Pain is a major symptom in chronic inflammatory arthropathies such as rheumatoid arthritis and affects the health status of arthritis patients negatively. There has been much debate about the role of pain in juvenile chronic arthritis and this review deals with the controversies about this subject. Pain in children is best understood as a multifactorial concept in which pain is the result of somatosensory, behavioural and environmental factors. The role of the different factors contributing to pain will be assessed with special reference to mechanisms relevant to children with chronic pain, the various instruments to measure pain, such as visual analogue scales and algometry, and the treatment of chronic pain in juvenile chronic arthritis. For a true understanding of chronic pain in children, these multidimensional assessments should be integrated into a biobehavioral model, by means of which a better understanding should lead to new therapeutic interventions for one of the most common symptoms of rheumatic diseases in childhood: pain.

Cytokines are important mediators of the immune response as well as the inflammatory response. Those concerned primarily with cell growth, differentiation and activation of cells within the immune system are called interleukins, of which there are now 18. Exposure to antigenic and environmental stimuli causes T cells to differentiate and polarise into Th1 or 2-like cells with different cytokine profiles, and requiring different cytokines for differentiation (IL-12 for Th1 and IL-4 for Th2). Homeostasis is usually restored as these cells are mutually inhibitory. Autoimmune diseases have been associated with a persistent imbalance with more Th1-like cells, which are thought to contribute to pathology. With regard to juvenile chronic arthritis (JCA), there is some preliminary evidence of this imbalance in the oligoarticular subgroup. Imbalance of pro-inflammatory cytokines, IL-1 and TNF with their natural inhibitors has also been shown to contribute to persistence of inflammation. In the case of JCA, there has been some evidence that these imbalances could account for some of the disease phenotypes. Furthermore, the tendency to imbalance is genetically determined.

Juvenile arthritis (JA) is a term that covers a number of different disease entities, of which only three present with significant Human Leukocyte Antigen (HLA) associations. (1) Pauciarticular JA with late onset and a strong male proponderance is associated with HLA-B27 and represents the group of juvenile spondyloarthropathies related to adult ankylosing spondylitis. (2) Early onset pauciarticular JA with a preponderance of females and a frequent occurance of chronic iridocyclitis and the frequent presence of anti-nuclear antibodies is associated with alleles from three different regions of the HLA system: HLA-A2, which shows a very strong correlation with early age of onset; DR8, DR11 and DR12 as well as DQA1*0401, *0501, *0601 and finally DPB1*0201. These alleles show no linkage disequilibrium in the control population. (3) Rheumatoid factor positive polyarticular JA is associated, as is adult rheumatoid arthritis, with DR4. Concerning the possible mechanisms of the immunopathogenesis, it is speculated that the normal function of HLA molecules, namely the presentation of antigenic peptides, plays a major role. Data collected on HLA associations in early onset pauciarticular JA have been interpreted as indicating that alleles of the DQA1 locus (*0401, *0501, *0601) are probably responsible for presenting the hypothetical arthritogenic peptides. It is speculated that the pathogenic process includes the presentation of HLA-A2 or HLA-DPB1*0201 derived peptides presented by DQ molecules. It is clearly stated that typing for HLA alleles has very little or no importance for clinical diagnosis and prognosis.

Epidemiological research in the field of paediatric rheumatology is important for reasons such as the identification of possible aetiological factors, description of the natural history, identification of biologically homogeneous disease groups and health care planning. This review will focus on the epidemiology of 'idiopathic' juvenile arthritis (JA) where data are available for comparison in terms of time, space and ethnic origin. Methodological issues that make comparisons of data difficult, such as case definition, source population and case ascertainment, will be discussed in relation to the data presented. The incidence and prevalence of JA cover a wide range, but, in studies that use similar methodology, an incidence of 5-18 and a prevalence of 30-150 per 100,000 children under the age of 16 is found in Europe and on the American continent. Studies from other parts of the world indicate differences in age of onset and subgroup distribution related to geographical location and/or race.

The classification of chronic childhood arthritis has challenged physicians for a century. Currently used classifications are all based on clinical characteristics and because they are frequently used imprecisely, communication of scientific data has been difficult. The new classification of the International League of Associations of Rheumatologists (ILAR) represents the results of an international effort to clarify the classification of this group of diseases based on identification of clinically homogeneous groups. This classification process is ongoing, and will reflect the results of scientifically based studies as they become available.

Degenerative changes of the spinal column have long been and continue to be confused with the presence of spinal distress and pain. All parts of the spine undergo degenerative changes as we age. The purpose of this chapter is to describe the degenerative process and its clinical consequences. The disc degenerative process will be discussed; its consequences on the facet joint and osteophyte formation are considered. The prevalence of disc degeneration, the role of physically demanding work and leisure and the interference of spinal deformity is clarified. A section particularly important for the clinician deals with the clinical consequences of the degenerative process in disc herniation, degenerative spondylolisthesis, spondylolysis and stenosis. This chapter tries to put the degenerative changes of the spine into the context of a normal ageing process.

The main challenge of surgery in the treatment of low back pain lies with the poor knowledge of the aetio-pathogenesis of this symptom. Surgical treatment requires the precise diagnosis of a surgically curable lesion. In low back disorders this research of a precise source of nociception remains elusive even in the presence of radiological abnormalities. Indeed, surgery may not be performed to treat a symptom (low back pain), but an objective condition or disease. Surgical treatment for low back pain is the subject of many controversies, but a certain numbers of attitudes can be (generally) agreed upon in a variety of low back disorders: (i) intervertebral disc herniation; (ii) degenerative spinal disease; (iii) spinal stenosis; (iv) lytic spondylolisthesis. However, there is a wide choice of attitudes, techniques and procedures for each of those indications and numerous conflicting result reports have been published. This chapter will try to present the best available consensus regarding the indications and results of different surgical procedures in spinal disorders. Most of all, physicians should bear in mind that, in spine surgery perhaps more than in other fields, unreasonable patient (and surgeon) expectations will most likely lead to poor outcomes.

Low back pain is a very common but benign and, in general, self-limiting disease indicating that only a small proportion of patients will require sophisticated imaging studies. Recent studies have highlighted the fact that a simple relationship of structural abnormalities to low back pain is impossible because similar alterations can be found in symptomatic as well as in asymptomatic individuals. these findings question our current criteria for the diagnosis of low back pain disorders with regard to their discriminative power in differentiating diseased and non-diseased individuals. Structural abnormalities demonstrated by imaging studies should therefore only be interpreted in the light of the clinical findings. This review shows that only a few studies contribute to our understanding of the clinical efficacy of imaging studies in the evaluation of low back pain disorders. There is an absolute need for comprehensive, well conducted studies on the impact of specific imaging modalities on diagnosis and treatment of lumbar spinal disease.

The purpose of this chapter is to promote a model to prevent chronicity and disability from non-specific low back pain (NSLBP). Delayed recovery is defined in this chapter as the period between 4 and 8 weeks after onset of NSLBP during which a patient has not yet returned to work. The recognition of predictors associated with delayed recovery at onset of the problem helps health care providers in their treatment plan. An algorithm can be useful for health care providers and employers in guiding the employee back to work. A multidisciplinary return to work programme is an essential part of the algorithm.

Problem situations in the patient-health care relationship may relate to the patient or to the health care provider characteristics or to the way they interact; they may also relate to the general social context. Such situations force the clinician dealing with non-specific low back pain patients to look beyond the traditional biomedical model that assumes a linear connection between pathology and symptomatology. The introduction of the biopsychosocial model approximately 10 years ago has improved the understanding of common low back pain. This chapter gives some insight into areas relating to factors that may hamper the patient-therapist relationship and thus complicate treatment and recommendation outcomes. It emphasizes the necessity to involve the patient in the decision-making. Recognizing the patients' psychological, social and cultural background as well as the level of education and employability are important to make successful recommendations. This knowledge is not new but the difficulty is to implement it in today's cost effectiveness driven society. However the benefit at the end may be the decrease of chronicity and/or permanent disability, suffering for the patient and frustration for the clinician. Identifying the underlying cause of non-compliance or of unexpected delayed recovery is an exciting issue. The cause may or may not be biomedical. If a specific cause can be identified, it has to be diagnosed and evaluated. If the clinical examination has ruled out specific or emergency conditions, another perspective may be needed and the course of action could then be determined.

A wide variety of mechanical and non-mechanical disorders are associated with the clinical symptom of low back pain. Mechanical disorders are the cause of the vast majority of low back pain. Despite this frequency, the specific cause of mechanical low back pain can not be elucidated in spite of extensive diagnostic evaluation in a majority of individuals. Specific causes of low back pain are associated with less frequently occurring systemic illnesses including rheumatic, infectious, neoplastic, gynaecological and vascular disorders. The diagnostic process is more successful in identifying systemic disorders as the specific cause of low back pain. Non-surgical management is effective therapy with most patients with mechanical disorders of any form. Systemic illnesses require interventions directed specifically at healing the affected organ system.

With the emergent concept of evidence-based practice, various countries have produced clinical guidelines for the management of acute low back pain since 1993-94. By and large the evidence-base for these proposals is consistent, though over the last 4 years it has increased considerably, and there has been a slight change of emphasis in several aspects. As all the guidelines are based on the same evidence, the similarity between them is not surprising. The common features are diagnostic triage along with periodic assessment to guide management strategies. There has been progressive reduction in the recommendation of rest as a treatment option, and early activation is increasingly recognized as a potent intervention. There has been a progressive recognition that psychosocial factors are important determinants for the risk of chronicity, and that such factors need to be addressed clinically. Specific therapeutic recommendations vary, but these are probably less important than the overall strategy. It is obviously hoped that clinical management should improve as a result of these initiatives, but effective dissemination and implementation are persisting concerns, and the effectiveness of clinical guidelines in changing clinical practice is still unproven.

Uncertainty is the rule rather than the exception when it comes to the underlying causes of 'common' or 'non-specific' low back pain. It may be called many names, depending on whether the diagnostic term is descriptive, anatomopathological or physiopathological. Classifications have been devised, including various criteria: symptoms and signs, duration, treatment, consequences of low back pain on the patients' daily life, etc. Because back pain frequently runs a recurrent course, functional and pain outcomes need to be considered separately: chronic disability and chronic pain may not be parallel. Thus, pain duration (e.g. acute, transient, recurrent, chronic) is only one element in the definition of chronicity. These difficulties in defining and classifying non-specific low back pain may lead to communication problems among health professionals as well as between patients and health professionals. These difficulties raise questions such as: what kind of diagnostic term should we use to avoid dramatization of non-specific low back pain? how can we improve the definition of long-term low back pain? and how can we assure and reassure the patient that this condition is benign in the majority of the population?

Musculoskeletal disorders, of which osteoarthritis (OA) is the most common, incur significant economic, social and psychological costs. Costs of illness have risen over recent decades accounting for up to 1-2.5% of the gross national product for those countries studied so far, including the USA, Canada, the UK, France and Australia. Arthritis has a significant impact on psychosocial and physical function and is known to be the leading cause of disability in later life. There are also significant out-of-pocket costs and loss of earnings due to changes in occupation and roles in domestic duties. Current guidelines for the management of OA of hip and knee include the recommendation of inexpensive but effective interventions. Although the guidelines have not had a specific economic evaluation, cost reductions may be expected. OA is a very common disease and will become an increasing economic burden as the population ages.

Non-pharmacological therapies are very important in osteoarthritis. Each form of this treatment should be individually devised, taking into account the anatomical distribution, the phase and the progression rate of the disease. Indications, contraindications, dosage and precautions are as important in non-pharmacological therapy as they are in drug treatment. Therapeutic exercises decrease pain, increase muscle strength and range of joint motion as well as improve endurance and aerobic capacity. Exercise programmes should be designed, conducted and regularly supervised by professionally trained physiotherapists. Weight reduction is of proven benefit in obese patients with osteoarthritis of the knee. Walking aids, crutches, shoe insoles, braces and patellar taping are useful tools in some form of osteoarthritis. Patient education and the management of the psychosocial consequences are priority tasks. Therapeutic heat and cold, electrotherapy, ultrasound, acupuncture, hydrotherapy and spa treatment are widely used, although the effects and benefits have not been fully established. Non-pharmacological therapies should undergo rigorous randomized controlled trials in a similar manner to pharmacological studies.

Although intra-articular therapy is widely used in the treatment of osteoarthritis (OA), those controlled clinical trials which include placebo groups suggest that there is little to be gained over joint aspiration alone, or even over a simple needle prick. Glucocorticoids may however offer a small additional symptom benefit over one or two weeks. Viscosupplementation may offer a slightly longer benefit. Intra-articular radiotherapy probably confers no benefit. Serious adverse effects are rare but local effects may occur in up to 10% of patients treated with viscosupplements. Future research should always include a placebo group in clinical studies, should clarify the possible benefits of viscosupplementation and should include in vitro work to consider the biological basis for possible actions of intra-articular therapy.

Therapy for osteoarthritis (OA) is aimed at relieving symptoms and at maximizing function. Therapies can be considered as either symptom modifying OA drugs (SMOADs) or as disease modifying OA drugs (DMOADs). Currently available agents fall into the category of SMOADs. Analgesic medications, particularly paracetamol and capsaicin, have proven efficacy in OA and are recommended first line therapies. Non-steroidal anti-inflammatory drugs (NSAIDs) do appear to provide extra symptomatic benefit for some patients but have greater toxicity. Newer generation NSAIDs may have safety advantages which remain to be confirmed in practice. Further therapies are being developed which aim to prevent cartilage damage and/or aid cartilage restoration, but these DMOADs remain in the experimental stage.

X-ray, magnetic resonance imaging (MRI) and arthroscopy are the methods most widely used to assess the status of osteoarthritic joints. How do these methods compare? As diagnostic tools, what is the relative sensitivity of X-ray versus MRI, arthroscopy versus MRI and arthroscopy versus X-ray? Which imaging modalities can be used for predicting progression? Scintigraphy and MRI can assess the degree of cellular activity in the tissues of a joint, which may help in prognosis. Are the methods proven and are they reliable? Recommendations for clinical trials in knee osteoarthritis, state it is essential that reproducible radiographs are obtained for reliable assessment of progression. Two radiographic views of the knee have been proposed; which provides the more reliable assessment, the knee in extension or semi-flexed? Compared with standard radiography, does microfocal radiography make a difference to patient numbers required for drug trials?

Biochemical markers for osteoarthritis (OA) may serve different purposes. Since markers reflect ongoing dynamic metabolic processes in the joint tissues (cartilage, synovium, bone, etc.), they are most likely to be useful to predict prognosis and response to treatment, to monitor response to treatment, and for disease staging. Markers are currently being used at the research level for these purposes. The goal of using these markers to assess the disease process in the OA clinical trial setting or in the clinical routine has, however, not yet been reached.

Several epidemiological studies have shown a lower incidence and prevalence of hip fractures in people with osteoarthritis (OA) and vice versa which has led to numerous studies examining the association between OA and osteoporosis more generally. There is felt to be an inverse relationship between these two diseases and the evidence for and against this association is discussed. The evidence for an association with osteoporosis is stronger for large joint OA than hand OA or primary generalized OA. A number of possible mechanisms for this association are discussed such as genetic factors, common risk factors, role of subchondral bone in cartilage damage and growth factors. The incidence and prevalence of one disease in the presence of the other is discussed. Despite the inverse relationship seen in some studies, there is currently no evidence that treatment of one disease can have a detrimental effect on the other.