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Biomedical subjects

P Holmstrup

Publications and source records attributed to P Holmstrup.

At least 37 records · Page 2Linked to original sources
PubMed1995

Bacterial-stimulated cytokine production of peripheral mononuclear cells from patients of various periodontitis categories.

Periodontitis is a general term for disease categories, including juvenile periodontitis (JP), rapidly progressive periodontitis (RPP), and adult periodontitis (AP), which may or may not share a common etiology and pathogenesis. These disease categories are characterized by differences in progression of tissue destruction and differences in age group susceptibility, but not, to our knowledge, by differences in cytokine responses of inflammatory cells. The present study examined blood cell counts and interindividual variation in the ability of PBMC of patients in three different categories of periodontitis to produce cytokines after stimulation with different oral bacterial species in vitro. The AP group had a significantly lower production of IL-1ra when stimulated with Porphyromonas gingivalis (P.g.) and Actinobacillus actinomycetemcomitans (A.a.) (P < 0.05). Streptococcus sanguis (S.s.), which is associated with normal periodontal conditions, induced extremely high levels of IL-1 alpha and TNF alpha production in all groups. The RPP group had a significantly higher number of monocytes (MC) than the AP group (P < 0.05). Additionally, JP patients had a significantly higher concentration of polymorphonuclear granulocytes compared to juvenile controls (P < 0.05). In conclusion, IL-1 alpha, TNF alpha, or IL-6 production by peripheral blood MC after in vitro stimulation with oral bacterial type stains may not distinguish different categories of periodontitis. The results support the hypothesis that the cytokine IL-1ra is produced in different concentrations in the two groups: RPP and AP. Furthermore, elevated MC concentration in the RPP group compared to the AP group may be an important pathogenic feature in RPP.

Adolescent↗
PubMed1994

Periodontal diseases in HIV-infected patients.

Periodontal diseases may be the first clinical sign of human immunodeficiency virus (HIV)-infection. Since the immunosuppression and subsequent susceptibility may alter the responses of the oral tissues as well as the microflora, both periodontal treatment and result of therapy may be modified. The periodontal diseases in HIV-seropositive patients include common as well as less conventional forms of gingivitis and periodontitis, and bacterial, mycotic and viral infections are seen. Neoplasias may also involve the periodontium; most common are Kaposi's sarcoma and non-Hodgkin's lymphoma. Recent studies of unselected groups of patients indicate that periodontal health in at least some groups of HIV-seropositive patients is better than previously reported.

Gingival Neoplasms↗
PubMed1994

Identification of Candida albicans types related to healthy and pathological oral mucosa.

This study comprised 100 healthy dentate adults and 53 patients with either chronic erythematous oral candidosis or oral leukoplakic lesions. The presence of yeasts was determined by microscopical examination of PAS-stained smears and by culture. Biopsy material was obtained from all lesions. The isolated yeasts were identified to species level. Strain phenotypes of 147 Candida albicans isolates were determined on the basis of the ODDS & ABBOTT procedure (25, 26). Yeasts were found in the mouth of healthy dentate individuals both by culture and by smears. The identification of hyphae in healthy mucosa indicates that the presence of these structures is not an unequivocal sign of candidal infection. The results support the view that tobacco smoking may be a predisposing factor for candidal infection. Also, the results have shown an association between the occurrence of yeasts and the type of leukoplakic lesions. Finally, the strain differentiation has indicated an oral mycoflora in patients with candidal lesions disappearing after antimycotic treatment which was more homogeneous in composition than in patients with irreversible lesions; furthermore, certain strains may possess properties which may be important in the development of pathological conditions and premalignant changes.

Adult↗
PubMed1994

Keratin staining pattern in clinically normal and diseased oral mucosa of lichen planus patients.

The keratin pattern in oral epithelia is related to the type of terminal differentiation observed morphologically (keratinization/nonkeratinization) and to the presence or absence of epithelial dysplasia. Furthermore, it has been suggested recently that inflammatory phenomena influence the keratin expression in human gingiva. The aim of the present study was to describe the keratin pattern in oral lichen planus (OLP) lesions, which are well known to be characterized by hyperkeratinization and severe inflammatory changes, in order to elucidate the role of inflammation in keratin expression of oral epithelia. Tissue sections were stained with antikeratin antibodies directed to groups of keratins (AE1 and AE2) and to single keratin proteins (Nos. 5, 8, 13, and 19). The keratin pattern in OLP lesions differed in some respects from that of leukoplakias and frictional keratoses as characterized in previous studies. No consistent patterns for use in a diagnostic context were found. However, the changes in OLP lesions did not mimic those previously described in inflamed gingival specimens and in oral epithelial dysplasias. Thus, the results encourage further studies on the potential diagnostic use of keratin expression in premalignant oral lesions. Furthermore, the study suggests that the inflammatory reaction seen in OLP lesions does not influence keratin expression in a way comparable with the suggested influence of inflammation in gingival specimens.

Antibodies, Monoclonal↗
PubMed1994

A comparison of the effect of epidermal growth factor, platelet-derived growth factor, and fibroblast growth factor on rat periodontal ligament fibroblast-like cells' DNA synthesis and morphology.

An enhanced formation of bone, dentin, and collagen fibers in periodontal wounds after application of polypeptide growth factors has recently been reported. However, the complex environment in vivo makes it impossible to determine the specific effects of growth factors on various cells involved in the wound-healing process. We have therefore investigated the mitogenic and morphogenic effects of recombinant epidermal growth factor (rEGF), natural platelet-derived growth factor (nPDGF), and natural fibroblast growth factor (nFGF) on periodontal ligament fibroblast-like cells. A cell line was established from rat PDL tissue. The cell line was characterized according to morphology, growth pattern, cytoskeletal proteins, and growth kinetics. The mitogenic effect of growth factors was assessed by incorporation of [3H]thymidine in the cellular DNA for 4 hours. Differences between groups of observations were assessed by the Student t-test. The morphogenic effects of growth factors were described with respect to growth pattern, cell orientation, and cell and nucleus form after a random photographic recording. The fibroblast-like cell type and the non-transformed phenotype of the cell line have been identified by the presence of parameters considered to be characteristic of a normal fibroblast-like cell line. The morphogenic analysis of both experimental and control cultures showed a monolayer of adherent cells with spindle or stellate morphology, a random alignment and round or elongated nuclei. Incorporation of [3H]-thymidine was increased in a dose-dependent manner by all growth factors. Maximal effect on the DNA synthesis was: rEGF, 131%; nPDGF, 274%; and nFGF, 182%.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Ligature-induced marginal inflammation around osseointegrated implants and ankylosed teeth.

The purpose of the investigation was to gain more understanding of marginal inflammatory reactions around osseointegrated implants. The significance of the lacking periodontal ligament of implants was examined in the initial breakdown phase of supporting tissues by comparing clinical and radiographic manifestations of ligature-induced marginal inflammation related to osseointegrated implants with those around ankylosed and normal control teeth in 8 cynomolgus monkeys (Macaca fascicularis). Bilateral extraction of the first and second mandibular molars was carried out initially, and 12 weeks later 2 implants were placed in each side. Ankylosis of the second maxillary molars was established by extracting and replanting the teeth after a drying period. When ankylosis and osseointegration were established, ligature-induced marginal inflammation was induced in the right or left side at random around implants, ankylosed teeth and normal control teeth (second maxillary premolar) for 7 weeks. Although the clinical manifestations as expressed by plaque score, gingival score, probing depth and attachment loss were quite similar, the radiographic features differed. Significant loss of bone height was limited to implants and ankylosed teeth and did not occur in relation to normal control teeth. Furthermore, the bone loss around implants was significantly greater than the loss around ankylosed teeth. Bone loss was limited to implants and ankylosed teeth; the study therefore suggests that the presence of marginal inflammation around implants and ankylosed teeth may have more serious implications than does marginal inflammation around teeth with a periodontal ligament. However, variations in microbiota and susceptibility of different jaw positions to periodontal breakdown may influence the results of this study.

Alveolar Bone Loss↗
PubMed1993

Scanning electron microscopic observations of early plaque formation in vivo on enamel specimens treated with delmopinol.

The aim of this double blind, cross-over, scanning electron microscopic (SEM) study was to compare the effect of topical application of 0.5% delmopinol HCl (aqueous solution) with placebo on early supragingival plaque formation on enamel specimens attached to a maxillary premolar. 3 subjects underwent 2x (placebo and delmopinol treatment, respectively) 7 treatment periods (1/2, 1, 2, 8, 24 hours; 3, 7 days) of undisturbed dental plaque accumulation, during which 2 ml of placebo and delmopinol HCl 0.5%, respectively, were applied topically to all teeth 2x daily. At the end of each period, the specimen was retrieved and processed for SEM. For the specimens obtained after 24 h or less, the number of visible micro-organisms was estimated. For the 3- and 7-day specimens, the area covered by plaque was calculated planimetrically. Large inter-individual differences were observed in the number of bacteria attaching during the first 24 h, with apparently no major differences between delmopinol and placebo. 1 subject showed a bacterial colonization predominated by curved rods throughout the first 8 h. Compared to placebo, the area of the specimens covered by plaque was reduced after 3 and 7 days of delmopinol use, with coccoid cells as the predominant morphotype. Plaque maturity, characterized by the appearance of corncob formations and high numbers of different morphotypes, was not observed on the delmopinol specimens, in contrast to the placebo specimens. The study shows that topical application of 0.5% delmopinol HCl delays and interferes with dental plaque maturation.

Adult↗
PubMed1993

Epithelial alpha-naphthyl acetate esterases in the green vervet monkey gingiva before and after periodontal surgery and during tooth eruption.

To provide enzymatic information on de novo formed junctional (JE) and sulcular epithelium (SE), we performed periodontal surgery on 24 teeth. Ten to 14 days postoperatively, all experimental and 16 control teeth were extracted with adjacent buccal gingiva. In addition, specimens from unerupted and partly erupted teeth containing enamel epithelium (EE) were examined. Fixed cryostat sections were cut in series, stained with HE, or incubated with and without substrate for demonstration of alpha-naphthyl acetate esterase activity and for control purposes, respectively. The distribution and intensity of the alpha-naphthyl acetate esterase activity of newly reformed JE and SE was identical to that of the original JE and SE, i.e. suprabasal and very strong. In contrast, both the oral gingival epithelium (OGE) and the EE displayed a very weak enzyme reaction. These observations indicate that the presence of alpha-naphthyl acetate activity of original and reformed JE and SE is probably site specific and of nondevelopmental origin. Heavy inflammation after healing was associated with enhanced epithelial proliferation of OGE and, in addition, marked esterase activity of these proliferations and corresponding OGE. This points at a possible inflammatory induction of the marked esterase activity seen in JE and SE as well as site-specific, connective tissue influences. Further investigation is needed to elucidate the effect of inflammation on the esterase activity.

Animals↗
PubMed1993

Miconazole chewing gum for treatment of chronic oral candidosis.

A chewing gum containing the antifungal drug miconazole may be convenient for topical treatment of oral candidosis. Therefore a trial was performed to examine the effect and tolerance of miconazole chewing gum in comparison with miconazole gel in the treatment of oral candidosis. The study group consisted of 32 patients with oral candidosis harboring yeasts, predominantly Candida spp. Half of the patients chewed one piece of chewing gum (dose: 3.6 mg of miconazole) four times daily; the other half dispersed a 2% gel (dose: 50 mg of miconazole) in the oral cavity four times daily. After 6 wk of treatment, there was no clinical evidence of yeast infection in either of the two groups. No significant differences between the two groups were found in clinical, mycologic, and cytologic investigations conducted after 3 and 6 wk of treatment or at the follow-up examination 4 wk after termination of the treatment. The results indicate that miconazole released from chewing gum is as effective as miconazole gel. The chewing gum reduced the dosage of miconazole for treatment of oral candidosis, and the patients approved the chewing gum as a pleasant medicament.

AIDS-Related Opportunistic Infections↗
PubMed1993

Marginal periodontitis and cytokines: a review of the literature.

Recent research on the immunopathogenesis of marginal periodontitis has focused on cytokines, because these mediators govern biological activities in inflammatory tissue destruction. Several studies have been carried out to elucidate the involvement of cytokines in periodontitis, including cytokine measurements in samples from gingival tissue, gingival crevicular fluid, and in supernatants of stimulated in vitro grown cells from gingival tissue and peripheral blood. The results, summarized in this review, suggest that cytokines are involved in the progress of periodontitis. Furthermore, cytokines may be valuable as markers of tissue breakdown. At the present stage, however, there are difficulties in detecting and quantifying cytokines by immunochemical methods and, in particular, by bioassays. Increased knowledge of the cytokine network may open new pathways of periodontitis treatment by controlling processes involved in tissue breakdown.

Cytokines↗
PubMed1993

Non-human primates used in studies of periodontal disease pathogenesis: a review of the literature.

The inability to examine initiation and progression of periodontal disease and to assess certain therapies in humans has led to a great interest in the use of animal models in periodontal research. Some of the most prominent animals used are non-human primates. This article reviews the characteristics of non-human primate models in periodontal health, in the transition from health to gingivitis to periodontitis, and in experimental gingivitis and periodontitis. Where possible, the results of these studies are compared with results from human studies. Only a few studies have compared in detail the anatomy, physiology, immunology, and tissue interactions in monkeys with those of humans. With the exceptions of differences and variations in size of the dentition, the number of each tooth type as well as larger canines, presence of diastemata between anterior teeth, and an edge-to-edge relationship of the incisors, the dental and periodontal anatomy of non-human primates seem quite similar to that of humans. Clinically healthy gingiva can be established and maintained in non-human primates, and gingivitis as well as periodontitis occur in these animals. It is possible to induce experimental periodontitis by placement of peri-dental silk ligatures or orthodontic elastics as well as by surgical removal of alveolar bone. Although the most appropriate model for studies of periodontal disease pathogenesis in non-human primates appears to involve the application of silk ligatures, some difficulties may occur in establishing periodontal break-down by using this model. Many clinical, histological, microbiological, and immunological characteristics of spontaneous and experimental marginal inflammation in most non-human primates are similar to those in humans. The most significant differences between small non-human primates and humans are the very limited number of lymphocytes and plasma cells in the inflammatory infiltrate of squirrel monkeys (Saimiri sciureus) and marmosets. Therefore, the use of squirrel monkeys and marmosets may not be appropriate in many studies of periodontal disease pathogenesis. The most significant microbial differences between macaque species and humans are a lower proportion of Actinomyces species, the presence of a catalase-producing Prevotella melaninogenica strain, and the high carrier rate for Actinobacillus actinomycetemcomitans in subgingival plaque of macaque species. The significance of these differences is presently unknown. It is concluded that the use of many non-human primate species due to the apparent close anatomic and biologic similarities to humans is appropriate in experimental studies of periodontal disease, provided the use of laboratory animals is requisite and lower species are not applicable.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1993

Ligature-induced marginal inflammation around osseointegrated implants and ankylosed teeth: stereologic and histologic observations in cynomolgus monkeys (Macaca fascicularis).

The aim of the investigation was to provide quantitative and qualitative histologic data on marginal inflammation around osseointegrated implants. The significance of the lack of a periodontal ligament in the initial breakdown phase of supporting tissues in implants was examined by comparing stereologic and histologic manifestations of ligature-induced marginal inflammation around osseointegrated implants with those around ankylosed and normal control teeth in 8 cynomolgus monkeys (Macaca fascicularis). Clinical and radiographic findings have been reported elsewhere. The marginal connective tissue around ligated implants was infiltrated by a significantly increased total number of lymphocytes, plasma cells, and neutrophils compared to non-ligated implants and teeth. The total number of lymphocytes around ligated implants was significantly higher than around ligated ankylosed and normal control teeth. There were, however, no significant differences in the total number of plasma cells and neutrophils within the ligated group. Osteoclasts were exclusively observed around ligated implants and ankylosed teeth. Although variations in microbiota and susceptibility of different jaw positions to periodontal break-down may influence the results of the present study, the results seem to substantiate the theory that marginal inflammation around implants and ankylosed teeth may have more serious implications than does marginal inflammation around teeth with a periodontal ligament. Since presence of osteoclasts was not related to the absence of cervical cementum with inserting gingival fibers around ligated ankylosed teeth, the increased susceptibility of bone loss of implants is probably not caused by the absence of these tissue components. In contrast, the histologic observations seem to support that the increased susceptibility for bone loss around implants may be related to the absence of a periodontal ligament.

Alveolar Process↗
PubMed1992

Plaque-induced marginal tissue reactions of osseointegrated oral implants: a review of the literature.

An intimate contact between bone and titanium implants was first demonstrated in 1969, and since then the bone-implant interface of osseointegrated implants has been investigated extensively. However, investigations of the marginal tissues and the microflora associated with osseointegrated implants have almost exclusively been carried out over the last decade. This review covers the clinical, radiographic, histologic, and microbiologic studies of marginal tissues of osseointegrated oral implants. In general, successfully osseointegrated implants exhibit low amounts of plaque concomitant with the absence of marginal inflammation. However, plaque accumulation may cause inflammatory reactions around the implants, sometimes giving rise to mucosal hyperplasia. Apparently, keratinized mucosa is not a requisite for the maintenance of peri-implant health if oral hygiene is adequate, but the presence of peri-implant keratinized mucosa is generally advocated. Alveolar bone loss around successful implants is minimal, but significant focal loss may occur due to plaque-induced inflammation or perhaps repeatedly extensive implant load. The progression of plaque-induced alveolar bone loss of osseointegrated implants may be different from that of teeth. It is unknown whether simultaneous marginal inflammation and excessive implant load further increase the loss of alveolar bone height. Both the light microscopic and ultrastructural characteristics of marginal tissues of implants and teeth are similar except for a lack of root cementum with inserting gingival collagen fibers of implants. Clinical inflammatory reactions are histologically characterized by an increased number of inflammatory cells infiltrating the connective tissue. The scattered subgingival microbiota associated with osseointegrated implants surrounded by healthy or slightly inflamed marginal tissues is similar to that of teeth with healthy gingiva. The microbiota associated with implants affected by marginal inflammation and bone loss is complex and consists predominantly of gram-negative anaerobic rods; this, again, is a similarity to periodontal disease.

Alveolar Bone Loss↗
PubMed1992

Oral mucosa and skin reactions related to amalgam.

Documented cases of oral mucosa and skin affections related to amalgam restorations are rare, although the exact incidence is unknown. Lesions of the oral mucosa may be due to specific immunologic or non-specific toxic reactions toward products generated from restorations. The immunologic reaction most probably involved in mucosal affections related to amalgam is the delayed or cell-mediated (type IV) reaction. Such reactions are seen in contact allergy, and the term "contact lesions of the oral mucosa" has been used. There is a much lower tendency of sensitization through mucous membranes than through skin, and it is questionable whether mercury released from amalgam restorations is able to sensitize a patient. A chronic toxic reaction may be established due to repeated or constant influence to toxic agents in low concentrations over long periods. Such reactions are most frequently localized to the contact zone with the toxic agent. Chronic toxic reactions may possibly be seen in areas of the oral mucosa in direct contact with amalgam fillings. Since the clinical features of these lesions do not differ from those of lesions due to contact hypersensitivity, the diagnosis is obtained by exclusion based on a negative patch test.

Dental Amalgam↗
PubMed1992

The effect of insulin-like growth factor-I and human growth hormone on periodontal ligament fibroblast morphology, growth pattern, DNA synthesis, and receptor binding.

Repopulation of the detached root surface by cells from the periodontal ligament (PDL) is a prerequisite for new attachment formation. Stimulation of PDL-cell growth may therefore serve as an essential method to enhance formation of new attachment. Studies have demonstrated that insulin-like growth factor-I (IGF-I) has a mitogenic effect on fibroblasts originating from various connective tissues and cell-lines. Further, human growth hormone (hGH) is known to regulate the plasma concentration of IGF-I and to mediate cellular biological effects. In the present study we examined the effect of IGF-I and hGH on morphology, growth pattern, and DNA synthesis. The expression of IGF-I and hGH receptors on the surface of cultured PDL fibroblasts is also described. A primary fibroblastic cell line was established from rat PDL tissue, and blind, photographic recordings of morphology and growth pattern, as well as incorporation of [3H]thymidine in cellular DNA, was carried out in the presence and absence of IGF-I and hGH. The presence of specific membrane receptors was investigated by binding of [125I]IGF-I and [125I]hGH. The analysis of photographs showed that IGF-I and hGH had no effect on morphology and growth pattern. Incorporation of 3H-thymidine, however, was increased in a dose-dependent manner by IGF-I, whereas hGH alone or in combination with IGF-I produced no dose-dependent response. Maximum effect (% of control) on DNA synthesis was 176% for IGF-I and 91% for hGH.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Reactions of the oral mucosa related to silver amalgam: a review.

Lesions of the oral mucosa caused by amalgam restorations are rare. They may be due to Type IV contact hypersensitivity or toxic reactions to products generated by the restorations. Hypersensitivity reactions to amalgam seem to be related to mercury in almost all cases. The basis for requiring allergologic examination of patients suspected of contact hypersensitivity to amalgam is the presence of whitish or reddish, sometimes ulcerative oral mucosal lesions with a clear anatomic relation to amalgam fillings. The clinical features of lesions due to toxic reactions from amalgam restorations do not differ from those of lesions due to contact hypersensitivity, and the diagnosis is obtained by exclusion based on a negative patch test. Amalgam accidentally implanted in the oral mucosa results in amalgam tattoos which are flat lesions of bluish, blackish or slate grey color. Implanted amalgam does not produce an acute tissue response and need not be removed except for diagnostic reasons.

Dental Amalgam↗
PubMed1991

Immunohistochemical distribution of keratin proteins in human gingival heterotransplants in nude mice.

Clinically healthy human gingivae from deciduous molar regions were transplanted to subcutaneous sites of nude mice (nu/nu NC). Transplants were harvested after posttransplantation periods of 5, 6, 7, 8.5, 10.5 and 12 weeks and examined histologically after staining with hematoxylin-eosin (H.E.), bisbenzimide, and a panel of mouse monoclonal anti-keratin antibodies in an indirect fluorescence technique. Central parts of transplants contained human connective tissue covered by human stratified squamous epithelium which were unkeratinized in 5- to 7-wk-old transplants and most frequently (75%) parakeratinized in 8.5-wk to 12-wk transplants. Comparison of keratin expression before and after transplantation revealed a progressive keratin reconstitution, i.e., keratin markers of basal/suprabasal cells preceded those of suprabasal/spinous cell layers and immunohistochemical markers of keratinization preceded routine histologically observed parakeratinization. Original keratin staining and essential features of histodifferentiation were reconstituted and maintained after 8.5 wk but graft recovery rate decreased drastically 12 wk after transplantation. This study shows that the human gingiva/nude mouse model is useful in experimental studies of the gingival keratin profile in the period 8.5 to 10.5 wk after transplantation.

Adolescent↗