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Notes: Inequalities in health care provision: the relationship between contemporary policy and contemporary practice in maternity services in England Aim. The project Addressing Inequalities in Health: new directions in midwifery education and practice (Hart et al. 2001) was commissioned by the English National Board for Nursing, Midwifery and Health Visiting (ENB). Here, we draw on those research findings to consider current midwifery policy and practice in England. Background. Little guidance on providing equality of care exists for midwives. The Code of Conduct [United Kingdom Central Council for Nursing, Midwifery and Health Visiting (UKCC) 1992] makes no specific requirement for midwives to address issues of inequalities of health in their practice. Recent policy documents emphasize the need to work towards reducing inequalities and to target practice to `disadvantaged clients' without giving guidelines on how to identify and care for target groups. Methods. In-depth studies of midwifery education and service provision were conducted in three very different parts of England. Three months of fieldwork were undertaken at each site, comprising a series of interviews with midwifery educators, managers, students, midwives and service users. Focus groups were also held and observation of classroom sessions and midwifery practice undertaken. Findings. A lack of clear and specific strategies concerning inequalities in health was evident at managerial level. Patchy knowledge of current policy was also evident amongst practising midwives. Specific projects with disadvantaged clients usually resulted from a particular midwife's personal interest or evident local need. All midwives emphasized the importance of `equality of care'. How this was operationalized varied, and `individualized' or `woman-centred' care was assumed to encompass the concept. In the few examples where care was systematically targeted in accordance with policy directives, the midwife's public health role was increased. Conclusion. In the absence of a co-ordinated strategic vision driven by managers, practitioners find difficulty in prioritizing care and targeting resources to disadvantaged clients in line with policy directives. Tensions between policy and practice in the care of `disadvantaged' women clearly exist. Successful implementation of policy at practice level needs: commitment from managers; clarity of purpose in documentation; and provision of specific targets for practitioners. However, the latter should remain flexible enough for the delivery of care to be appropriate and sensitive to individual needs.

Notes: The gut flora is a vast interior ecosystem whose nature is only beginning to be unravelled, due to the emergence of sophisticated molecular tools. Techniques such as 16S ribosomal RNA analysis, polymerase chain reaction amplification and the use of DNA microarrays now facilitate rapid identification and characterization of species resistant to conventional culture and possibly unknown species. Life-long cross-talk between the host and the gut flora determines whether health is maintained or disease intervenes. An understanding of these bacteria–bacteria and bacteria–host immune and epithelial cell interactions is likely to lead to a greater insight into disease pathogenesis. Studies of single organism–epithelial interactions have revealed the large range of metabolic processes that gut bacteria may influence. In inflammatory bowel diseases, bacteria drive the inflammatory process, and genetic predisposition to disease identified to date, such as the recently described NOD2/CARD15 gene variants, may relate to altered bacterial recognition. Extra-intestinal disorders, such as atopy and arthritis, may also have an altered gut milieu as their basis. Clinical evidence is emerging that the modification of this internal environment, using either antibiotics or probiotic bacteria, is beneficial in preventing and treating disease. This natural and apparently safe approach holds great appeal.

Notes: Inflammatory bowel disease involves an interaction between genetic susceptibility, a host mucosal immune response and the enteric flora. However, the relapsing and remitting course underlines the importance of other modifiers, such as psychological stress. Doctors and patients share the view that stress plays a role in the initiation and perpetuation of disease. Levels of chronic perceived stress have been shown to correlate with symptom relapse and mucosal appearance, and stress management therapy has been shown to be beneficial. Animal models provide further evidence that stress may play a role in disease initiation and reactivation.Elucidation of the gut–brain–immune axis has provided insight into the mechanisms by which stress may result in gut inflammation. Stress can alter intestinal physiological function. Stress can increase gut permeability, increase ion secretion by a mechanism involving neural stimulation or mast cells, increase mucin release and deplete goblet cells. Stress causes parasympathetic activation via a mechanism involving corticotropin releasing factor, ultimately affecting mucosal mast cells. Stress also results in increased bacterial adherence and decreased luminal lactobacilli. As a result of all these changes luminal antigens may gain access to the epithelium, causing inflammation.

Notes: Background: When the subgingival presence of periodontal pathogens is studied in groups of patients or populations, mostly a number of the deepest sites is sampled. The mean clinical parameters of these deep sites are also frequently used as a the descriptor of the clinical situation of these subjects. It can be questioned, whether these 4 deep sites are capable of predicting a full-mouth situation.Aim: The purpose of the present retrospective study was to investigate to what extent the experienced progression of periodontitis as measured in the deepest approximal pocket in each quadrant reflects the disease progression at the approximal sites on a full-mouth level.Methods: A data set of a 7-year longitudinal study of 158 young subjects (69 male, 89 female, 15–25 years of age at baseline) was used. Clinical assessments included plaque index (PI), pocket depth (PD) and attachment loss (AL) at baseline (1987) and follow-up (1994). Measurements were made at the approximal surfaces of all teeth. The deepest pocket in each quadrant was determined at follow-up. Changes of the clinical parameters between baseline and follow-up were calculated both as full-mouth mean scores as well as for these 4 deepest sites. A regression analysis was used to evaluate the relationship between full-mouth score and the 4 test sites.Results: For disease progression between baseline and follow-up, significant correlation coefficients were observed between the 4-site and full-mouth mean changes (PD: 0.80, AL: 0.70, PI: 0.77). Regression coefficients were 0.51 for PD, 0.35 for AL and 0.55 for PI. The precision of the estimate for the full-mouth mean, as predicted by the 4-site mean, is determined by the residual standard deviation. This was for PD 0.31 mm, for AL 0.31 mm and for PI 0.29. Compared to the between-patient standard deviation of the full-mouth means, the residual standard deviations were high.Conclusion: In the present population, a reasonable to good correlation between full-mouth and 4-sites data was observed. However, the high residual standard deviation in the regression analysis illustrates the inaccuracy for the 4-sites data when used as a descriptive for changes in the periodontal condition on a full-mouth level. Data evaluating progression of periodontitis based on a limited number of diseased sites should be interpreted cautiously.

Notes: Objectives: Current literature is ambivalent on the use of barrier membranes for regeneration of intraosseous defects. One of the reasons for unpredictable results may be related to infection before, during and after the surgical procedure. Therefore, the purpose of the present controlled study was to evaluate both the use of membranes (MEM) and antibiotics (AB), separately and in combination.Methods: In all, 25 patients with two intraosseous periodontal defects each were randomized in two groups: AB+ group receiving systemic antibiotics (n = 13) and AB– group without antibiotics (n = 12). After raising flaps and after debridement, both defects in each patient were covered by a bioresorbable membrane (MEM+). However, just before suturing the flaps in a coronal position, the membrane over one of the two defects was removed at random (MEM–). This protocol resulted in four groups of defects: (i) MEM– AB–; (ii) MEM+ AB–; (iii) MEM– AB+ ; (iv) MEM+ AB+. Patients were monitored clinically and microbiologically for 1 year. Data were analyzed in repeated measures ancova's and adjusted means for clinical variables were obtained from the final statistical model.Results:  Reduction in probing pocket depth (PPD) at 12 months postoperatively varied between 2.54 and 3.06 mm between the four treatment modalities, but overall no main effect of MEM or AB was found. Gains in probing attachment level (PAL) at 12 months postoperatively varied between 0.56 and 1.96 mm for the 4 treatments. In the overall analysis for PAL, no main effect of MEM or AB was found. Gains in probing bone level (PBL) 12 months postoperatively ranged from 1.39 to 2.09 mm between the treatment groups. Again, overall, no main effects of MEM or AB were found for PBL. Explorative statistical analyses indicated that smoking and not MEM or AB is a determining factor for gain in PBL (P = 0.0009). Nonsmokers were estimated to gain 2.04 mm PBL compared to 0.52 mm in smokers. The prevalence of several periodontal pathogens, at the day of surgery or postoperatively, and specific defect characteristics, were not determining factors for gain in PAL and PBL.Conclusions:  Neither the application of barrier membranes nor the use of systemic antibiotics showed an additional effect over control on both soft and hard tissue measurements in the treatment of intraosseous defects. In contrast, smoking was a determining factor severely limiting gain in PBL in surgical procedures aimed at regeneration of intraosseous defects.