal rats or donors with CIA were used, or when Con A-stimulated AA lymphoid cells were irradiated before transfer. Synergy between separate immune effector mechanisms may represent a general phenomenon in the pathogenesis of inflammatory joint disease.
Animals↗
Pulmonary hypertension in systemic lupus erythematosus: effect of vasodilators on pulmonary hemodynamics.
Hemodynamic studies of the response of the pulmonary vasculature to vasodilator drugs were performed in 3 patients with systemic lupus and pulmonary hypertension. In one patient isoproterenol infusion produced a reduction in total pulmonary resistance, but increased pulmonary blood flow and pulmonary artery pressure. No significant change in pulmonary artery pressure or resistance was noted with nifedipine in any of the patients. One woman with associated pulmonary infiltrates improved symptomatically with high dose steroids.
Adult↗
Infection with Mycoplasma pulmonis modulates adjuvant- and collagen-induced arthritis in Lewis rats.
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Administration, Intranasal↗
Budd-Chiari syndrome in a patient with the lupus anticoagulant.
Lupus anticoagulant is an immunoglobulin that interferes with prothrombin conversion to thrombin and is manifested biochemically by prolongation of the partial thromboplastin time. Paradoxically, bleeding is rare in association with this anticoagulant, and deep leg vein thromboses, pulmonary emboli, and cerebrovascular accidents have been described in patients with this clotting inhibitor. This report describes the first case of Budd-Chiari syndrome associated with the lupus anticoagulant. The patient presented with abdominal pain and massive ascites. The Budd-Chiari syndrome was confirmed by liver biopsy and venography. No medical condition known to predispose to an increased thrombotic tendency could be identified, and the presence of the lupus anticoagulant in the patient's plasma may provide an explanation for his hypercoagulability and development of the Budd-Chiari syndrome.
Adult↗
A case of Wegener's granulomatosis presenting with jaw claudication.
The major manifestations of Wegener's granulomatosis have been well described. Jaw claudication has not been recognized as one of the symptoms associated with this disease. We report the first case of Wegener's granulomatosis presenting with jaw claudication. Documentation of different histological types of vasculitis producing similar symptoms broadens our concepts of systemic vasculitis and emphasizes the need for tissue biopsy for diagnosis.
Diagnosis, Differential↗