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PubMed1994

Connective tissue diseases.

The connective tissue diseases are musculoskeletal disorders that have an autoimmune basis. They can affect the internal organ systems and may have numerous ocular manifestations. This chapter discusses both the systemic and ocular findings of certain connective tissue diseases, specifically cranial arteritis, Sjögren's syndrome, rheumatoid arthritis, scleroderma, and lupus erythematosus. Treatment for the clinical manifestations of each disease is also reviewed.

Connective Tissue Diseases↗
PubMed2005

Central nervous system involvement in systemic connective tissue diseases.

Systemic connective tissue diseases can affect the brain, meninges, spinal cord, cranial and peripheral nerves. Different pathogenic mechanisms, particularly autoantibody or T-cell mediated lesions, appear to be involved. The neurological manifestations of the connective tissue diseases and their diagnostic possibilities including newer imaging techniques are reviewed. Early recognition of neurological abnormalities can help in the differential diagnosis and in defining the underlying disease in order to initiate treatment and prevent progression of lesion or cognitive function loss.

Central Nervous System Diseases↗
PubMed1998

[Pathology of diseases of extracardiac origin. VI. Disease of the connective tissue and heart].

Connective tissue diseases encompass a wide group of nosologic entities of unknown etiology, characterized by multisystemic organ involvement, sharing an immunologic pathogenetic mechanism, producing a variety of inflammatory manifestations, and whose primary lesion is always a diffuse vasculitis. Any part of the cardiovascular system may be involved, including the pericardium, the myocardium, the endocardium and valves, the coronary arteries, the aorta, the pulmonary vasculature, the peripheral arteries, veins, arterioles, venules, and the capillary beds of almost every organ subsystem. Pathologic studies disclose a high prevalence of heart involvement, but the presence and extent of pathologic findings correlate poorly with clinical manifestations. With the advent of echocardiography-Doppler, milder and earlier cases are now recognized. Although these patients continue under the care of rheumatologists and internists, when cardiac involvement arises, cardiologists must be aware of the characteristics, outcome and management of connective tissue diseases.

Connective Tissue Diseases↗
PubMedDate not supplied

[Components of the extracellular tissue matrix as potential "markers" of connective tissue, cartilage and bone metabolism in diseases of the locomotor system].

Inflammatory and degenerative joint diseases are characterized by active degradation of the extracellular matrix of articular cartilage, bone and connective tissue. At the same time, specific changes in the neosynthesis of extracellular matrix components are seen. Thus, quantitative measurement of matrix related compounds and their metabolites in body fluids might provide a specific and sensitive tool for evaluating connective tissue involvement in rheumatic joint disease. The different components are linked to and may as such reflect different pathways of the pathological process, e.g.: Serum hyaluronan and serum procollagen type III peptides: fibroblast activation, early and late stage, respectively fibroproliferative tissue reaction. Synovial proteoglycans and glycosaminoglycans: degradation of proteoglycans derived from the extracellular matrix of cartilage; degree and activity of articular cartilage destruction. Serum keratan sulphate: proteoglycan metabolism (?). Urinary hydroxy pyridinium crosslinks (pyridinoline and deoxypyridinoline): degradation of mature cartilage and bone collagens; cartilage and bone catabolism. Cross-sectional and longitudinal clinical studies have shown that the quantitative measurement of some of these components may be of relevance in monitoring connective tissue disease. Further prospective studies are needed to prove the definite value of extracellular matrix-related components in early diagnosis and follow up of rheumatic joint and bone disease.

Arthritis↗
PubMedDate not supplied

Gastrointestinal systemic sclerosis in serologic mixed connective tissue disease.

Mixed connective tissue disease is a clinical entity defined by overlapping features of progressive systemic sclerosis, systemic lupus erythematosus, polymyositis, rheumatoid arthritis, and distinct serologic findings. Esophageal dilatation and dysmotility have been the only gastrointestinal manifestations reported. Three patients with serologic findings of mixed connective tissue disease and extensive gastrointestinal involvement compatible with the changes found in progressive systemic sclerosis are presented. Gastrointestinal manifestations of progressive systemic sclerosis are reviewed and were found to be indistinguishable from the findings in these patients.

Adult↗
PubMed1999

Mixed connective tissue disease.

Mixed connective tissue disease deserves to be a distinct disease entity due to the persistent citation of this disease in the literature since the original description by Sharp in 1972, in spite of the presence of several criticisms against the independency of this disease. The characteristic features of mixed connective tissue disease are: 1) the presence of anti-U1snRNP antibody with high titers in sera, 2) an increased frequency of HLA-DR4 in the leukocytes, and 3) death due to pulmonary hypertension.

Autoantibodies↗
PubMed1989

Increase of plasma beta-endorphins in connective tissue massage.

1. Connective tissue massage produces relief of pain and increases microcirculation in a number of vascular beds. 2. The concentration of plasma beta-endorphins has been measured in 12 volunteers before and 5, 30 and 90 min after a 30-min session of connective tissue massage. 3. There was a moderate mean increase of 16% in beta-endorphin levels from 20.0 to 23.2 pg/0.1 ml (P = 0.025), lasting for about 1 hr with a maximum in the test 5 min after termination of the massage. 4. It is assumed that the release of beta-endorphins is linked with the pain relief and feeling of warmth and well-being associated with the treatment.

Adult↗
PubMedDate not supplied

[The aging of connective tissue. Molecular and cellular aspects].

Connective tissues are made of cells and extra-cellular matrix. The predominant cells in vascular connective tissue are smooth muscle cells, fibroblasts and endothelial cells. All these cells actively synthesize the macromolecules of the extracellular matrix. This matrix comprises four types of macromolecules: collagens (11 types known), proteoglycans (8 to 10 types known); elastin and structural glycoproteins (more than a dozen known). Ageing of the connective tissue concerns therefore ageing of its cells and the extracellular matrix. For all connective tissue cells, the limit of proliferation (limit of Hayflick) was verified. The ageing of the matrix is different according to the macromolecules considered: rigidification (cross-linking) of collagen, degradation of elastin, decrease and alteration of the proteoglycans ratio. Structural glycoproteins such as fibronectin may be increased in the plasma and the tissues. Connective tissues diseases are implanted on these qualitative and quantitative modifications of the connective tissues.

Aging↗
PubMed2005

[MCTD--mixed connective tissue disease].

Mixed connective tissue disease is a disease entity characterized by overlapping symptoms of lupus erythematosus (LE), systemic sclerosis (SSc), polymyositis/dermatomyositis (PM/DM) and rheumatoid arthritis (RA). Diagnostic criteria include high titers of antibodies against U1RNP as well as the presence of at least 3 of 5 of the following clinical features: edema of hands, synovitis, myositis, Raynaud phenomenon and acroscierosis. In terms of the pathogenesis, genetic as well as infectious (viral) factors appear to play a role. The acceptance of MCTD as a distinct disease entity is controversial. Terms such as "undifferentiated connective tissue disease" or "overlapping syndromes" are not helpful. One-quarter of MCTD patients transform into LE, while one-third progress to SSc. Therapeutic recommendations are glucocorticoids in combination with immunosuppressive agents and endothelin receptor antagonists. Double blind studies are not available. The prognosis is relatively good. Causes of death include pulmonary hypertension, infections and both pulmonary and cardiac failure.

Diagnosis, Differential↗
PubMed2003

[Hormonal life in systemic lupus and other connective tissue diseases].

Among connective tissue diseases, systemic lupus erythematosus is the illness that is most concerned by hormonal life events. The sex ratio is 9/1, and symptoms begin mostly during the third decade, sometimes during birth pill contraception or during pregnancy. As soon as systemic lupus is under control of an efficient treatment, pregnancy is no longer contra-indicated. A medical multidisciplinary surveillance is required. Complicated pregnancy concerns mother and baby. Lupus flares are more frequent during the second and third trimesters as well as during the post-partum period. Usually the intensity is moderate. Severe flares concern patients with renal involvement, hypertension and renal insufficiency and are mostly seen in patients with unplanified pregnancy and yet with still active lupus. Foetal death occurs in 10-30% of the cases, depending on the lupus activity and severity (renal lupus). Prematurity remains an important cause of morbidity (30% of live births). Foetal deaths and prematurity are even more frequent if the patient has an antiphospholipid syndrome. Neonatal cutaneous lupus and auriculo-ventricular congenital heart block is infrequent (1% of SLE patients with anti-Ro/SSA antibodies). Among other connective tissue diseases, polymyositis has a very severe obstetrical prognosis for both mother and foetus. Among primary vasculitis, polyarteritis nodosa, as found during pregnancy, can herald a very bad prognosis.

Animals↗
PubMed2003

[Extracardiac manifestations of undifferentiated connective tissue dysplasia].

Undifferentiated connective tissue dysplasia (UDCTD) is a common type of congenital mesenchymal defect. Among the visceral manifestations of UDCTD, cardiac anomalies have been studied in detail while the nature, extent, and clinical significance of changes in other viscera are much less known. The review summaries data on currently accepted extracardiac manifestations of UDCTD, such as venous insufficiency, tracheobronchial dyskinesia, nephroptosis, genital prolapse, gastrointestinal disorders, hemostatic pathology.

Connective Tissue↗
PubMed1996

Functional anatomy of the levator palpebrae superioris muscle and its connective tissue system.

AIMS/BACKGROUND: The connective tissue system of the levator palpebrae superioris muscle (LPS) consists of the septa surrounding its muscle sheath, the superior transverse ligament (STL) commonly referred to as 'Whitnall's ligament' and the common sheath which is the fascia between the LPS and the superior rectus muscle (SRM). The anterior band-like component of the common sheath is called transverse superior fascial expansion (TSFE) of the SRM and LPS. It mainly extends from the connective tissue of the trochlea to the fascia of the lacrimal gland. A detailed description of the relation between the LPS and its connective tissue is presented. Furthermore, the course of the LPS in the orbit is described. The study was conducted to provide a morphological basis for biomechanical and clinical considerations regarding ptosis surgery. METHODS: Postmortem dissections were performed in 16 orbits from eight cadavers. The microscopical anatomy was demonstrated in six formalin preserved orbits from six cadavers which had been sectioned in the frontal and sagittal plane and stained with haematoxylin and azophloxin. Surface coil magnetic resonance imaging in the sagittal and coronal plane was performed in five orbits from five normal volunteers using a T1 weighted spin echo sequence. RESULTS: The STL and the TSFE surround the LPS to form a fascial sleeve around the muscle which has attachments to the medial and lateral orbital wall. The TSFE, which is thicker than the STL, blends with Tenon's capsule. The STL and the fascial sheath of the LPS muscle are suspended from the orbital roof by a framework of radial connective tissue septa. MR images show that the TSFE is located between the anterior third of the superior rectus muscle and the segment of the LPS muscle where it changes its course from upwards to downwards. In this area, the LPS reaches its highest point in the orbit (culmination point). The culmination point is located a few millimetres posterior to the equator and superior to the globe. CONCLUSION: Whitnall's ligament can be considered to consist of two distinct parts--the TSFE inferior to the LPS and the STL superior to the LPS. Since the medial and lateral main attachments of Whitnall's ligament are situated inferior to the level of the culmination point of the LPS, the ligament itself is unlikely to suspend the levator muscle. However, a suspension of the LPS may be achieved by the radial connective tissue septa of the superior orbit. The TSFE in connection with the globe may have an additional supporting function. The elasticity of Whitnall's ligament and its connections with highly elastic structures including Tenon's capsule, may provide the morphological substrate for the previously proposed passive (that is, without orbicularis action) lowering of the lid during downward saccades.

Adult↗
PubMed1990

Dermal and subdermal tissue filling with fetal connective tissue and cartilage, collagen, and silicone: experimental study in the pig compared with clinical results. A new technique of dermis mini-autograft injections.

The early reaction to the injection of silicone, collagen, and lyophilized heterologous fetal connective and cartilage tissues into the limiting zone deep dermis-superficial subcutaneous tissue was histologically examined in the pig and compared with clinical results. The inflammatory reaction to lyophilized heterologous fetal tissue is considerably more intense than that to collagen and silicone and lasts for several weeks. Therefore, it is not recommended for soft tissue filling in the face. Admitting an inferior antigenicity of fetal tissues, the authors suggest that enzymatically denaturalized collagen should be manufactured from heterologous fetal connective tissue, to be then further tested. The reaction of tissue to silicone and collagen is minimal. Silicone is preferred for dermal injections since in clinical experience it remains in the site of injection much longer. For subdermal injections, however, collagen is preferred. Based on experience with over 600 patients since 1958, the first author continues using liquid silicone. The lack of complications is probably a result of the fact that only small amounts (milliliters) of silicone were used in wrinkles or small depressions in the dermal layer and that from the beginning injection into the subcutaneous tissue was avoided. Since 1988 a new technique for the treatment of wrinkles and skin depressions with injections of dermal miniautografts has been used with satisfactory results.

Animals↗
PubMed1980

Age-related changes and scar formations of perianal connective tissue.

Changes in perianal connective tissue were studied using specimens from juvenile cadavers and resected tissue from adults. The fibers of the anal sphincter muscles lie in a connective tissue mesh which anchors the muscle fibers, the anal mucosa and skin, and the entire anal canal. The connective tissue mesh is present in the newborn and has similar patterns in every age group, but the ratio of the amount of connective tissue/muscle tissue (C/M ratio) increases with age. The increase of the C/M ratio may have a role in the development of weakness of the sphincters and mucosal or rectal prolapse in the elderly. After injuries or operation no pure collagen scar formation was observed in the sphincter muscles, but there was an increase in the C/M ratio. In inflammatory bowel diseases, when severe anal stenosis is present, the connective tissue web and sphincter are intact and the scar formation is confined to the submucosal and subcutaneous layers.

Adult↗