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PubMed1994

[Clinical and serologic course of patients with mixed connective tissue disease].

The so called mixed connective tissue disease (MCTD), continues to be a controversial entity, while some authors considered it a good characterized disease, others think that is an undifferentiated connective tissue disease. OBJECTIVE. To analyse the clinical and serological evolution of a group of patients diagnosed of MCTD, with particular consideration to the meaning of anti-nRNP and anti-Sm antibodies. METHOD. We have studied 20 patients diagnosed of MCTD and 112 with systemic lupus erythematosus (SLE). Anti-nRNP and anti-Sm antibodies were detected through counter immunoelectrophoresis, immunoblotting and ELISA. RESULTS. After an average time of evolution of 10 years, 70% (14/20) of the patients diagnosed of MCTD fulfill criteria for SLE (6 cases), scleroderma (6 cases) or polymyositis (2 cases). Anti-nRNP response is persistent, directed mainly against the 70 Kd and A-nRNP polypeptides and qualitatively higher in MCTD in SLE (absorbencies 2.64 vs 1.25. The immunoblotting test detected anti-Sm antibodies in 5 patients (25%) and ELISA test in 14 (70%). CONCLUSIONS. Clinical and serological evolution suggest that MCTD is an undifferentiated connective tissue disease. Anti-nRNP antibodies are characteristic, although anti-Sm antibodies can be detected with ELISA regardless whether on not patients fulfill SLE criteria.

Adolescent↗

PubMed1993

Chemically separated connective tissue grafts: clinical application and histological evaluation.

Subepithelial palatal connective tissue grafts, separated from the epithelium either chemically (n = 5) or surgically (n = 2) were inserted in patients presenting with gingival recession. Biopsies at the grafted tissue and a portion of non-keratinized mucosa were taken 12 months later. Histology showed keratinization of the newly formed epithelium, and interestingly a deep projection of epithelium into the connective tissue in almost all biopsies, sometimes with an enlargement and a cyst-like space. We conclude that chemical separation of epithelium and connective tissue is clinically feasible for connective tissue grafts and that the subepithelial connective tissue grafting technique should be modified to avoid this projection of epithelium.

Connective Tissue↗

PubMed1998

The clinical significance of antinuclear antibodies in connective tissue disease.

Antinuclear antibodies (ANA) are often present in connective tissue diseases. In 279 non-selected patients with connective tissue disease, inflammatory and degenerative joint disease, in some patients with chronic infectious diseases and malignancies and in the presence of some unclear pathologic conditions in patients whose serum reacted positively to ANA, we analyzed the type of immunofluorescence and the presence of extractable antinuclear antibodies (ENA). In systemic lupus erythematosus, the prevailing immunofluorescence is type H (homogenous) (60.6%), anti-Ro/SS-A appears in 24.2%, anti-Sm and anti-RNP in 12.1%. In Sjögren's syndrome, type S prevails (47.6%), anti- Ro/SS-A and anti-La/SS-B are present in 52.4%, only anti-Ro/SS-A in 28.6%. In systemic sclerosis, the prevailing immunofluorescence is type S (37.5%), in 75% a positive anti-Scl-70 antibody is present. In mixed connective tissue disease, anti-RNP appears in 85.7%. In dermatopolymyositis, the anti-Jo-1 antibody is present in 33.3%. In undifferentiated connective tissue disease, type S immunofluorescence appears in 70%. In rheumatoid arthritis the prevailing immunofluorescence is type H (homogenous) (46.4%) and type S (speckled) (41.0%), while the presence of ENA is rare (anti-Ro/SS-A in 4.6%). In spondylarthritis, type S immunofluorescence appears most often (62.5%). Patients with chronic infectious disease, malignancies, undefined conditions and degenerative joint disease present with various types of immunofluorescence; the presence of ENA is extremely rare in these patients. The results of this study underline the significance of ANA and, particularly ENA, in the diagnosis of connective tissue disease. These antibodies however, can also be identified in various infectious and malignant diseases as well as in inflammatory and degenerative joint diseases.

Adult↗

PubMed1987

Three-dimensional structures of the connective tissue papillae of the tongue in newborn dogs.

Connective tissue papillae underlying epithelial cell layers of the lingual papillae of newborn mongrel dogs were exposed by long term hydrochloric acid treatment and observed by scanning electron microscopy. Each of the filiform papillae of ovoid shape (100-130 microns in diameter) contained a connective tissue papilla representing a smaller elliptical protrusion (90-100 microns in length, 70-80 microns in width). Its overview showed a horse-shoe shaped, opening anteriorly. Its posterior curvature projected a conical node with a rounded apex. Each of the fungiform papillae (150 microns in diameter) contained a connective tissue papilla of rounded shape (100 microns in diameter) whose upper surface was facetted with several slight depressions. The entire surface of the connective tissue papillae was found to be covered by networks of collagenous fibers of varying thickness, running in various directions. The basal surface of the epithelium revealed regularly distributed round holes that corresponded to the connective tissue papillae. In the filiform papillae, a small elliptical bulge was seen on the anterior side of each hole. Light microscope observation indicated that the anterior column of the filiform papillae contained a granular layer with moderate keratohyaline granules, whereas the posterior column did not show such a granular layer.

Animals↗

PubMed2006

Undifferentiated connective tissue diseases (UCTD).

The term undifferentiated connective tissue diseases is used to define conditions characterized by the presence of signs and symptoms suggestive of a systemic autoimmune disease that do not satisfy the classificative criteria for defined connective tissue diseases (CTD) such as systemic lupus erythematosus (SLE), Sjögren's syndrome (SS), rheumatoid arthritis (RA) and others. A small percentage of patients presenting with an undifferentiated profile will develop during the first year follow up of a full blown CTD, however an average of 75% will maintain an undifferentiated clinical course. These patients may be defined as having a stable undifferentiated connective tissue diseases (UCTD). The most characteristic symptoms of UCTD are represented by arthritis and arthralgias, Raynaud's phenomenon, leukopenia, while neurological and kidney involvement are virtually absent. Eighty percent of these patients have a single autoantibody specificity, more frequently anti-Ro and anti-RNP antibodies. Stable UCTD are considered as distinct clinical entities and therefore it has been proposed to define those conditions as UCTD. Classificative criteria have also been proposed and a work to better define them is still under way.

Autoantibodies↗

PubMed2004

Bovine metalloprotease characterization and in vitro connective tissue degradation.

Metalloproteases that selectively hydrolyze connective tissue proteins may tenderize meat without creating texture problems associated with myofibrillar protein degradation. Our objective was to characterize the activity of bovine placental proteases to determine whether they can improve meat tenderness through disruption of the connective tissue matrix. Enzymes were extracted, crudely purified, and proteolytic activity was assessed against gelatin and collagen under varying pH and temperature conditions using both SDS-PAGE and zymography. Gelatin zymography revealed proteolysis between 57 and 63 kDa, with decreased activity as buffer pH decreased from pH 7.4 to 5.4 (37 degrees C). Proteolytic activity was pronounced at 37 degrees C, moderate at 25 degrees C, and absent at 4 degrees C following 48-h incubation (pH 7.4). Placental enzymes were metalloproteases inhibited by excess EDTA. Maximum proteolysis was achieved in the presence of Ca2+, with or without Mg2+ and Zn2+. Absence of Ca2+ decreased proteolytic activity. Complete degradation of both the 125- and 120-kDa proteins of the alpha-chains of gelatin was achieved following enzyme incubation for 6 h at 37 degrees C or 24 h at 25 degrees C. No degradation was observed following enzyme incubation with native Type I collagen. Given the marked decrease in enzyme activity at pH 5.4 and 4 degrees C (standard industry conditions), bovine placental metalloproteases would not be expected to contribute to connective tissue degradation or improve meat tenderness.

Animals↗

PubMed1989

Skin is a window on heritable disorders of connective tissue.

A skin biopsy contains the macromolecules present in most connective tissues: collagens, elastin, glycoproteins, and proteoglycans. The specific combination and assembly of these matrix components and their interactions with other structures (e.g., epidermal appendages, nerve and vascular networks) and cells are responsible for the distinction among specific regions of the dermis. The matrix components are interactive and interdependent and modification of one of them, by extrinsic (environmental) and/or intrinsic (systemic, genetic, age-related) factors, may have consequences on the tissue as a whole. The skin, therefore, provides a window through which it is possible to examine how mutations in one connective tissue macromolecule can change the interactions among matrix components and affect tissue structure and organization. Light and electron microscopic studies of skin from patients with inherited connective tissue disorders (e.g., Ehlers-Danlos syndrome, osteogenesis imperfecta, Marfan syndrome, cutis laxa) have led us to the following generalizations about what components change, how individual collagen or elastic fibers are altered and how individual alterations affect overall dermal organization: 1) There is a limited change in the repertoire of collagen fibrils in the skin; 2) there appears to be a greater range of abnormal structure in dermal elastic fibers than in the collagen fibrils; 3) the morphology of the fibroblastic cells may provide clues to the defect in matrix components; 4) similar structural abnormalities result from different molecular defect; 5) a molecular defect in one connective tissue molecule has consequences for the structural properties of other connective tissue components; and 6) although structural alterations in connective tissue fibers are rarely specific for a given disease, there are characteristic patterns of structural change in the matrix that may be used to confirm a diagnosis. These generalizations show that mutations rarely affect only a single aspect of macromolecular function and because of the interactions of matrix components in this complex organ (skin) often disturb the organization of the entire dermis. Genotype-phenotype relationships are important to understand if effective therapies are to be designed. The structure of skin should provide the next level of integration in our efforts to determine how mutations produce disease.

Collagen↗

PubMed1983

Skeletal framework of mammalian heart muscle. Arrangement of inter- and pericellular connective tissue structures.

We have studied the connective tissue of mammalian heart muscle in order to obtain an integrated description of extracellular structures and their dispositions relative to cardiac myocytes. Light microscopy and several types of electron microscopy have been employed in these investigations. The epimysium, the sheath of connective tissue that surrounds the muscle, contains relatively large fibers of collagen and elastin. In papillary muscles of rat, the large collagen fibers of the epimysium form a weave pattern at slack length (sarcomere lengths 1.8 to 2.0 micron) but are well aligned in states of stretch along the long axis of the muscle (sarcomere length 2.3 to 2.5 micron). We propose that the epimysial collagen network protects the sarcomeres from being stretched beyond lengths favorable to maximal force production. The endomysium is defined as the connective tissue that surrounds and interconnects myocytes; it consists of intercellular struts (bundles of collagen fibrils, often attached near Z-band level), a weave of bundles of collagen fibrils that envelopes myocytes, and a collagen fibril-microthread-granule lattice that bridges cells and fills the extracellular matrix. In contracted muscles festoons of sarcolemma are attached to Z-bands, thus forming regions for transmission of force across the sarcolemma. Perimysial bundles of collagen connect epimysium to endomysium and surround groups of myocytes. Collagen fibers often have a twisted configuration, probably for enhanced tensile strength. Superimposed on the large extracellular structures is the polyanion-rich lattice comprised of unit collagen fibrils, microthreads, and granules. Amorphous ground substance forms a matrix in which the fibrils of collagen fibers are embedded; it appears continuous with the cell coat in regions of fiber attachment. Elastic fibers interconnect cells and helically wind around myocytes. Circumferential forces from elastin stretched about shortened, thickened myocytes in systole should promote elongation in tandem with intramyocyte forces of elongation.

Animals↗

PubMedDate not supplied

Mapping by monoclonal antibody detection of glycosaminoglycans in connective tissues.

Chondroitin sulphate proteoglycans are widespread connective tissue components and chemical analysis of cartilage and other proteoglycans has demonstrated molecular speciation involving the degree and position of sulphation of the carbohydrate chains. This may, in turn, affect the properties of the glycosaminoglycan (GAG), particularly with respect to self-association and interactions with other extracellular matrix components. Interactions with specific molecules from different connective tissue types, such as the collagens and their associated glycoproteins, could be favoured by particular charge organizations on the GAG molecule endowed by the sulphate groups. So far, it has not been possible to identify and map chondroitins of differing sulphation in tissues, but we have now raised three monoclonal antibodies which specifically recognize unsulphated, 4-sulphated and 6-sulphated chondroitin and dermatan sulphate. These provide novel opportunities to study the in vivo distribution of chondroitin sulphate proteoglycans. We demonstrate that chondroitin sulphates exhibit remarkable connective tissue specificity and furthermore provide evidence that some proteoglycans may predominantly carry only one type of chondroitin sulphate chain.

Animals↗

PubMed1980

Changes in the differentiation pattern of oral mucosal epithelium following heterotopic connective tissue transplantation in man.

Anterior palatal connective tissue was transplanted into wound beds created within the alveolar mucosa of the lower anterior vestibulum in seven adults females. Six months postoperatively, the epithelial lining of the inverted transplants was biopsied and compared histologically, histometrically, and stereologically to the neighboring mucosal epithelium. The data suggest that (1) connective tissue of the lamina propria is primarily responsible for the structural specificity of the overlying epithelium, (2) inductive stimuli are not confined to superficial layers but also originate from deep portions of the lamina propria, (3) these stimuli influence both the epithelial differentiation and the type of epithelium-connective tissue interface, and (4) the epithelial response to the inductive stimuli in man may depend on the individual type of epithelial differentiation pattern originally prevailing at the recipient site. The transplant-lining epithelium assumed features resembling that of the hard palate in subjects with an alveolar mucosal epithelium with cheek-type characteristics. In subjects with an alveolar epithelium displaying a mixed differentiation pattern, the transplant-lining epithelium continued to generate a mixed pattern or else shifted to more palate-like characteristics.

Adult↗

PubMed2000

Relation between myofibers and connective tissue during muscle injury repair.

The connective tissue framework in skeletal muscle combines the contractile myofibers into a functional unit, in which the contraction of myofibers is transformed into movement via myotendinous junctions (MTJs) at their ends, where myofibers attach to tendons/fascia. The cytoskeletal contractile myofilament apparatus adheres through subsarcolemmal and transmembrane molecules to the surrounding extracellular matrix, with integrin and dystrophin associated chains of molecules being the two main adhesion complexes. In shearing type of muscle injury both myofibers and the connective tissue framework are ruptured and thereby the functional tendon-muscle-tendon units are disrupted. The stumps of the ruptured myofibers are separated and at the same time joined by a connective tissue scar, through which the ends of regenerating myofibers try to pierce, but as the scar becomes more compact the ends attach to the scar by new mini-MTJs. During the early phase ruptured myofibers try to compensate for the lost MTJ attachment by reinforcing their integrin mediated lateral adhesion, which returns to normal low level after formation of the mini-MTJs and at which time complementary increase of dystrophin and associated molecules on lateral sarcolemma takes place. The stumps appear to remain separated by and attached to the interposed scar for many months, possibly for ever, i.e. the original tendon-muscle-tendon units may have become permanently divided into two consecutive units. Remarkably, axon sprouts are able to penetrate through the interposed scar to form new neuromuscular junctions on those abjunctional stumps which were denervated by the rupture.

Athletic Injuries↗

PubMed1994

How connective tissues temporally process mechanical stimuli.

Connective tissues have the capacity to adapt to a changing mechanical environment. Considerable experimental evidence suggests, however, that tissues respond to only a small portion of mechanical loads they experience and thus ignore the majority of the load they experience. Evidence suggests that tissues 'temporally process' these external mechanical signals in specific ways: 1) they respond in a trigger-like manner after a relatively few events or cycles of loading; 2) they respond only to some window of strain magnitude; 3) they exhibit a refractory period after a response; 4) they have a memory for previous stimuli. These characteristics do not necessarily mirror distinct cellular phenomena but rather reflect typical features of experimental and theoretical models. The manner in which tissues temporally process mechanical signals can be explained by energy transfer over short periods of time from the matrix to the second messenger systems. Much of the energy input into connective tissues during deformation is recovered, and relatively little is 'lost' and thus potentially transferable to the cells. Since evolutionary principles suggest that a pathway of response needs to be defined by biologically optimal use of energy, it is logical that cells would have evolved mechanisms to respond to a small finite level of integrated stimuli in order to rapidly respond (fitness) especially in times of environmental duress.

Adaptation, Physiological↗

PubMed1985

Fate of bone marrow-derived cultured mast cells after intracutaneous, intraperitoneal, and intravenous transfer into genetically mast cell-deficient W/Wv mice. Evidence that cultured mast cells can give rise to both connective tissue type and mucosal mast cells.

Both connective tissue mast cells and mast cells grown in vitro are derived from multipotential hematopoietic stem cells, but these two mast cell populations exhibit many differences in morphology, biochemistry, and function. We investigated whether the phenotype of cultured mast cells or their progeny was altered when the cells were transferred into different locations in vivo. Cultured mast cells were immature by ultrastructure, and stained with alcian blue but with neither safranin or berberine sulfate, a fluorescent dye that binds to the heparin of connective tissue mast cell granules. By contrast, mast cells recovered from the peritoneal cavity of congenitally mast cell-deficient (WB X C57BL/6)F1-W/Wv (WBB6F1-W/Wv) mice 10 wk after intraperitoneal injection of cultured WBB6F1-+/+ or C57BL/6-bgJ/bgJ mast cells stained with both safranin and berberine sulfate. Staining with berberine sulfate was prevented by treatment of the cells with heparinase but not chondroitinase ABC, suggesting that the adoptively transferred mast cell population had acquired the ability to synthesize and store heparin. Furthermore, the recovered mast cells were indistinguishable by ultrastructure from the normal mature peritoneal mast cells of WBB6F1-+/+ mice, and contained substantially more histamine than mast cells studied directly from culture. Intravenous injection of cultured mast cells resulted in the development of safranin-and berberine sulfate-positive mast cells in the peritoneal cavity, spleen, skin, and glandular stomach muscularis propria. Mast cells also developed on the glandular stomach mucosa, but these cells stained with alcian blue rather than safranin, and did not stain with berberine sulfate. This result suggests that cultured mast cells can give rise to mast cells of either the connective tissue type or mucosal phenotype, depending on anatomical location. Furthermore, transplantation of cultured mast cells into WBB6F1-W/Wv mice had no measurable effect on the anemia of the recipient mice, suggesting a possible strategy for repairing the mast cell deficiency of WBB6F1-W/Wv mice without affecting other bone marrow-derived populations such as erythrocytes. Intravenous injection of representative connective tissue type mast cells (30-50% pure peritoneal mast cells derived from WBB6F1-+/+ mice) gave results similar to those obtained with cultured mast cells: mast cells developing in the peritoneal cavity, skin, spleen, and glandular stomach muscularis propria of WBB6F1-W/Wv recipients stained with safranin and berberine sulfate, whereas mast cells developing in the mucosa of the glandular stomach stained only with alcian blue.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1988

Studies of the tissue reaction induced by transvenous pacemaker electrodes. I. Microscopic examination of the extent of connective tissue around the electrode tip in the human right ventricle.

The purpose of this study was to investigate the extent of connective tissue of the human right ventricle induced by cardiac pacing electrodes. Between January 1984 and July 1987, 34 consecutive patients with VVI-pacing systems were autopsied in the Department of Pathology at the University of Frankfurt/M. The surrounding tissue of these 34 electrodes (17 Siemens Elema 412 S, five Medtronic 6957, one Medtronic 6959, one Medtronic 4011, three Biotronik D2K, three Biotronik K 10, two Osypka FY 62, one Biotronik N, and one Siemens Elema 588) in the right ventricle were investigated histologically. The tissue was stained with Giemsa and the thickness of the connective tissue layer was measured. Stimulation threshold data at various times were known in four of eight screw-in electrodes, in seven of 17 vitreous carbon electrodes and in two of seven smooth surface electrodes. Electrode surface area, implantation time, age of the patient and cause of death were comparable for all three electrode groups. However, a significant difference was found in the extent of connective tissue between the porous surface and screw-in electrodes (128 +/- 55 vs 397 +/- 269 micron, P less than or equal to 0.01) and porous surface and smooth surface electrodes (128 +/- 55 vs 307 +/- 117 micron, P less than or equal to 0.01). No relation (r = 0.106) was found between the duration of implantation and the extent of connective tissue for the vitreous carbon electrodes (Siemens Elema 412 S).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1974

Oxytalan connective tissue fibers: a review.

Oxytalan connective tissue fibers are a separate and distinct fiber type. Although current histochemical methods cannot distinguish pre-elastic from oxytalan fibers, the two fiber types are readily distinguished by electron microscopy. Oxytalan fibers are found in periodontal membranes of all teeth of man, monkeys, rats, guinea pigs and mice. Increased numbers and size of oxytalan fibers are observed in periodontal membranes of teeth subjected to increased stress, such as those used for bridge abutments. Edwards (1968) observed increased size and number of oxytalan fibers in periodontal membranes of dog incisors subjected to orthodontic forces. Some oxytalan fibers serve to support the blood and lymphatic vessels leading to the teeth. Oxytalan fibers appear to have a protein component and a stainable component digestible with beta-glucuronidase after peracetic acid digestion. Oxytalan fibers develop in repair tissues of the periodontal membrane. Although oxytalan fibers probably develop in relation to tumors developed from dental tissues, electron microscopy must be employed to distinguish oxytalan from developing elastic tissues inasmuch as histochemical methods are inadequate.

Adolescent↗

PubMed1998

Respiratory complications in mixed connective tissue disease.

The term mixed connective tissue disease is used to identify the patients with combined clinical features of systemic lupus erythematosus, scleroderma or progressive systemic sclerosis, and polymyositis-dermatomyositis. A prerequisite for the diagnosis of mixed connective tissue disease is the presence, in the serum, of high titers of antibodies against uridine-rich RNA-small nuclear ribonucleoprotein (snRNP). Respiratory and nonrespiratory features of the disease follow those seen in systemic lupus erythematosus, scleroderma, or progressive systemic sclerosis, and polymyositis-dermatomyositis. Respiratory involvement is observed in 20% to 80% of patients. Major respiratory manifestations and their incidences described include interstitial pneumonitis and fibrosis (20% to 65%), pleural effusion (50%), pleurisy (20%), and pulmonary hypertension (10% to 45%). Other pulmonary features consist of pulmonary vasculitis, pulmonary thromboembolism, aspiration pneumonia, pulmonary hemorrhage, pulmonary nodules, pulmonary cysts, obstructive airways disease, mediastinal lymphadenopathy, pulmonary infections, hypoventilatory respiratory failure, and diaphragmatic dysfunction. Pulmonary hypertension is a serious complication; rapid deterioration and death have occurred in spite of corticosteroid and cytotoxic chemotherapy.

Adult↗

PubMed2001

Type II alveolar epithelial cells and interstitial fibroblasts express connective tissue growth factor in IPF.

Connective tissue growth factor (CTGF) is a growth and chemotactic factor for fibroblasts encoded by an immediate early gene that is transcriptionally activated by transforming growth factor-beta. Previous studies have shown that both CTGF messenger ribonuclear acid (mRNA) and protein are expressed in renal fibrosis and bleomycin-induced pulmonary fibrosis in mice. The aim of the present study was to investigate the localization of CTGF protein and its mRNA expression in the fibrotic lung tissue of patients with idiopathic pulmonary fibrosis (IPF). Using human fibrotic lung tissue obtained from eight autopsy cases and four biopsy cases with IPF, immunohistochemical staining, in situ hybridization, and reverse transcription-polymerase chain reaction (RT-PCR) were performed. The cellular immunoreactivity for CTGF was markedly increased in the lung tissue of patients with IPF, compared to normal lungs. The immunolocalization of CTGF was confined predominantly to proliferating type II alveolar epithelial cells and activated fibroblasts. In the normal lung, type II alveolar epithelial cells stained for CTGF were sparsely distributed. CTGF mRNA was localized in proliferating type II alveolar epithelial cells and activated fibroblasts in the interstitium of fibrotic lung tissues. RT-PCR analysis showed that CTGF mRNA was expressed at a higher level in fibrotic lungs than in normal lungs. In both an autocrine and a paracrine manner, type II alveolar epithelial cells and activated fibroblasts may play a critical role in pulmonary fibrosis by producing connective tissue growth factor which modulates fibroblast proliferation and extracellular matrix production.

Adult↗

PubMedDate not supplied

[The role of vitamin K in the metabolism of connective tissue biopolymers (review)].

Metabolism of connective tissue biopolymers was studied under conditions of various content of vitamin K in the body. The data obtained suggest the existence of a new metabolic effect of vitamin K--its participation as an allosteric activator in regulation of glucosamine synthetase (EC 5.3.1.19). The anabolic effect of vitamin K on connective tissue is apparently related to an increase in the rate of biosynthesis of glucosamine-6-phosphate--general precursor of glycosaminoglycans, glycoproteins and hexosamine-containing glycolipids.

Animals↗