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M Malmström

Publications and source records attributed to M Malmström.

86 records · Page 5Linked to original sources
PubMed1975

Teeth loss and the inflammation of teeth-supporting tissues in rheumatoid disease.

To compare the state of dentition between rheumatoid and control patients, ortopanthomograms were taken of 126 rheumatoid and 119 control patients. This roenthenologic examination revealed a signficantly higher incidence of teeth loss among the rheumatoid patients than among the control patients. To determine whether the dental periapical lesions of patients with rheumatoid disease differ histologically from corresponding lesions in control patients, the dental periapical lesions of 43 rheumatoid and 23 control patients were examined with a routine histochemical technique. No differences were detected however between these two patient groups either as regards the histologic features of their periapical lesions or as regards the incidence of these lesions, whether granulomas or radicular cysts. Furthermore, examination of the gingival tissues from 21 rheumatoid patients did not either reveal any distinguishing histologic feature. Amyloid was sought in the teeth-supporting tissues of both rheumatoid and control groups with techniques involving light, polarization and fluorescence microscopy. In neither group was amyloid detected with certainty with any of these techniques. The higher incidence of teeth loss among rheumatoid patients invited further investigation into the relationship between dental health and rheumatoid disease.

Adolescent↗
PubMed1975

Immunoglobulin clases IgG, IgM, IgA and complement component C3 in dental periapical lesions of patients with rheumatoid disease.

To identify the immunoglobulin classes present in dental periapical lesions and to determine how, if at all, the distribution of immunoglobulin classes IgG. IgM and IgA differ in the dental periapical lesions of rheumatoid and control patients, paraffin-embedded and frozen tissues from the dental periapical lesions of 36 rheumatoid and 22 control patients were examined by the direct immunofluorescence technique. In addition, both rheumatoid and control tissues were examined for the presence of complement component C3, albumin and fibrinogen. Neither the greater frequency and abundancy with which IgG and to a lesser degree, IgA occurred in the dental periapical lesions of rheumatoid patients than in the corresponding lesions of control patients, nor the more frequent occurrence of complement component C3 in these same lesions, was statistically significant. No difference in the distribution of the various immunoglobulin classed could be discerned between the rheumatoid and control group. Albumin was distributed almost equally between the two patient groups. The greater abundance of fibrinogen among control patients was, however, statistically significant. These results do not provide evidence that an immunologic reaction takes place in the dental periapical lesions of patients with rheumatoid disease similar to that which characterizes rheumatoid inflammation. However, the presence of such a reaction cannot be excluded without more extensive investigation.

Adult↗
PubMed1975

IgG rheumatoid factor in dental periapical lesions of patients with rheumatoid disease.

To detect "hidden" IgG rheumatoid factor in tissues from dental periapical lesions, 26 rheumatoid and 14 control patients were examined by the direct immunofluorescence technique for binding of FITC-labelled IgG before and after pepsin digestion. Whereas free rheumatoid factor was detected in only 1 rheumatoid tissue before digestion with pepsin, this tissue as well as 8 other rheumatoid tissues strongly bound heat-aggregated IgG after the digestion procedure. Six of these 9 tissues also bound native IgG. In no control tissue was free rheumatoid factor detected and in only 1 was "hidden" rheumatoid factor revealed after pepsin digestion. Hence, presence of IgG rheumatoid factor correlated positively with the presence of rheumatoid disease, and evidence was established that certain features of rheumatoid inflammation occur in dental periapical lesions of many patients with rheumatoid disease.

Adult↗
PubMed1975

Occurrence of amyloid in the teeth-supporting tissues of patients with rheumatoid diseases. An immunohistochemical study.

An investigation was carried out to determine whether amyloid could be detected in the dental periapical lesions or gingival buccal fold, or in both, of patients with rheumatoid disease but in whom amyloidosis had not been diagnosed. Tissue from the dental periapical lesions of 36 rheumatoid and 23 control patients, as well as from the gingival buccal fold of 11 of the rheumatoid and 11 of the control patients, were examined by the direct immunofluorescence technique and by polarization microscopy of sections stained with Congo red. Amyloid was observed almost 5 times more often, or in 19% of the dental periapical lesions of rheumatoid patients: it was detected by immunofluorescence in 7 rheumatoid patients and 1 control patient, and by polarization microscopy in 6 of these 7 rheumatoid patients as well as in the 1 control. Rectal biopsies performed on these 8 patients were positive in only 1 of the rheumatoid patients. Amyloid was not detected in any of the gingival biopsies. Serum samples from the rheumatoid and the control patients were tested for the presence of the nonimmunoglobulin amyloid fibril-related serum component, protein ASC. Nineteen of the 36 rheumatoid patients, including the 7 whose dental periapical lesions contained amyloid, had protein ASC in their serum.

Adult↗
PubMed1975

Free rheumatoid factor in dental periapical lesions and gingivae of patients with rheumatoid disease.

To determine whether evidence of rheumatoid inflammation, in the form of free rheumatoid factor, might be found in the teeth-supporting tissues of patients with known rheumatoid disease, tissues from the dental periapical lesions of one group of 50 rheumatoid and 23 control patients, and from the marginal gingivae of a second group of 58 rheumatoid patients were examined by the direct immunofluorescence technique that employed fluroesceinisothiocyanate (FITC)-labelled aggregated human IgG. The gingival tissues contained no free rheumatoid factor. Free rheumatoid factor-producing plasma cells were, however, detected in the dental periapical lesions of 3 of the 50 rheumatoid patients, i.e. in 6%, and in 1 of the control patients i.e., in 4%. This control patient had suffered from nephritis 10 months prior to the investigation. Because free rheumatoid factor did occur, albeit infrequently, in the dental periapical lesions of rheumatoid patients, a search for IgG rheumatoid factor, known to occur in greater abundance than the IgM type although "hidden", was indicated.

Adult↗
PubMed1969

Jaw fractures.

Explore the source record for details and available documents.

Accidents↗
PubMedDate not supplied

Tumor necrosis factor-alpha and receptors for it in labial salivary glands in Sjögren's syndrome.

OBJECTIVE: Modulation of TNF-alpha by neutralizing antibodies, soluble receptors and TNFR: Fc fusion proteins are being developed for the therapeutic modulation of immune inflammation. It is becoming increasingly important to understand the state and involvement of the TNF-alpha/TNFR system in various rheumatic diseases. Tumor necrosis factor-alpha (TNF-alpha) affects its target cells through binding to two different receptors, TNFR-p55 and TNFR-p75. Mitogenic, cytostatic and cytotoxic effects of TNF-alpha on various cells have been reported. In Sjögren's syndrome (SS) focal sialadenitis leads to salivary gland destruction and loss of function. Although TNF-alpha is one possible mediator in these processes, nothing is known about the spatial distribution of TNF-alpha in relation to its receptors/target cells in salivary gland tissue. METHODS: Labial salivary glands (LSG) were obtained from 16 SS patients and 13 healthy controls and stained using the immunohistochemical peroxidase-anti-peroxidase (PAP) method for TNF-alpha, TNFR-p55 and TNFR-p75. RESULTS: TNF-alpha, TNFR-p55 and TNFR-p75 staining was absent, weak or relatively inextensive in controls compared to SS patients. Infiltrating mononuclear inflammatory cells in SS patients displayed moderate to strong TNF-alpha and TNFR expression. In addition, resident vascular endothelial cells, ductal epithelial cells and fibroblasts co-expressed TNF-alpha and TNFR. In contrast, acinar end piece cells did not express TNF-alpha or TNFR-p75 although TNFR-p55 was expressed. CONCLUSION: The interrelated localization of TNF receptors and their ligand TNF-alpha in inflammatory and in endothelial cells suggests a proinflammatory role of TNF-alpha in SS. The expression of TNF-alpha and its receptors in fibroblasts and ductal cells may contribute to ductal hyperplasia and glandular fibrosis. However, in contrast to expectations, the cellular localization of the TNF-alpha/TNRF system argues against its role in acinar cell atrophy.

Antigens, CD↗
PubMedDate not supplied

Fibroblast markers in labial salivary gland biopsies in progressive systemic sclerosis.

Labial salivary gland (LSG) biopsies from 13 patients were studied. Three were normal glands, five showed fibrosis induced by progressive systemic sclerosis (PSS) and five more had PSS-induced fibrosis combined with and focal sialadenitis compatible with Sjögren's syndrome (SS). Monoclonal antibodies to proline-4-hydroxylase (alpha PH or 5B5-A) and the carboxyterminal domain of human type I procollagen (alpha pC or M-38) were used as fibroblast markers. Immunostaining was done with avidin-biotin-peroxidase complex (ABC). Using various sample controls (including cultured fibroblasts and specimens enriched for lymphocytes, plasma cells, granulocytes, monocytes and dendritic cells) as well as analysis of various LSG resident cells, the specificity of the alpha PH and alpha pC markers for fibroblasts was established. Cross reactions were only seen with plasma cells and acinar cells containing the beta subunit of PH or disulfide isomerase involved in SS-SH interchange reactions in these secretory cells. All fibroblasts in fibroblast monolayer cultures at their logarithmic phase of growth stained with the fibroblast markers studied, but false negative staining was seen with resting, mature fibroblasts in dense connective tissue in LSG sections. Therefore, it can be concluded that proline 4-hydroxylase and the COOH-terminal domain of type-I procollagen both indicate fibroblast involvement in collagen (type l) synthesis and thus identify active but not resting fibroblasts. PH+ fibroblast-like cells and pC+ fibroblasts were both more frequent in PSS LSGs than in normal glands, suggesting active local fibroblast involvement in PSS.(ABSTRACT TRUNCATED AT 250 WORDS)

Antibodies, Monoclonal↗
PubMedDate not supplied

Oral parameters for the diagnosis of Sjögren's syndrome.

Agreement is probably world wide in the medical profession that patient history is the most relevant part of the patient examination, but at the same time the most demanding part because there is no substitute to lack of knowledge and experience. These form the basis for an often subconscious process of selecting the most important pieces of information to help in decision making. We describe a stepwise forward discriminant analysis with a jackknife-validation in analysis of questionnaires as to diagnosis of Sjögren's syndrome. The second topic of current interest, also due to the need of generally acceptable criteria for diagnosis and classification, is the place of labial salivary gland (LSG) biopsy in such sets of criteria. In the histopathological part of our work we describe findings of a postmortem LSG study from the coroner's office.

Diagnosis, Differential↗