Dental Public Health in Action: Delivering a domestic violence and abuse screening and identification training programme in North Staffordshire-based dental practices.

Domestic violence and abuse (DVA) is a significant public health problem both globally and in the UK. Dental professionals are aptly place to detect the signs of DVA and support patients to disclose DVA. However, dental professionals may lack confidence to identify and refer patients experiencing DVA; training needs in these areas were identified in Staffordshire. Glow DVA charity and the local Dental Public Health teams worked collaboratively to develop DVA training and resources specific to the needs to the dental team; these were provided to participating dental practices in the North-Staffordshire region. Feedback from the training was positive and the training was refined to better meet the needs of the dental team.mKey challenges included obtaining dental team buy in, securing funding for the continuation of the initiative and minimising the disruption to the dental team when attending training sessions or when managing a DVA disclosure. The implementation of the training highlighted the importance of DVA champions within the third sector organisations to develop and evolve the project, within dental practices to support implementation, and within the local Dental Public Health team to facilitate dental team buy-in and sustained engagement. Future plans include developing the patient-facing resources, finding ways to formally accredit dental teams for taking part in the DVA programme, and evaluating the impact of the training programme on DVA screening, identification and referral.

Antibodies to protein P in systemic lupus erythematosus.

A synthetic peptide was used to develop an enzyme linked immunosorbent assay (ELISA) to detect antibodies to the ribosomal proteins P0, P1, and P2. Significantly increased levels of IgG antibodies to protein P were found in 16% (18/116) of patients with systemic lupus erythematosus but slightly increased levels were detected in 2% (2/98) of patients with rheumatoid arthritis and one normal control subject. No association was observed between the presence of IgG antibodies to protein P and either lupus psychosis or depression. Sequential studies in individual patients failed to show an association between antibody levels and the development of psychosis.

Effect of cocaine on tritium overflow evoked from vasa deferentia previously loaded with [3H]noradrenaline by stimulation using different types of electrode.

In mouse and guinea-pig vasa deferentia previously incubated with [3H]noradrenaline, electrical stimulation applied through parallel electrodes (transmurally) increased overflow of tritium 2- to 5-fold above the resting value. Electrical stimulation applied using methods involving more substantial conduction of nerve impulses in neuronal elements in the tissues evoked a tritium overflow which was smaller (70%) than that evoked by transmural stimulation. Cinchocaine (25 microM), tetrodotoxin (0.5 microM) or the absence of calcium effectively abolished evoked overflow in both tissues whichever method of stimulation was used. In mouse vas deferens, cocaine (10 microM) did not alter overflow evoked by either transmural or axonal stimulation while 100 microM produced a reduction. In guinea-pig vas deferens, cocaine (10 microM) produced a statistically significant increase in evoked overflow of about 50% or more with both transmural and axonal stimulation. As in mouse vas deferens, 100 microM cocaine produced a reduction. It is concluded that the action of cocaine is independent of these methods of stimulation and that some difference in the arrangement of the noradrenergic nerves in the two species may account for the differential effect of cocaine observed.

Concentrations of glycosaminoglycans in synovial fluids and their relation with immunological and inflammatory mediators in rheumatoid arthritis.

The dimethylmethylene blue assay showed higher concentrations of glycosaminoglycans in many synovial fluids from patients with rheumatoid arthritis (RA) than in autologous sera or sera or synovial fluids from normal subjects. These results were taken to suggest that the glycosaminoglycans in RA synovial fluid were abnormally raised and derived from cartilage. To discover what stimulated such glycosaminoglycan release in RA joints relations were sought between synovial fluid concentrations of glycosaminoglycans and immunological and inflammatory mediators. It was shown that RA synovial fluid glycosaminoglycan concentrations correlated with synovial fluid C3d concentrations but not with synovial fluid rheumatoid factor concentrations, polymorphonuclear leucocyte numbers, myeloperoxidase concentrations, or the ability of the synovial fluids to release free radicals from normal polymorphonuclear leucocytes. A correlation was found between synovial fluid C3d and interleukin 1 concentrations as judged by both lymphocyte activating factor activity and immunoassay, but no significant correlation was detected between interleukin 1 and glycosaminoglycan concentrations. It is suggested that in the rheumatoid joint locally produced cytokines, in addition to interleukin 1, together stimulate glycosaminoglycan release from cartilage and render it vulnerable to attack by other processes.

Complement-mediated inhibition of immune precipitation in rheumatoid vasculitis.

Complement-mediated inhibition of immune precipitation (CMIP) was measured in patients with rheumatoid arthritis (RA), rheumatoid vasculitis (RA VASC), patients with skin vasculitis not associated with a systemic connective tissue disease and normal healthy controls. CMIP was impaired in 100% (14/14) of the RA vasculitic patients, 60% (12/20) of the RA patients and 22% (2/9) of the dermovasculitic patients. The degree of impairment of CMIP was significantly greater in the RA vasculitic patients compared to the non-vasculitic patients. This difference was due to the significantly lower complement levels and the presence of higher concentrations of an inhibitor of CMIP in the RA vasculitic sera. The levels of this inhibitory activity correlated significantly with IgM rheumatoid factor concentration. Serial studies in three patients with RA vasculitis treated with corticosteroids and immunosuppressive drugs showed significant clinical improvement in two patients, which was associated with improvement in CMIP, reduction in circulating immune complex levels and reduction in IgM rheumatoid factor concentrations.

Autoantibody analysis in chronic graft-versus-host disease.

Chronic graft-versus-host disease (cGVHD) bears clinical similarities to connective tissue diseases which are characterized by a spectrum of autoantibody formation. A wide range of autoantibody analyses in 19 allogeneic and 16 autologous bone marrow transplant (BMT) patients has determined that the most commonly detected antibody is IgM anti-cytoplasmic factor (ACF) occurring in 37% and 20% of allogeneic and autologous group respectively and of a type not normally seen in connective tissue disease. The antigen is as yet unidentified. These results suggest that autoantibody formation post-BMT is unrelated to the graft-versus-host process. Ophthalmic examination revealed evidence of a Sjögren-like syndrome in 20% autologous and 47% allogeneic patients, suggesting that the development of dry eyes post-BMT is not uniquely a feature of cGVHD.

Immunological involvement in the pathogenesis of pristane-induced arthritis.

Evidence is presented that the development of arthritis induced in mice by 2,6,10,14-tetramethylpentadecane (pristane) involves the immune response. Mice irradiated (500 rad) before injection of pristane failed to develop arthritis. By contrast, irradiated mice given lymphoid cells from normal donors and challenged with pristane developed arthritis. Other experiments showed that lymphoid cells from irradiated mice given pristane suppressed the development of arthritis in recipients challenged with pristane. Finally, the incidence of arthritis was significantly higher in CBA/Igb mice given pristane than in the allotypic congenic strain CBA/H, suggesting that a gene linked to the heavy chain immunoglobulin locus controls the development of arthritis.

Isolation and analysis of complement activating aggregates from synovial fluid of patients with rheumatoid arthritis using monoclonal anti-C3d antibodies.

The complement activating aggregates in synovial fluids of patients with rheumatoid arthritis (RA) have been isolated using monoclonal IgM anti-C3d antibodies attached to solid phases, and the content of the material bound has been analysed. High levels of aggregated IgG bearing C3d were found in RA synovial fluids, and IgG was the major immunoglobulin bound from such synovial fluids by anti-C3d Sepharose. A strong correlation was shown between levels of aggregated IgG bearing C3d and complement activation, as judged by C3d levels. Significant (but less strong) relationships were also observed between C3d levels and both complement consuming and C1q binding activity. C3d levels and levels of aggregated IgG bearing C3d were both significantly associated with the numbers of polymorphonuclear leucocytes (PMNs) found in RA synovial fluids. From these results it is concluded that the aggregated immunoglobulins bearing C3d (particularly IgG) isolated from RA synovial fluids are responsible for activating complement and attracting PMNs into the joint space. Radioimmunoassay showed no correlation, however, between levels of aggregated IgG (or IgM) bearing C3d and rheumatoid factor (RF) activity bound by anti-C3d. In addition, the material bound by anti-C3d Sepharose from most synovial fluid polyethylene glycol precipitates did not contain either IgM or IgG RF. Thus both techniques show that the majority of complexes bearing C3d do not contain RF. As the complement fixing aggregates apparently contain only immunoglobulin and complement components the results raise the problem of how the aggregates are formed. It is suggested that RA IgG may remain aggregated after either antigen or antibody (RF) has dissociated from the complex.