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Biomedical subjects

M Malmström

Publications and source records attributed to M Malmström.

At least 55 records · Page 3Linked to original sources
PubMed1990

An electron microscopic study of oral lesions in erythema multiforme.

The ultrastructure of oral lesions in 6 patients with erythema multiforme (EM) and of one apparently clinically healthy oral mucosa in one patient with recurrent EM during remission is described. Alterations were observed in epithelium, basal lamina and lamina propria. Both intercellular and intracellular oedema, intracellular vacuolization, decreased numbers of desmosomes, and also loss of cytoplasmic organelles and occasional nuclei were noted in the epithelium. Inflammatory cells--mainly lymphocytes--were found intra-epithelially. Several discontinuities together with some evidence of duplication of the basal lamina were seen in five of the six lesional mucosa specimens. The inflammatory infiltrate in the lamina propria consisted mainly of lymphocytes, although plasma cells, neutrophilic and eosinophilic leukocytes, macrophages and mast cells were also found. Some of the mast cells were partly degranulated. The apparently clinically healthy oral mucosa in the patient with EM in remission showed mild inflammatory changes. The changes observed in the lesional mucosa in EM are thus according to our study mostly non-specific inflammatory alterations and are not pathognomonic for EM.

Adolescent↗
PubMed1990

Herpes simplex virus antigens and inflammatory cells in oral lesions in recurrent erythema multiforme. Immunoperoxidase and autoradiographic studies.

Herpes simplex virus (HSV) antigens were sought in 15 biopsy specimens from both lesional mucosa and clinically healthy looking oral mucosa between attacks in patients with erythema multiforme (EM). Four of the eight biopsy specimens obtained from lesional EM mucosa stained positively with HSV-1-and/or HSV-2-specific antisera applied in direct immunoperoxidase staining. Of the 16 tissue specimens used as controls, two displayed positive staining with HSV-1 and/or HSV-2. Five of the seven biopsy specimens from macroscopically healthy oral mucosa obtained between attacks from patients with recurrent EM stained positively with HSV-1 and/or HSV-2. Of the six tissue specimens used as controls, three stained positively. Most of the local inflammatory mononuclear cells belonged to the T cell series, mainly to the CD-4 subset. A small proportion of the local T cells were blast transformed as assessed by CD-25 expression and [3H]thymidine incorporation. This, together with the findings showing a lower degree of activation in the biopsy from macroscopically healthy looking mucosa between attacks suggest an active role of the cell-mediated immune response in the genesis of oral lesions in EM. The persistence of HSV antigens, and the well-established role of HSV as a precipitating factor in recurrent EM, suggest that HSV may be involved, but since HSV seems to be present in other mucosal lesions as well as in clinically healthy mucosa, quite frequently an additional, hitherto unknown factor must be present in order that EM may occur.

Antigens, Viral↗
PubMed1989

Immunoelectron microscopic study of distribution of T cell subsets in oral lichen planus.

Monoclonal anti-CD4, anti-CD8, and anti-CD18 antibodies were applied in avidin-biotin-peroxidase complex staining using a pre-embedding immunoelectron microscopy technique. Although most of the local T cells in situ were of CD4+ subtype, local CD8+ cells generally had a lower nucleus/cytoplasm ratio and contained more cell organelles than CD4+ cells. This suggests a local activation of CD8+ subpopulation, rather than activation of the numerically predominant CD4+ cells. Topographical analysis disclosed that all lymphocytes, regardless of location, were CD18+ and that most of the CD8+ cells were located subbasally and intraepithelially, whereas CD4+ cells often occurred in small clusters deeper down in the subepithelial lymphocyte-rich band. Furthermore, CD8+ cells were often in close contact with macrophages, whereas CD4+ cells were in some instances in direct contact with plasma cells. This indicates that CD4+ cells may be involved in T cell-dependent B cell-mediated immunoglobulin synthesis, whereas CD8+ cytotoxic lymphocytes and tissue macrophages may be involved in the local pathogenetic process leading to basement membrane alterations.

Antibodies, Monoclonal↗
PubMed1989

PHA stimulation of peripheral blood lymphocytes in oral lichen planus. Abnormality localized between interleukin-2 receptor ligand formation and gamma-interferon secretion.

Peripheral blood T cell function in five oral lichen planus (OLP) patients and five healthy controls was assessed using different activation parameters. Staining with monoclonal antibodies against interleukin-2 receptor and MHC locus II coded Ia antigen, 3H-thymidine incorporation and gamma-interferon secretion were determined in phytohaemagglutinin (PHA) stimulated peripheral blood mononuclear cell cultures at days 0, 1, 3 and 5. The peripheral blood T cell subsets and spontaneous MHC locus II antigen expression were similar in OLP patients and in controls whereas the spontaneous lymphocyte proliferation was lower in OLP patients than in controls (p less than 0.01). This may reflect a slight in vivo preactivation and its effect on lymphocyte recirculation. The PHA-induced expression of IL-2 receptor and T cell proliferation were similar in both groups whereas gamma-interferon secretion and MHC locus II antigen expression were low in OLP patients compared with controls (p less than 0.01). The results suggest a defect in OLP T cell activation disclosed by in vitro PHA stimulation and localized between IL-2 receptor ligand binding and gamma-interferon secretion.

HLA-D Antigens↗
PubMed1989

Lymphocyte activation in oral lichen planus.

The current study analyses the ultramorphology, lymphocyte activation marker expression, DNA synthesis, and gamma-interferon and immunoglobulin production of inflammatory cells in oral lichen planus (OLP) lesions. According to these four different aspects of lymphocyte activation, only a minor fraction, 5% at the most, of all T cells in situ were activated. However, it is this minor fraction, and not the resting T cells without signs of activation, which may prove decisive for the outcome of the local immune-inflammatory process in OLP. We also studied both spontaneous and phytohaemagglutinin (PHA) stimulated peripheral blood T cell function. 3H-thymidine incorporation and gamma-interferon secretion were determined. Interleukin-2 (IL-2) receptor and major histocompatibility complex (MHC) locus II coded la antigen were stained with monoclonal antibodies. The peripheral blood T cell subsets and spontaneous MHC locus II antigen expression were similar in OLP patients and healthy controls, whereas spontaneous lymphocyte proliferation was lower in OLP patients (p less than 0.01). The PHA induced expression of IL-2 receptor and T cell proliferation were similar in both groups. Gamma-interferon secretion and MHC locus II antigen expression were low in OLP patients compared with the controls (p less than 0.01). The results suggest a defect in OLP T cell activation disclosed by in vitro PHA stimulation and occurring between IL-2 receptor ligand binding and gamma-interferon secretion. The findings of our peripheral blood mononuclear studies do not, however, provide an easy or straightforward explanation of the changes observed in the disease itself, particularly with respect to local pathogenesis.

Humans↗
PubMed1989

Basement membrane changes in oral lichen planus.

In recent years ultrastructural morphological alterations in the basement membrane have been observed in a number of mucocutaneous diseases. Varying degrees of fragmentation and branching are seen, but such changes are not specific to any disease. In this respect, oral lichen planus has been studied extensively and clear correlations observed between the clinical type of lesion and type of basement membrane change. The nature of these changes has been studied using different immunohistochemical methods, including immunoelectron microscopy, and immunoreactivity to various basement membrane components has been noted even in the branches of the subbasal basement membrane. Thus these changes probably reflect various proliferative or degenerative changes in basal cells. Using the same technique the topographical distribution of T cell subsets and their relationship to the basement membrane pathology have been studied. Inflammation topography, analysis of lymphocyte differentiation markers, signs of CD8+ cell activation and association of CD8+ cells with mononuclear phagocytes all suggest that the local inflammatory cells are active participants in the local pathogenetic process.

Basement Membrane↗
PubMed1989

Mast cells and their mediators.

Mast cells (MC) are the most important cells in hypersensitivity reactions. Their functions in other pathological conditions are, however, not completely understood. At least two different MC subtypes have been isolated and it seems that due to environmental changes further differences in the morphology and functions of MC:s exist. The activation of MC:s can be both due to immunological and non-immunological factors and results in a release of different mediators and production of so called newly generated MC mediators. The functions following mediator release are complicated and several other inflammatory cells are involved in these reactions. Due to the more slowly effect of the newly generated mediators and the interaction of different cell types the effects of these reactions are often spread over a long time. It seems that MC:s may play an important part not only in hypersensitivity reactions but also in other pathological conditions as in inflammatory disorders.

Humans↗
PubMed1989

Cellular and molecular aspects of inflammation.

Cellular host reaction to noxious agents and damaging events consists of inflammatory, immune and repair responses. These are usually involved in different phases of the host reaction in a well co-ordinated manner, contributing to the well-being of the host. However, when they are excessive, uncontrolled or occur in a vulnerable anatomic location, they can contribute greatly to injury. In general, the effects of the initiating stimulus are much enhanced by secondary involvement of amplification loops, leading to recruitment of nonspecific cells. The number of initially stimulated and/or actively involved cell is, therefore, usually low but of crucial importance for the outcome of the process. As important as understanding of the mechanisms responsible for initiation and amplification of the host response is knowledge of the negative feedback loops responsible for down-regulation of the whole process.

Cell Line↗
PubMed1988

Evaluation of lymphocyte activation in skin lesions of patients with mixed connective tissue disease and discoid lupus erythematodes.

Biopsy specimens from mixed connective tissue disease (MCTD) and discoid lupus erythematodes (DLE) skin lesions were stained with monoclonal antibodies to differentiation and activation antigens. In addition, the blast cells were studied by combining autoradiography with immunoperoxidase staining. In both disease conditions most of the inflammatory cells in situ were positive for T11 antigen, the CD4/CD8 ratio being low. Only a few of the cells were pan-B positive B cells. The expression of various activation antigens did not differ significantly between MCTD and DLE biopsy specimens; the number of T9, Tac, and 4F2 antigen carrying cells was relatively low, whereas Ia-positive cells were more numerous. 3H-Thymidine incorporating T blasts comprised less than 1% of all inflammatory cells. T4 and T8 marker-carrying blast cells were present in about equal proportions. These findings suggest that Ia antigen-expressing T cells are important from the pathogenetic point of view in both MCTD and DLE. Because the local proliferation of T cells was extremely low according to the lack of interleukin-2 receptor and OKT9 markers and 3H-thymidine incorporation, it seems probable that most of the T cells are recruited from the circulation to the site of the inflammation.

Adult↗
PubMed1988

Topical treatment of oral leukoplakia with bleomycin.

Ten patients with oral leukoplakia were treated topically with bleomycin. We found the method convenient but only successful where sufficient attention was paid to the activity of the bleomycin-dimethylsulphoxide solution. The initial epithelial dysplasia disappeared completely in five of the 10 patients, while in the remainder the dysplastic grade remained the same. Following treatment the thickness of the keratotic layer increased in four patients, became thinner in five and remained unchanged in one. Although clinically the results of treatment only appear some 3 months after bleomycin application, once the lesions are cured their recurrence seems to be slower than after surgery. Nevertheless we strongly emphasise that 3-monthly follow-ups are mandatory for patients with oral leukoplakias whether or not they have been treated successfully.

Administration, Topical↗
PubMed1988

Lymphocyte activation in oral lichen planus in situ.

The current study evaluated the activation of T-cell mediated cellular immune response in the oral lesions in lichen planus (OLP). Analysis was made of the ultramorphology, lymphocyte activation marker expression, DNA synthesis, and gamma-interferon production of the inflammatory cells in OLP lesions. According to these four different aspects of lymphocyte activation, only a minor fraction, 5% at the most, of all T-cells in situ were activated. This minor fraction, however, not the resting T-cells without these signs of activation, may decide the outcome of the local immune-inflammatory process in OLP. Of the inflammatory cells in situ, however, 81 +/- 5% were Ia positive. This finding may be the result of an Ia inducing capacity of the gamma-interferon produced locally by the activated T-cells.

Antigens, Surface↗
PubMed1987

Mandibular dentinoma.

Dentinoma is a rare odontogenic tumor showing the inductive effects of odontogenic epithelium on the connective tissue. A case of the tumor occurring in the region of the missing right mandibular second permanent premolar of an 11-year-old male is described. The tumor and the impacted right mandibular second deciduous molar were surgically removed. Histologically, areas of hyalinized collagen, osteodentin and tubular dentin were seen in a stroma varying from mesenchymal to more mature. Immunostaining for the distinct types I, III and IV collagens were negative in the hyalinized areas. Type IV collagen stained as a halo corresponding to the basal membrane zone surrounding the groups of odontogenic epithelial cells. Recovery was uneventful. There was no recurrence of the tumor during the first 10 months of follow-up.

Child↗
PubMed1987

A long-term clinicopathologic survey of patients with Jessner's lymphocytic infiltration of the skin.

Skin biopsies from 6 patients with Jessner's lymphocytic infiltration (JLI) were studied using monoclonal antibodies in peroxidase staining, on some occasions combined with [3H]thymidine incorporation visualized by autoradiography. Ninety-one +/- two percent of all inflammatory mononuclear cells in situ were T11-positive T lymphocytes, whereas B lymphocytes were few. Forty-nine +/- nine percent of cells were Ia-positive, suggesting involvement of T cells in the local pathogenetic mechanisms, but interleukin-2 receptor-carrying cells as well as [3H]thymidine-incorporating cells accounted for less than 2% of all inflammatory cells, suggesting that T blasts account for only a small minority. Similarly, PCA-1 plasma cells were few in situ, there was no immunoglobulin or complement deposition at the dermal-epidermal junction and serum antinuclear and anti-DNA antibodies as well as complement levels were normal, and no visceral involvement was revealed during the survey period. According to our findings, JLI of the skin seems to be sufficiently distinctive to be appreciated as an entity. T lymphocytes in JLI do not seem to proliferate in the site of inflammation but are merely accumulated from the circulation.

Adult↗
PubMed1987

Ultrastructure of oral leukoplakia and lichen planus. II. A correlated scanning and transmission electron microscopic study of epithelial surface cells.

Nine cases of homogenous leukoplakia and 21 cases of lichen planus (11 reticular and 10 erosive) were studied under the scanning and transmission electron microscopes. Characteristic differences between leukoplakia and lichen planus in surface patterns of the epithelial surface cells were noted. Microridges in leukoplakia form parallel and anastomosing rows whereas the picture in lichen planus is irregular with microridges varying in width. The transmission electron microscopic findings confirm and correlate with these findings, the microridges representing invaginations of the plasma membrane. The keratin patterns exhibited by the surface cells were also characteristic regarding type and site of lesion. Scanning electron microscopy can be used as an additional diagnostic aid in differentiating these lesions.

Epithelium↗
PubMed1987

Ultrastructure of oral leukoplakia and lichen planus. I. Basal region and inflammatory cells.

Nine cases of homogenous leukoplakia and 21 cases of lichen planus (11 reticular and 10 erosive) were studied under the electron microscope. The changes found in leukoplakia were limited to occasional breaks in the basal lamina and modest changes in the cytoplasm of the basal cells. The basal lamina in lichen planus was found to exhibit 3 distinctly different pictures reflecting the clinical types of lichen planus. The structural abnormalities in the basal cells increased with increasing severity of the lesions. The inflammatory infiltrate in lichen planus was found to contain mainly small-to-medium-sized lymphocytes but plasma-cells with widely dilated rough endoplasmic reticulum containing a granular substance were frequently seen. Similar changes are seen in other disorders and, therefore, specific diagnostic criteria cannot be established on the basis of the present material.

Basement Membrane↗
PubMed1987

T lymphocyte activation state in the minor salivary glands of patients with Sjögren's syndrome.

Local lymphoplasmacytoid infiltration of the diseased exocrine glands is a cardinal sign of Sjögren's syndrome (SS). The state of T lymphocyte activation present in these local infiltrations was studied by three different techniques: determination of interleukin 2 (IL2) receptor (Tac) on cell surface membrane; autoradiography combined with immunoperoxidase staining of T cell epitopes; and electron microscopic analysis of the lymphoblast subclasses. Although 64 (SEM 4)% of the local inflammatory cells expressed Ia antigen, only 4 (SEM 1)% of them displayed the T cell activation antigen Tac. Autoradiography-immunoperoxidase double labelling showed that less than 1% of all T cells in situ were [3H]thymidine incorporating blasts. This finding suggests that although T lymphocyte is the dominant cell in situ, only a few of these cells have passed the G0/G1 interphase, and even fewer have been pushed to the S phase of the cell cycle by IL2. Transmission electron microscopy showed that few T blasts were present, even though there were many plasma cells. This result further confirms the impression that only a minor T cell subpopulation in situ is blast transformed despite the fact that many of the local T lymphocytes in the diseased salivary glands in SS are Ia positive.

Adult↗