PubMed HealthSearch

Biomedical subjects

R N Powell

Publications and source records attributed to R N Powell.

At least 19 recordsLinked to original sources

Patient attendance compliance in periodontal therapy.

Attendance compliance of patients presenting for periodontal therapy during one calendar year at two practice locations (Perth, Western Australia and Darwin, Northern Territory) was observed over a period of three to four years, depending on whether the patients were seen in the earlier or latter part of the initial year. Both venues (full-time practice and visiting practice every quarter) gave very similar results, of around 10 per cent of patients who dropped out after initial consultation, without commencing treatment. As well, both venues showed a similar trend of subsequent patient 'attrition' after the initial phase of treatment, with the retention of approximately 40 per cent of the original group of patients after three to four years. Of these, a very high proportion (90 per cent) were totally compliant with maintenance recall appointments.

Appointments and Schedules

A 3-year community-based periodontal disease prevention programme for adults in a developing nation.

A field trail of a community programme for improving periodontal health of adults was carried out in a geographically remote, unsophisticated rural population in the South Pacific islands of Tonga. The 3-year project (1986-89) involved three village communities, each with a population of approximately 1200. Village N received supplies of toothbrushes and toothpaste without charge, health education (videos, talks, posters) and periodic dental scaling (ultrasonic). Village K received the same as N except that dental scaling was not provided. Village E received none of the services provided to the villages N and K. Baseline and final examinations of 20-44-year olds showed that unsupervised self-care promoted at the community level, when supplemented with periodic removal of subgingival calculus, significantly improved periodontal health. Improvement was age dependent.

Adult

Modulation of Langerhans cell surface antigen expression by recombinant cytokines.

This study examined the influence of cytokines on surface antigen expression by gingival Langerhans cells (LC) in organ culture, interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-alpha) upregulated the expression of CD1a, HLA-DR and HLA-DP antigens on LC. TNF-alpha, interleukin-4 (IL-4), and transforming growth factor beta (TGF-beta) suppressed CD29 expression, while other cytokines, including interleukin-3 and granulocyte-macrophage colony stimulating factor, were without effect. No cytokines induced CD3, CD4, CD23, CD25 or CD45 RA antigen expression in organ culture. Since TNF-alpha and IL-6 can be secreted by keratinocytes, these molecules, together with interleukin-1, are likely to play a role in the local control of LC number and function within the epithelial milleu. Thus, alterations in cytokine secretion by keratinocytes may at least in part be responsible for variations in LC number and antigen expression which occur in oral mucosal disorders.

Antigens, CD

Human gingival Langerhans cells stimulate allogeneic lymphocytes: requirement for MHC class II antigens.

Langerhans cells (LC) are antigen-presenting cells which express high levels of Class II MHC antigens on their plasma membranes. While the expression of these antigens on gingival LC has been documented, their functional significance is unclear. In this study, the mixed epithelial cell-lymphocyte culture reaction (MECLR) between stimulator cells (LC) and allogenic lymphocytes was used as an in vitro model for investigating the role of the MHC Class II antigens HLA-DR, -DQ, and -DP in alloantigen presentation by gingival LC. In epithelial cell suspensions prepared from human gingiva, MHC Class II antigen expression (HLA-DR, -DP, -DQ) was confined to CD1a-positive LC. Depletion of Class II antigen-bearing LC from epithelial cells using monoclonal antibodies (L243, B7/21, and SK10) and complement inhibited the ability of epithelial cells to stimulate proliferation in the MECLR. Pre-treatment of epithelial cell suspensions with the same monoclonal antibodies suppressed proliferation in the MECLR, as did direct addition of these antibodies to co-cultures of epithelial cells and lymphocytes. These results indicate that HLA-DQ and -DP, together with DR antigens on gingival LC, are involved in LC-lymphocyte interactions. Since LC are potent antigen presenting cells, alterations in the expression of MHC Class II antigens on the surface of these cells will influence their ability to stimulate lymphocytes during the initiation of the cellular immune response to the accumulation of dental plaque.

Antibodies, Monoclonal

Disturbances of tooth form and eruption in the microphthalmic (mi) mouse: a light and electron microscopic study.

Changes in the surrounding alveolar bone occur during tooth eruption. The microphthalmic (mi/mi) mouse suffers from osteopetrosis and lack of bone resorption; tooth form and eruption were examined in both affected mi/mi mice and unaffected litter-mates to determine the effect of osteopetrosis on tooth development and eruption. Paraffin sections of mandibles from 3, 7, 10, 13, 15 and 20-day-old mice were examined by light microscopy after staining with haematoxylin and eosin and for stable acid phosphatase activity. Mandibles from 15- and 20-day-old mice were examined by scanning electron microscopy. The ultrastructure of odontoblasts was observed in 15-day-old mice. Tooth eruption was significantly reduced in the mi/mi mice; the bone of affected mice increased in area with increasing age and marrow spaces narrowed. There was little bony remodeling in the mi/mi mouse, as indicated by layers of reversal lines. This lack of bone resorption affected tooth eruption and root formation. No abnormalities were detected in odontoblasts, suggesting functional normality, but the wide predentine layer in the mi/mi mouse may indicate an alteration in dentine mineralization.

Animals

Ultrastructure of the tibial epiphyseal growth plate in microphthalmic (mi/mi) mice.

Osteoclasts from growth plates of affected (mi/mi) and control (mi/+) microphthalmic mice, from newborn to 15 days old, were examined. Osteoclasts from unaffected mice were generally large, multinucleated cells with distinct ruffled borders and clear zones. Osteoclasts from the mi/mi litter mates were predominantly mononucleated, lacking in ruffled borders, clear zones and an abundance of organelles, features not normally associated with a functioning resorptive cell. The lamina limitans was more distinct in mi/mi mice. By 15 days, no evidence of bone resorption was seen in mi/mi mice. The immature appearance of osteoclasts and the lack of bone marrow cavity formation in mi/mi mice may result from either a fusion defect or from a limited life span of osteoclasts.

Animals

The regulation of Langerhans cell T6, DR and DQ antigen expression: an hypothesis.

A hypothetical model of the maturation pathway of Langerhans cells (LC) within an epithelial environment is presented. This model is based on in vitro studies using human gingival organ culture. In this model, T6 (CD1) antigen is induced on a T6(-) intraepithelial population by Interleukin-1 secreted by epithelial cells. This process is abrogated by a locally produced Interleukin-1 inhibitor, ILS. These T6(+) LC then express first HLA-DR and subsequently HLA-DQ surface antigens under the influence of either lipopolysaccharide or gamma interferon. The induction of these Class II antigens on LC is inhibited by prostaglandin E2. It is postulated that these Class II antigen positive LC are then available to function as antigen presenting cells. This hypothesis is consistent with in vitro studies and several in vivo observations. The basis of the hypothesis is the demonstration that locally produced factors may exert an influence on LC behaviour within an epithelial environment.

Adjuvants, Immunologic

Human gingival Langerhans cells as accessory cells in mitogen induced T cell responses.

Peripheral blood and gingival tissue was collected from patients undergoing surgery for the treatment of periodontal disease. Both unfractionated peripheral blood mononuclear cells and a T cell-enriched, monocyte-depleted lymphocyte population were isolated from the blood samples while a gingival epithelial cell suspension was prepared from the oral aspect of the gingival tissue. The blood cells (1 X 10(5)) were then co-cultured with the gingival epithelial cells (1 X 10(5) and 1 X 10(4)) in 200 microliters aliquots in microtitre trays for three days to see if the epithelial cells could act as accessory cells in the lymphocyte response to the mitogen, phytohaemagglutinin (PHA). Lymphocyte proliferation was assessed by measuring the uptake of [6-3H] thymidine during the last 18 hours of culture. Removal of monocytes from peripheral blood mononuclear cells led to a significant, but not total, reduction in the proliferative response to PHA. When gingival epithelial cells were added to the T cells they restored their response to PHA in a dose dependent fashion. As Langerhans cells were the only potentially immunocompetent cells seen in the epithelial cell suspensions, it is concluded that these cells are acting as accessory cells in the T cell response to PHA.

Adult

Immunohistological analysis of experimental gingivitis in humans.

Immunohistological analysis of experimental gingivitis in humans was carried out to provide a baseline for the study of immunoregulatory mechanisms in chronic inflammatory periodontal disease. Using a panel of monoclonal antibodies in an avidin biotin immunoperoxidase technique, T cell subsets were identified and the pattern of Class II major histocompatibility complex (MHC) antigens determined. Twenty third-year dental students took part in the study. Following the cessation of oral hygiene procedures, gingival biopsies were taken from each of five students at days 0, 4, 8 and 21 during the development of the inflammatory lesion. Each student had one biopsy which healed uneventfully. The T4:T8 ratio showed only slight variation over the time course of the lesion varying from 2.18:1 at day 0 to 2.48:1 at day 4. At all stages the T cells displayed both HLA-DR and HLA-DQ antigens, but less than 10% had detectable IL-2 receptors. The predominant macrophage population was acid phosphatase + ve, adenosine triphosphatase -ve, HLA-DR+ and HLA-DQ+ antigens suggesting an activated phagocytic population. During the development of the lesion, the number of intraepithelial Langerhans cells (T6+) increased but there appeared to be a discrepancy between HLA-DR and HLA-DQ expression on these cells. Similarly, the keratinocytes expressed HLA-DR but failed to express HLA-DQ at any stage. These results suggest that the developing gingival lesion is a well controlled lesion and follows a similar pattern to a controlled delayed type hypersensitivity (DTH) response.

Adult

Differential expression of Class II (DR & DQ) antigens by human gingival Langerhans' cells and keratinocytes in vitro.

The expression of the Class II products DR and DQ on human gingival epithelium was examined using immunofluorescence and immunoperoxidase staining. Differential expression of Class II antigens was seen in chronic gingivitis in adults, with T6(+) DR(+) cells being more numerous than T6(+) DQ(+) cells. The periodontopathic organism Fusobacterium nucleatum (FN) induced DQ expression on Langerhans' cells (LC) during in vitro explant culture of gingival tissue. This effect was mimicked by endotoxin (LPS) from F. nucleatum and by E. coli LPS. These results indicate that differential expression of Class II products, a feature of chronic gingival inflammation, may result from the action of LPS on gingival LC.

Culture Techniques

In vitro modulation of T6 expression on gingival Langerhans cells by interleukin-1 inhibitors and ETAF.

T6 antigen is a highly specific marker for human Langerhans cells (LC). Previous studies have demonstrated that Interleukin-1 (IL-1) and an IL-1 inhibitor (ILS) modulate LC T6 expression (T6E) in explant culture. The present study examined the in vitro modulation of T6E by two molecules: epidermal-cell-derived thymocyte-activating factor (ETAF), and a bone-derived protein (BP) implicated in the control of bone homeostasis. The effect of purified ILS was also examined. ETAF mimicked the stimulatory effect of IL-1 on LC T6E, while BP depressed T6E in a manner resembling that seen with ILS. No agents altered Class II (DR and DQ) expression by LC. BP was a specific IL-1 inhibitor, and did not inhibit thymocyte proliferation in the standard IL-1 bioassay in the absence of IL-1. These results demonstrate that molecules resembling IL-1 or ILS can modulate T6E, and implicate locally produced ETAF and ILS in the regulation of T6E in the oral mucosa in vivo.

Antigens, Differentiation, T-Lymphocyte

Phenotypic and functional analysis of T cells extracted from chronically inflamed human periodontal tissues.

T-cell subsets extracted from chronically inflamed periodontal tissues were identified using monoclonal antibodies, and their functional activity was analysed using the autologous mixed lymphocyte reaction (AMLR). Tissue was obtained from a total of 33 adult periodontitis (AP) patients and 6 normal/marginal gingivitis (N/MG) patients. All AP patients had received repeated oral hygiene instruction and root planing prior to the surgery, and the majority (30 out of 33) had at least one site with greater than 6 mm loss of attachment from the cementoenamel junction within the surgical field. The N/MG patients had no loss of attachment, and probing depths were less than 3 mm. Single cell suspensions were obtained following collagenase digestion (90 minutes at 37 degrees C) and mechanical disruption of the tissue. T-cell subsets were identified using an indirect immunofluorescence assay on cells obtained from 19 AP patients and the 6 N/MG patients. The mean (+/- standard error) helper:suppressor (T4:T8) ratio for the AP patients was found to be 0.94 +/- 0.48 compared with 1.65 +/- 0.16 for the N/MG group and 1.51 +/- 0.12 for peripheral blood controls. HLA-DR positive macrophages were identified and were found to include both acid phosphatase (AcP) positive and adenosine triphosphatase (ATPase) positive populations. Functional analysis was carried out using cells extracted from the remaining 14 AP patients. Cells from six of these 14 patients were found to be capable of spontaneous proliferation. Co-culture experiments using autologous T and non-T populations revealed that cells from only four patients were able to respond in an AMLR while those from only one of the 14 patients were able to stimulate the AMLR.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult