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In a single-blind trial, five treatments for painful stiff shoulder were compared for a 4-week assessment period in 60 patients. The treatments were acupuncture, steroid injection with placebo and with active tolmetin sodium, physiotherapy in the form of ultrasound and 'placebo' physiotherapy with placebo tolmetin sodium. Objective assessment was gained by use of goniometer readings to monitor shoulder abduction. Pain was measured by visual analogue scales and by a 4-point scale. Comparative assessment was also recorded and at the end of the study a success or failure was recorded for each patient's treatment. With very few exceptions all patients improved markedly, both in terms of the subjective and objective parameters. No differences between the treatments were detected. The incidence and severity of side-effects was low. It is suggested that the results show that the painful stiff shoulder may be a self-limiting condition and that any beneficial effect was really due to natural recovery. This is an important consideration because patients do not always receive immediate attention when referred to an out-patient department and the use of physiotherapy and acupuncture in such cases, perhaps, should be critically examined.

In clinical practice, at the outpatient clinic of oral medicine, we attend to many patients diagnosed with benign migratory glossitis, with varying intensity of pain ranging from mild to severe. Treating this disease is a formidable challenge for clinicians. Therefore, we performed a systematic review of benign migratory glossitis to identify the best evidence-based treatment available for this condition. We believe that this article may be useful in guiding clinicians on the choice of treatment.

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Osteoarthritis is a worldwide heterogeneous group of conditions that leads to joint symptoms, which are associated with defective integrity of articular cartilage, in addition to related changes in the underlying bone at the joint margins. The prevalence of the disease after the age of 65 years, is about 60% in men and 70% in women. The aetiology of osteoarthritis is multifactorial, with the end result being mechanical joint failure and varying degrees of loss of joint function. The pathophysiological events associated with osteoarthritis are beginning to be understood. Essential inflammatory cytokines, such as IL-1beta and TNF-alpha, are involved initiating a vicious cycle of catabolic and degradative events in cartilage, mediated by metalloproteinases, which degrade cartilage extracellular matrix. The role of inflammation in the pathophysiology and progression of early osteoarthritis is supported further by the observation that C-reactive protein levels are raised in women with early knee osteoarthritis and higher levels predict those whose disease will progress. The synovium from osteoarthritis joints stains for IL-1beta and TNF-alpha. Nitric oxide, which exerts pro-inflammatory effects, is released during inflammation. Cartilage from patients with rheumatoid arthritis and osteoarthritis spontaneously produces nitric oxide in vitro. In experimental osteoarthritis, nitric oxide induces chondrocyte apoptosis, thus contributing to cartilage degradation. Hence unregulated nitric oxide production in humans plays a part in the pathophysiology of the disease. These recent observations suggest that therapy can now be targeted at specific sites of pathophysiological pathways involved in the pathogenesis of osteoarthritis. The novel strategies under consideration for the treatment of osteoarthritis can be divided into five main areas. These are COX-2 inhibitors, nitric oxide synthesis inhibitors and anti-oxidants, chondrocyte and bone growth promoters, metalloproteinase and cytokine inhibitors and gene therapy.

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