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At least 397 records · Page 22Linked to original sources
PubMed1987

[Connective tissue framework of the greater omentum].

Tissue samples of the greater omentum were intraoperatively collected from 17 patients on whom laparotomy was performed for different indications. The connective tissue framework of the unstained omentum was investigated, using a stereomicroscope. Histological sections were prepared from large saw-cuts of the plastinated omentum. The greater omentum of man was found to possess a connective tissue framework with blood and lymphatic vessels and was also found to be embedded in adipose tissue. The latter is made up of fatty organs differentiated in size. Round to oval organs are formed by fat cells. These organs are delimitated from their environment by a tender connective tissue capsule and are connected, through a pedunculated structure, to a vascular cord of the connective tissue framework. Connective tissue fibres radiate from the framework into the capsule which is made up of a submesothelial connective tissue layer and the mesothelium. The peduncle of a fatty organ consists of connective tissue as well as of supplying blood and lymphatic vessels. Fatty organs surrounded by connective tissue fibres were visualised even in highly adipose regions by means of plastinated saw-cuts of the greater omentum.

Adipose Tissue↗
PubMed2005

[Interstitial lung disease in mixed connective tissue disease].

INTRODUCTION: The authors analyzed the incidence of interstitial lung disease in mixed connective tissue disease. They were seeking an answer to the following problems: the nature of the pathological course of mixed connective tissue disease complicated by and the therapy to be used in interstitial lung disease. PATIENTS AND METHODS: 179 patients were followed up during a period of 15.9 +/- 6.1 years. Interstitial lung disease was diagnosed using high resolution computed tomography. The diagnosis of interstitial lung disease was not obvious in 5 patients thus open lung biopsy was performed, which confirmed common interstitial pneumonitis. The patients were followed-up, and the data of computed tomography and respiratory function tests were detected 6 months, and then 4 years after the acute lung disease complicated by mixed connective tissue disease. RESULTS: Out of the 179 mixed connective tissue disease patients 96 (53.6%) had interstitial lung disease. The onset of interstitial lung disease was the most frequent in the 2-4 years of the disease. Four years after the first appearance of interstitial lung disease severe fibrosis was diagnosed in 24 patients (25%). A honey comb formation in the lung developed only in one patient. For the treatment of interstitial lung disease, corticosteroid treatment had to be combined with cyclophosphamide in 51 cases. In 4 patients (24%), pulmonary arterial hypertension evolved 2-4 years following interstitial lung disease. The high pulmonary arterial pressure decreased using pulsed corticosteroid treatment, cyclophosphamide, prostacyclin analogue, anticoagulants therapy and the 4 patients stay alive. The pulmonary arterial hypertension was caused by obliterative vasculopathy. CONCLUSION: Pulmonary involvement is found in more than half of the patients with mixed connective tissue disease. Early diagnosis of interstitial lung disease is possible by computed tomography. Interstitial lung disease can be treated by the combination of corticosteroids and cyclophosphamide. The authors were the first to detect the coexistence of interstitial lung disease and pulmonary arterial hypertension in mixed connective tissue disease. Subsequent respiratory alterations in these patient necessitate regular patient follow up.

Adult↗
PubMedDate not supplied

New connective tissue attachment formation on various biomaterials implanted in roots.

To determine whether connective tissue attachment can occur on implant materials by repopulating periodontal ligament (PDL)-derived cells and whether the new connective tissue attachments formation is influenced by the type of implant materials, periodontal tissue regeneration on four materials implanted into root cavities of cat canines was observed under conditions where PDL-derived cells could populate the surface of the materials. New connective tissue attachment occurred on bioactive materials such as bioglass and hydroxyapatite, while little or no cementum deposition was seen on bioinert materials such as titanium alloy and partially stabilized zirconium. Results showed that PDL-derived cells can form new connective tissue attachments on implant materials and that the formation of new connective tissue attachment is influenced by bioactivity of the materials.

Animals↗
PubMed2006

[Pulmonary arterial hypertension in connective tissue disease].

INTRODUCTION: Pulmonary arterial hypertension (PAH) is one of the most severe complications of connective tissue diseases. PAH is defined by mean arterial pulmonary pressure > 25 mmHg at rest (or 30 mmHg during exercise) during right heart catheterisation. STATE OF THE ART: About 10% of cases of PAH are related to connective tissue diseases. PAH may be observed in any of the connective tissue diseases; it is mostly encountered in systemic sclerosis (prevalence estimated to 8%), and is more frequent in the limited form of the disease with anticentromeres antibodies, in the presence of Raynaud's phenomenon, of antinuclear antibodies, decreased CO diffusion capacity, and during the perimenopausal period. Histopathological lesions are similar to that of idiopathic PAH (with plexogenic lesions being more rare); mutations have not been described. Venous thromboembolic disease (especially in lupus) and hypoxemia related to pulmonary fibrosis should be investigated. Screening for PAH is recommended in systemic sclerosis (by echocardiography every year and in case of dyspnea). Few clinical trials have been conducted specifically in PAH related to connective tissue diseases, therefore the treatment approach is similar to that of idiopathic PAH, with a poorer prognosis, including treatment with bosentan, epoprostenol and other prostacyclin analogs, and sildenafil. Immunosuppressive therapy may occasionally improve PAH in patients with systemic erythematosus lupus or mixed connective tissue disease. PERSPECTIVES: Respective indications of drugs and treatment associations need to be precised. CONCLUSION: The availability of efficacious treatments of PAH justifies its screening and early diagnosis in connective tissue diseases.

Antihypertensive Agents↗
PubMed1987

Specificity of a mouse monoclonal antibody raised against acute myeloid leukaemia cells for mast cells in human mucosal and connective tissues.

A mouse monoclonal antibody raised against acute myeloid leukaemia cells (YB5.B8 monoclonal antibody; Gadd, S. J. and Ashman, L. K. (1985): Leukaemia Res. 9, 1329-1336) has been found by an indirect immunoperoxidase technique to bind to scattered cells in frozen sections from a number of human tissues. They have been identified as mast cells in fixed sections of skin, tonsil and duodenum by simultaneous staining of glycosaminoglycan with Alcian blue in 0.7 N HCl. The antibody does not distinguish mast cells in mucosal tissues from those in connective tissue, although the level of expression by cells at both sites appears to be heterogeneous. With the exception of low affinity binding to B lymphocytes, no other bone marrow-derived cells were found to bind the antibody. In particular, basophils and eosinophils were not stained, suggesting that they are not related closely to mast cells and that the antigen detected by YB5.B8 monoclonal antibody is not an IgE Fc receptor. Therefore, among all mature haemopoietic lineages, the antibody is specific for mast cells.

Animals↗
PubMed1981

Pharmacological control of inflammatory connective tissue diseases.

The primary cause of the most common inflammatory rheumatic diseases in unknown. Microbial infection combined with an increased susceptibility due to genetically determined alterations in the immune system is probably of importance. Non-specific processes of inflammation and repair are the immediate causes of the clinical symptoms, and anti-inflammatory therapy is at present the corner stone in the control of these diseases. The highest priority in research should be given to drugs, which in controlled clinical trials have demonstrated ability to cause remission of disease activity. Important examples are D-penicillamine, glucocorticoids and the cytostatic drugs. The effects of these drugs on the metabolism of proteoglycans and collagen in granulation tissue and normal connective tissue may explain some of the beneficial effects, but also some of the side effects. Rational pharmacotherapy in the inflammatory rheumatic diseases may be a combination of anti-inflammatory drugs with immunotherapy and possibly antimicrobial therapy.

Anti-Inflammatory Agents↗
PubMed1986

Excessive hypercalcaemia and mixed connective tissue disease.

A 23-year-old female with extreme hypercalcaemia was treated with calcitonin, mitramycin and parathyroidectomy and normocalcaemia was achieved after 4 weeks. Nevertheless, the patient later died of cutaneous necrosis, impaired circulation and multiple organ failure. Serum immunoreactive parathyroid hormone was in the normal range and parathyroid tissue normal. Mixed connective tissue disease was diagnosed on the basis of high titers of antibody to extractable nuclear antigen, moderately elevated levels of antibody to nuclear antigen and only marginal elevation of anti-double standed DNA. The role of Cl. difficile toxin in the blood and an acinic cell tumour is unclear.

Adult↗
PubMed1998

Clinical usefulness of antibodies to U1snRNP proteins in mixed connective tissue disease and systemic lupus erythematosus.

OBJECTIVES: To determine whether the anti-68 kDaU1snRNP antibody is associated with mixed connective tissue disease and not with SLE; to evaluate correlations between anti-U1snRNP titers and disease activity; and to look for associations between anti-U1snRNP specificities and specific clinical features. PATIENTS AND METHODS: 40 patients with a positive double diffusion test for anti-68 kDa U1snRNP were studied, including 21 with mixed connective tissue disease, 14 with systemic lupus erythematosus and five with other connective tissue diseases. IgGs to 68 kDa U1snRNP were assayed using an ELISA. Clinical features, disease activity and antibody test findings were evaluated longitudinally in nine patients. RESULTS: Both proportions of patients with anti-68 kDa U1snRNP and titers of IgG to 68 kDa U1snRNP were similar in the mixed connective tissue disease and systemic lupus erythematosus groups. Patients with mixed connective tissue disease were significantly more likely to have anti-A U1snRNP or anti-C U1snRNP than those with systemic lupus erythematosus (P < 0.03 and P < 0.04, respectively). No significant correlations were found between any of the features of mixed connective tissue disease (e.g., Raynaud's phenomenon, myositis, or sausage digits) and a specific anti-U1snRNP antibody. During follow-up (mean, seven years; range, 1-25 years), changes occurred in the anti-U1snRNP profile and in the anti-68 kDa U1snRNP titer. These changes were not correlated with disease activity. CONCLUSIONS: IgGs to 68 kDa U1snRNP are not associated with a specific pattern of anti-RNP-positive connective tissue disease. No useful information can be gained by monitoring anti-68 kDa U1snRNP IgG titers over time. A Western blot profile including anti-A U1snRNP or anti-C U1snRNP indicates a high likelihood of U1snRNP-associated mixed connective tissue syndrome (MCTD).

Adolescent↗
PubMedDate not supplied

Connective tissue proteinases and inhibitors in abdominal aortic aneurysms. Involvement of the vasa vasorum in the pathogenesis of aortic aneurysms.

Recent studies have shown that increases in proteolytic activity are associated with abdominal aortic aneurysms (AAAs). We have studied samples of the dilated aortic wall, taken during corrective surgery for AAAs, in terms of the number, type, and tissue location of connective tissue proteinases and their inhibitors. Five distinct caseinolytic serine proteinases and six gelatinolytic metalloproteinases were resolved by molecular weight by use of sodium dodecyl sulfate-substrate gel electrophoresis. Isoforms of the Mr 92,000 neutrophil gelatinase were identified by immunoprecipitation of biosynthetically labeled organ culture media. About 50% of the total radiolabeled protein secreted by AAA organ cultures was identified as the Mr 30,000 glycoprotein, tissue inhibitor of metalloproteinase (TIMP), by immunoprecipitation. Both TIMP and gelatinase were localized to the vasa vasorum by immunoperoxidase staining. However, interstitial collagenase could not be detected by any method. These results suggest the involvement of the vasa vasorum in the maintenance and possibly the genesis of AAAs.

Aorta, Abdominal↗
PubMed1995

Silicone breast implants and the risk of connective-tissue diseases and symptoms.

BACKGROUND: Silicone breast implants have been linked to a variety of illnesses, the most controversial of which are connective-tissue diseases and symptoms. To study this relation, we analyzed data from 14 years of follow-up of the Nurses' Health Study cohort. METHODS: Women who were free from connective-tissue disease in June 1976 were followed through May 31, 1990, before there was widespread media coverage of the possible association of breast implants and connective-tissue diseases. Information was collected through biennial and supplementary mailed questionnaires and blinded reviews of medical records with the use of standardized criteria. Relative risk, the measure of association, was defined as the incidence rate of connective-tissue disease among women with breast implants divided by the corresponding incidence rate among women without breast implants. RESULTS: Among 87,501 women who were eligible for follow-up, 516 were confirmed as having definite connective-tissue diseases and 1183 as having breast implants (of which 876 were silicone-gel-filled, 170 saline-filled, 67 double-lumen, 14 polyurethane-coated, and 56 of unknown type). The mean (+/- SD) period of follow-up after surgery was 9.9 +/- 6.4 years (range, 1 month to 40.5 years). Three of the patients with definite connective-tissue disease--all had rheumatoid arthritis--had implants (one silicone-gel-filled, one saline-filled, and one double-lumen). The age-adjusted relative risk of a definite connective-tissue disease among women with any type of implant was 0.6 (95 percent confidence interval, 0.2 to 2.0), as compared with women without implants. For women with silicon-gel-filled implants, the comparable relative risk was 0.3 (95 percent confidence interval, 0 to 1.9). The relative risk of self-reported signs or symptoms of connective-tissue disease for women with implants was 1.5 (95 percent confidence interval, 0.9 to 2.4); the risk of having any 1 of 41 signs, symptoms, or laboratory features of connective-tissue disease was 0.7 (95 percent confidence interval, 0.3 to 1.6). CONCLUSIONS: In a large cohort study, we did not find an association between silicone breast implants and connective-tissue diseases, defined according to a variety of standardized criteria, or signs and symptoms of these diseases.

Adult↗
PubMed1999

Antinuclear antibodies: presence and specificity in autoimmune connective tissue disease in the dog.

Autoimmune connective tissue disease in both animals and humans present as multi-systemic disorders. Clinical signs referable to joints, musculoskeletal system and Dermatopathies are present. Autoantibody production is a regular feature of systemic autoimmune disease and these antibodies have diagnostic value in both human and veterinary medicine. In this study, we demonstrate that many of the commonly used diagnostic techniques developed for use with human patients may also be adapted for use in dogs. However, in some instances, 'canine specific' autoantibodies, distinct from analogous human antibodies may be detected in sera from dogs with a diagnosis of autoimmune disease. This finding indicates that dogs may develop 'dog-specific' autoimmune connective tissue disease.

Animals↗
PubMed1991

Overlap syndromes and mixed connective tissue disease.

While the etiology of connective tissue diseases remains unknown, the classification of individual cases will continue to depend on identifying certain patterns of clinical and laboratory features. As many as 25% of connective tissue disease patients present with an overlap syndrome with features of systemic lupus erythematosus, systemic sclerosis, polymyositis, or dermatomyositis, with rheumatoid arthritis and Sjögren's syndrome evolving concurrently or consecutively during the course of the disease. The term overlap syndrome is applied to what appears to be a heterogeneous group of disorders, but in recent years there have been attempts to identify antibody markers within this population to identify subsets with particular patterns of disease expression. Thus, anti-U1-ribonucleoprotein is associated with overlap syndromes in which features of systemic lupus erythematosus are accompanied by features of systemic sclerosis or myositis; antibodies to polymyositis-scleroderma, Ku, and U2-ribonucleoprotein are associated with overlaps of systemic sclerosis and polymyositis, and anti-Jo-1 is associated with polymyositis and pulmonary fibrosis. A practical reason for subdividing cases in this way relates to prognosis and treatment, but at a more fundamental level it is hoped that the study of the origin of these antibodies and their antigen targets will provide clues to pathogenesis and even etiology.

Humans↗
PubMed1994

Role of cytokines in controlling connective tissue gene expression.

Recently, the role of cytokines in controlling gene expression of connective tissue components has been increasingly emphasized. Many cytokines have been shown to have specific effects on gene expression of connective tissue components, and the roles of cytokines in controlling connective tissue metabolism during wound healing and in fibrosis have increasingly been discussed. In this article, the effects of cytokines on regulation of gene expression of connective tissue components, especially of type I collagen were described. We analysed transcriptional control of the alpha 1(I) collagen gene by TNF-alpha by means of DNA mediated transfection experiments using recombinant plasmids in which the promoter region of the human alpha 1(I) collagen had been fused to the chloramphenicol acetyl-transferase (CAT) gene, in human dermal fibroblasts. It was found that TNF-alpha reduced alpha 1(I) collagen transcription through at least up to -107 bp upstream of the human alpha 1(I) collagen promoter gene in dermal fibroblasts.

Animals↗
PubMed1993

When the lungs are involved by connective tissue disease.

Pulmonary involvement by a connective tissue disease can result in clinically important complications. Pathogenic mechanisms vary from granulomatous reaction and interstitial inflammation to primary vasculitis and immune complex-mediated disease. Understanding the pulmonary complications of connective tissue diseases is challenging in that several distinct patterns of involvement are associated with the same disease but the same lung abnormalities are found with several different diseases. Early recognition and treatment of pulmonary involvement may offer the patient a better chance of recovery from serious conditions that often carry a grim prognosis if undetected.

Arthritis, Rheumatoid↗