BACKGROUND:A Mediterranean-type diet rich in fish, fruit and vegetables and low in saturated fats has been associated with health benefits, including improved cardiovascular profile and benefit in RA. OBJECTIVE:To overcome obstacles to healthy eating by a community-based intervention promoting a Mediterranean-type diet in patients with RA living in socially deprived areas of Glasgow. METHODS:130 female patients with RA aged 30-70 years (median 55), disease duration 8 years were recruited from three hospital sites. The intervention group (n = 75) attended weekly 2-hour sessions for 6 weeks in the local community, including hands-on cooking classes backed up with written information. The control group (n = 55) were given dietary written information only. Both groups completed food frequency questionnaires (FFQs), and clinical and laboratory measures were assessed at baseline, 3 and 6 months. RESULTS:Significant benefit was shown in the intervention group compared with controls for patient global assessment at 6 months (p = 0.002), pain score at 3 and 6 months (p = 0.011 and 0.049), early morning stiffness at 6 months (p = 0.041) and Health Assessment Questionnaire score at 3 months (p = 0.03). Analysis of the FFQs showed significant increases in weekly total fruit, vegetable and legume consumption and improvement in the ratio of monounsaturated:saturated fat intake and systolic BP in the intervention group only. The cooking classes were positively received by patients and tutors; cost/patient for the 6 week course was 84 pounds (124 euro). CONCLUSIONS:Results demonstrate that a 6 week intervention can improve consumption of healthier foods. If implemented more widely it may prove a popular, inexpensive and useful adjunct to other RA treatment.

Non-steroidal anti-inflammatory drugs (NSAIDs) are among one of the most frequently prescribed classes of drugs. Both their benefits and harms arise due to inhibition of cycloxygenase (COX) of which there are two isoenzymes, COX 1 and 2. Both COX isoenzymes have a hydrophobic tunnel, through which the substrate accesses the active site. The tunnel is larger in the COX 2 isoenzyme with a side pocket, a property exploited in the development of specific COX 2 inhibitors [1]. The premise of the initial, COX 2 hypothesis was that the gastrointestinal side effects arose due to inhibition of COX 1 whereas their anti-inflammatory or analgesic properties were COX 2 mediated. Although now appreciated to be rather naı̈ve, the superiority of the selective COX 2 inhibitors in preventing gastro-duodenal mucosal ulceration over the non-selective NSAIDs is striking [2, 3]. There has been continuing scientific and media attention on reports that selective COX 2 inhibitors increase the risk of cardiovascular events. In an early study of major gastrointestinal events, an unexpected 5-fold increase in the risk of acute myocardial infarction (AMI) with rofecoxib was observed when compared with naproxen [4]. At the time, many suggested and aggressively pursued the hypothesis that the increased frequency of events was a spurious observation not due to any prothrombotic effects of rofecoxib, but the cardioprotective properties of naproxen. However, subsequent placebo-controlled studies of both rofecoxib, and celecoxib in chemoprevention also reported an approximate 2-fold increase in cardiovascular events with both drugs [5, 6]. More recently, attention has turned to the effects of the nonselective NSAIDs. As aspirin confers its cardiovascular benefits by inhibiting COX 1 [7], received wisdom has never considered the possibility that the non-selective NSAIDs could increase the risk of cardiovascular events. However, in February 2005, the Food and Drugs Administration (FDA) decided to advise that the risk of cardiovascular events for both selective COX 2 and non-selective NSAIDs is similar and has taken the step to categorize this as a class effect [8]. In the US, all COX 2 selective and non-selective NSAIDs now carry a black-boxed warning on the package insert advising patients of the potential increased cardiovascular risk [9]. The European Agency for the Evaluation of Medicine Products (EMEA) [10] and the Medicines and Healthcare Products Regulatory Agency (MRHA) [11] have, however, been much more reassuring with regard to non-selective NSAIDs and advised that ‘the data are insufficient to warrant changes in current prescribing’. The association between increased AMI risk and non-selective NSAIDs has been evaluated predominantly in observational studies [12–28]. These were primarily based on data from large population and hospital databases that recorded the prevalence of NSAID use combined with confirmed AMI diagnosis. While most studies also accounted for the presence of other risk factors, confounders and use of aspirin, few recorded the indication and duration of NSAID use [15, 16, 18]. Overall, a general direction of effect has been reported from the observational studies—with the exception of one study [21], which reported no effect between non-selective NSAID use and AMI, all studies showed a similar trend of increased risk of AMI compared with remote and non-use, ranging from relative risk of 1.00 (95% CI: 0.73–1.37) [21] to 1.47 (95% CI: 1.00–2.16) [22]. Although the size of the overall relative risk appears small, however, due to the large number of patients prescribed NSAIDs, the absolute risk may be considerable. In addition, these studies have presented data that suggested a differential risk between individual NSAID such as diclofenac, naproxen and ibuprofen, but there is insufficient evidence to conclude whether this truly represents a class effect. The main concern in the context of these studies is whether the small effect observed is a real one or due to unknown or unmeasured confounding factors, a limitation that is inherent to all observational studies. However, such studies may be the only feasible method to determine the potential harms of drugs if the effects are small. It has been advocated that the only method to resolve the issue would be to undertake a large randomized-control trial of non-selective NSAIDs vs placebo [29]. However, it is unlikely that such trial would ever be funded, and it would be unethical to randomize patients to an intervention that may be potentially harmful. Kearney et al. [30] have undertaken a meta-analysis of data of vascular events from randomized-controlled trials of selective COX 2 inhibitors. They found that in all studies selective COX 2 inhibitors increased the risk of vascular events, mainly AMI by 42% (rate ratio 1.42; 95% CI: 1.13–1.78). Trials that compared a COX 2 inhibitor with a traditional NSAID (n1⁄4 91 trials) showed no significant difference in the risk of vascular events (rate ratio 1.16; 95% CI: 0.97–1.38). There were no significant differences whether all non-selective NSAIDs were considered together, in combination, or alone when compared with COX 2 inhibitors. However, a comparison of non-selective NSAIDs with placebo showed differences between NSAIDs—naproxen was associated with the lowest risk (0.92; 95% CI: 0.67–1.21), but there were insufficient data to show a cardioprotective effect; whereas the rate ratios for ibuprofen and diclofenac were 1.51 (95% CI: 0.96–2.37) and 1.63 (95% CI: 1.12–2.37), respectively. This study thus confirms the findings of the epidemiological studies, but the number of cardiovascular events were small, a limitation acknowledged by the investigators. Furthermore, none of the comparative studies of COX 2 inhibitors with non-selective studies were conducted in patients with high cardiovascular risk or specifically powered to evaluate cardiovascular events. The MEDAL programme and PRECISION studies are pharmaceutical industry sponsored trials designed to address these concerns. The MEDAL programme consists of three studies (EDGE, EDGE II and MEDAL), and is a non-inferiority comparison of cardiovascular events between etoricoxib and diclofenac [31]. The EDGE studies where originally designed to compare the gastrointestinal tolerability of etoricoxib compared with diclofenac in osteoarthritis and rheumatoid arthritis, whereas the MEDAL study is specifically designed to compare cardiovascular events in 17 804 osteoarthritis and 5700 rheumatoid arthritis patients treated with either etoricoxib or diclofenac. All three studies will continue until the total number of confirmed thrombotic reaches 635 with at least 430 in the MEDAL study. The PRECISION study is a multi-centre comparative study Rheumatology 2006;45:1458–1460 doi:10.1093/rheumatology/kel353 Advance Access publication 31 October 2006

a Chlamydia reveal significant differences in cytokine levels and ratios the although lower levels of interferon (cid:1) (IFN- (cid:1) in SF found in the HLA-B27-positive ReA patients in

Osteolysis of the jaws has been reported in association with infection, cysts, neoplasia, and metabolic, endocrine, or hematologic abnormalities. Rare cases of idiopathic osteolysis have also been recorded. We report the case of a 10-year-old girl with mandibular basal and alveolar bone resorption that has continued over a period of 9 years. The patient has subsequently developed bilateral resorption of the ascending rami and condyles. The maxilla is uninvolved. Investigations included radiology, computerized tomography, scintigraphy, hematology, serum chemistry, endocrinology, histopathology, microbiology, and immunology. Neutrophil chemotaxis, chemiluminescence, and random migration values were low but within the normal range. These findings are interpreted as indicating an unusual variant of massive osteolysis.

This article reviews the available literature on the ultrasonographic examination of the head and neck as related to oral and maxillofacial surgery, presents clinical case summaries illustrating these applications, and evaluates the role of ultrasonography in current clinical practice.