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Biomedical subjects

M Malmström

Publications and source records attributed to M Malmström.

At least 19 recordsLinked to original sources
PubMed1992

Peptide-containing nerves in labial salivary glands in Sjögren's syndrome.

OBJECTIVE: The presence and spatial distribution of peptide-containing nerves in labial salivary glands from 10 Sjögren's syndrome patients were compared with those in salivary glands from 7 healthy controls. METHODS: Immunoperoxidase staining was used to demonstrate vasoactive intestinal peptide (VIP)-immunoreactive (IR) fibers, postganglionic sympathetic fibers containing the C-flanking peptide of neuropeptide Y (CPON), and sensory fibers containing calcitonin gene-related peptide (CGRP) and substance P. RESULTS: Acini, intralobular ducts, small arteries, and postcapillary veins were richly innervated by VIP-IR fibers, whereas CPON-, CGRP-, and substance P-IR fibers were restricted to blood vessels. Peptide-containing nerves were found surrounding, but not in the middle of, the highly inflamed mononuclear cell areas. CONCLUSION: This topologic distribution suggests involvement of VIP-IR fibers in vascular, motor, and secretory components of the reflex salivary secretion, whereas the distribution and the vasoactive actions of CPON, CGRP, and substance P suggest a role in the regulation of the salivary gland circulation, and thus of transcapillary flow. Excessive release may contribute to a neurogenic inflammation. Local depletion and absence of trophic neuropeptide stimuli may contribute to acinar atrophy.

C-Peptide↗
PubMed1992

Distribution of adhesion receptors in recurrent oral ulcers.

When activated under physiologic or pathologic conditions leukocytes adhere to one another or to other cell types. Adhesion receptors mediate these interactions. In the study reported here, the distribution of the adhesion receptors LFA-1 (CD11a/CD18), ICAM-1 (CD54), CD2 and LFA-3 (CD58) in recurrent oral ulcers (ROU) were studied. Nine tissue specimens from five female patients (mean age 33 yr, age range 21-40 yr) with ROU were studied using the avidin-biotin-peroxidase complex (ABC) method. The main mononuclear cell infiltrations were in lamina propria (LP) and the epithelium next to the basement membrane (BM), laterally to the ulcers. In this area, ICAM-1 was strongly expressed in capillaries and in postcapillary venules. LFA-1, LFA-3 and CD2 were expressed in 65 +/- 1.1%, 70 +/- 16% and 80 +/- 1%, respectively, of all mononuclear cells. The findings indicate that LFA-1/ICAM-1 and CD2/LFA-3 interactions may play roles in cell to cell adhesion events in ROU.

Adult↗
PubMed1992

Topology of innervation of labial salivary glands by protein gene product 9.5 and synaptophysin immunoreactive nerves in patients with Sjögren's syndrome.

Glandular secretion and integrity, local blood flow, salivary secretion, pain perception and neurogenic inflammation can all be controlled by the nervous system. Therefore, the pattern of innervation of labial salivary glands (LSG) was studied in 10 patients with Sjögren's syndrome using neuronal markers: protein gene product 9.5 (PGP 9.5), a cytoplasmic, noncytoskeletal epitope and synaptophysin, a glycoprotein present in presynaptic vesicles. PGP 9.5 immunoreactive nerve fibers were found surrounding the acini, salivary ducts and blood vessels. The rich innervation of LSG was even more evident in immunofluorescence stained sections analyzed using confocal laser scanning imaging. Synaptophysin immunoreactive nerve endings and preterminal varicosities also demarcated the LSG acini. Furthermore, in the small foci, PGP 9.5 and synaptophysin immunoreactive nerve fibers were found amid inflammatory mononuclear cells and in extensive inflammatory areas nerve fibers were found in the peripheral parts of such infiltrates. This suggests a possible neurogenic influence on the local cellular inflammation. When LSG patient samples were compared to unaffected glands from 7 controls, acinar atrophy was found in the areas devoid of a local delivery system of neurogenic trophic stimuli, suggesting this as a possible cause of glandular degeneration. It may become necessary to incorporate this neglected, but existing system into our current view on the local but possibly centrally controlled or influenced pathogenetic mechanisms of Sjögren's syndrome.

Humans↗
PubMed1991

Immune-inflammatory cells in recurrent oral ulcers (ROU).

Tissue lesions from eight patients with recurrent oral ulcers (ROU) were subjected to detailed immunohistopathologic studies. In five patients, a specimen of an unaffected area from the opposite site was obtained. The main inflammatory cells in situ were CD3 positive T lymphocytes, with CD4 cells forming approximately half (range 30-60%) and CD8 cells 20% (range 10-30%) of all cells. CD19 positive B lymphocytes formed 5-12% of all cells. Furthermore, 45% (range 15-65%) of all lymphoid cells had signs of previous antigenous contact and had helper/inducer CDw29 type. Suppressor/inducer CD45R cells formed only about 20% (range 7-50%) of all cells. Although this observation suggests involvement of antigen as a causative and/or triggering stimulus, elements of a non-specific inflammatory response were observed as well. Endogenous peroxidase-positive neutrophils were present at the ulcer site, and were occasionally observed intravascularly and in the extracellular matrix in areas characterized by inflammatory mononuclear cell infiltrates. Although the proportion of endogenous peroxidase-positive, recently recruited monocytes was low, CD11b and nonspecific esterase-positive mature tissue macrophages formed about 14% (range 5-35%) of all inflammatory cells in situ, particularly at the periphery of the lymphoid cell infiltrates. Mast cells were also observed in all samples studied, forming 2-5% of inflammatory cells in the richly vascularized connective tissue beneath the basement membrane. In the specimens from clinically unaffected areas, inflammatory cells were rare. Our observations stress the multifaceted nature and participation of multiple effector systems in the local tissue pathogenesis of ROU.

Adult↗
PubMed1990

Localization of lysozyme mRNA in the labial salivary glands by in situ hybridization in Sjögren's syndrome.

In this study, lysozyme mRNA in labial salivary glands has been localized with in situ hybridization technique using 35S-labeled hen lysozyme cDNA (cDNALZM) as a hybridization probe in normals and in patients with Sjögren's syndrome, 35S-DNALZM:mRNA hybrids were detected only in acinar serous cells, although lysozyme was identified in ductal cells using immunohistochemical techniques. Our results suggest that the serous acinar cells are the only site of lysozyme synthesis in small salivary glands. The presence of lysozyme in ductal cells may be a result of reabsorption from the saliva or concentration from the blood or surrounding tissues.

Autoradiography↗
PubMed1990

A six-year follow-up study of sports-related dental injuries in children and adolescents.

The records were analyzed of 106 patients with sports-related dental traumas treated in 1983 at the public oral surgery unit in Helsinki, Finland; 51 were examined six years after injury. The mean age was 11.8 years (range 7-24 years). The woman/man ratio was 1:3. In 39% of cases, the injuries had arisen from ice hockey or skating; 30% happened during school hours; 80% were uncomplicated crown fractures, concussions or subluxations. During the six-year follow-up, of 80 teeth in 51 patients, root resorption was found in 6 teeth (7.5%), periapical lesions were noted in 2 teeth (2.5%), and obliteration of the pulp was seen in 4 teeth (5%). Three teeth (3.7%) had suffered loss of vitality. The pulp had been extirpated in 13 of the traumatized teeth (16%). In all, 13.7% of the patients were found to have complications six years later. The results showed that long follow-up periods are needed after dental injury.

Adolescent↗
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↗