Redesigning the job is a strategy for preventing low back injuries at work or for accommodating injured employees who return to work. An evaluation of the physical job demands is necessary in either strategy. Several job demands are associated with low back pain and injury--heavy physical work, static or postural effort, dynamic work-load and exposure to wholebody vibration. Traditional work measurement studies emphasize a rigorous task analysis. By adding biomechanical, physiological and psychophysical measurements, a comprehensive evaluation is possible. There is no standard scheme for a workplace evaluation. The method depends on the end use of the analysis. Job evaluation for workplace design requires an emphasis on equipment and work conditions; evaluation for placement of injured employees should emphasize the operational demands of the tasks. Few studies considered the multifactorial aetiology of low back pain. Most studies that measured the magnitude of biomechanical, physiological and psychophysical stresses attempted to define peak work-loads. The attempt to evaluate the effects of subacute cumulative traumas is only in the beginning. Most ergonomic intervention programmes modify the loads, the design of objects handled, lifting techniques, workplace layout and task design. The effectiveness of these interventions in controlling medical costs or morbidity has not been clearly demonstrated. Consequently, occupational risk factors may be more important for evaluating disability. Job familiarity is the key to effective medical management. Ergonomic analysis procedures may be useful within rehabilitation settings that also provide placement services. The reason is that they facilitate communication between all elements involved in the rehabilitation process. Proper communication procedures are also crucial in implementing ergonomic interventions in the workplace. A health care provider should be part of a task force that oversees these interventions. Future effort should be directed to finding a method that health care practitioners could be competent to carry out effectively in a clinical setting. Expert systems offer promising results in disseminating ergonomic knowledge in primary and secondary health care facilities.

This chapter has reviewed the role of back school and educational programmes for the common and non-specific acute and subacute low back pain patient. The following seems to come out of this review. Education is an important part of patient care. However, several questions arise about the content of the education, the selection of patients, the patient compliance to instruction given, how the information is retained, and which outcome measures should be used. It is also important to realize that the back school is a modality or a tool that may be used as an adjunct, but as a sole treatment it seems to have less impact than in combination with other structured or goal-oriented programmes. When a back school is instituted in a hospital or in industry, it requires administrative and budgetary support and a multidisciplinary staff to successfully carry out the programme. The information given must be adapted to the needs of the participants and all members of the team must give the same information to the patient. A poorly structured back school where patients are dumped because the physician or other health care provider has nothing else to offer is a poor solution for the patient, a poor solution for the health care provider, and can only increase the patient's discomfort and health care costs.

This chapter has reviewed research on psychological and social factors associated with the onset and progression of low back pain. From this review it can be concluded that psychosocial traits appear to be important contributors to the course of pain and disability though methodologically well-designed longitudinal studies are rare. For this reason it is difficult to assess the relative importance of, for example, psychological distress compared with work stress. Furthermore, the mechanisms by which specific variables effect back pain remain unknown. The answer, no doubt, lies in longitudinal studies which employ multicausal models. It has been noted the psychosocial treatments which have proven effective for chronic pain populations are rarely assessed with acute pain patients. Some problems are the inaccessibility of acute back pain sufferers to psychologists, the difficulty of isolating the effect of one component of a multidisciplinary programme and the lack of uniform practice of psychosocial techniques. None the less, programmes which include psychosocial interventions appear to have superior results to those which do not. Since these techniques are often simple and inexpensive to include they should be incorporated into all treatment programmes where the potential for chronic pain syndrome exists. Gaps and flaws in current research methodologies have been identified and suggestions for future investigations have been proposed. In addition we have attempted to provide some practical guidelines for health care professionals to help them identify salient psychosocial issues which may effect the course of their patient's treatment. Recommendations for assessment and referral are also provided.

Controversial opinions have been published concerning the frequency of LBP among children and adolescents. Studies from orthopaedics or neurosurgical departments have reported low figures for prevalence of specific LBP due to serious disorders. Field surveys, on the contrary, have shown that cumulative life prevalence of non-specific LBP in children and teenagers can be comparable to the prevalence data for adult populations. Some specific diagnoses are more common or characteristic of children complaining of LBP. Age, gender, sports activities and family history of LBP have been found to be significantly associated with an increased prevalence in non-specific LBP among children. Low back pain among children and teenagers is common and should be recognized. This chapter provides guidelines for a clinical approach and differential diagnoses. Most back pain in these age groups is benign and should be treated as such.

At present, although there have been many epidemiological studies of risk factors for low back pain, there are few risk factors established in prospective studies; and our understanding of them remains relatively crude. Individuals in jobs requiring manual materials handling, particularly repeated heavy lifting and lifting while twisting, are at increased risk of back pain leading to work absence. In addition, exposure to whole-body vibration and job requirements for static postures are associated with back pain. Individual trunk strength has not been consistently demonstrated as associated with back pain; although there is some suggestion that when work requirements for heavy lifting exceed individual capacities, back pain is more likely to occur. The pattern of peak age at onset in the 20's is consistent with back pain development early in working life. Among other individual characteristics, only cigarette smoking has consistently been associated with back pain; and the biological mechanism for this finding is not understood. Evidence with respect to spinal flexibility, aerobic capacity, educational attainment and other variables is suggestive but not consistent. There is some evidence that the individual's relation to work, expressed as job satisfaction or supervisor rating, is also related to work absence due to back pain. While it is possible to describe, however crudely, the characteristics placing people at risk for back pain leading to work absence and/or medical attention, the problem of predicting chronicity and thus identifying patients for more intensive clinical intervention remains unresolved. At this time, only age of the patient and certain clinical features of the back pain such as the presence of sciatic symptoms, duration of the current episode, and history of prior episodes are consistently demonstrated predictors. In chronic patients, there is suggestive evidence that spinal flexibility, trunk strength, and certain psychological characteristics such as coping skills, fear and avoidance of pain or movement, job satisfaction, attribution of fault and hysterical or hypochondriacal features are associated with treatment failure. In addition, there is suggestive evidence that the availability of alternative work placement may allow for earlier return to work than otherwise. While the availability of disability compensation in excess of usual wages may serve as a disincentive to return to work. The latter-cited remain to be verified, while findings in chronic patients remain to be tested in acute. Further, the role of physical demands of work in duration of back pain episodes has not been well studied.

Current theories of the aetiology of RA point to a central role for the trimolecular complex comprising the MHC class II molecule on the surface of the APC, the antigenic peptide and the TCR on the disease-inducing T cell. Thus the arthritogenic T cell is an important target for new therapy. However, it cannot be directly identified because the causative antigen is unknown, so indirect techniques such as TCV and TCR peptide vaccination are required. In TCV, T cells thought to mediate the disease, in an activated and attenuated form, are injected into the patient, who then develops a specific immune response against these pathogenic T cells. TCV has been shown to be effective in protecting against and treating a variety of animal models of autoimmune disease, including AA, EAE and IDDM in NOD mice. The vaccines initially comprised clones and lines of T cells shown to be capable of transferring the disease, but later unseparated LN cells were also shown to be effective, paralleling more closely the human situation. Interestingly, it has become clear that TCV does not create its own regulatory network but amplifies a natural immunoregulatory network which forms as the disease develops. The major stimulating moiety on the vaccinating T cell is its receptor (anti-idiotypic response), although there is also an anti-ergotypic (anti-activated T cell) response. For this reason the technique of TCR peptide vaccination was developed, which utilizes only a short peptide from the TCR of the disease-causing cells to stimulate an immune response against them. This is effective in the prevention and treatment of EAE, where there is a preferential usage of TCR-V beta 8 by encephalitogenic T cells. The application of both these techniques to human autoimmune disease is in its infancy. Studies of TCV in MS and RA have not shown clear-cut clinical benefit, although immunological changes have been observed; comparison of methodology with the animal work and assessment of results are complex and further studies are in progress. Studies of TCR peptide vaccination in MS and RA are handicapped by the lack of a consensus on TCR usage in these conditions, but a limited study is underway in MS.

Over the last three years there has been a dramatic rise in the number of trials using monoclonal antibodies in the treatment of rheumatoid arthritis. So far, the numbers of patients treated in the individual studies have been small, and the study designs not comparable. All these trials have been conducted in a non-blinded, uncontrolled fashion. The patient populations tended to represent the severe end of the disease spectrum, being usually individuals for whom all other conventional and sometimes even unconventional experimental therapeutic approaches have failed. Clearly, therefore, larger controlled double blind studies in patients with less advanced stages of rheumatoid arthritis are needed. In the trials thus far, long-standing diseases afflicting the joints, usually with severe destruction, have frequently made clinical evaluation very difficult. Moreover, apparently with the exception of one or two reagents (16H5 and possibly B-F5) routine laboratory parameters which are helpful in determining disease activity such as CRP or the rheumatoid factor usually remain unaltered with anti-T cell therapy. In addition, in some individuals there was no clinical improvement despite sometimes severe CD4 cell depletion. The notion that the mere depletion of CD4+ cells is not sufficient to permanently suppress disease activity in autoimmune disease is further supported by studies carried out by Conolly and Wofsy in 1990. In a mouse lupus model, these investigators demonstrated that a small subpopulation of CD4+ T cells may be refractory to depletion by anti-CD4 and may be able to promote the full expression of the disease. Similar mechanisms could apply to certain individuals with human autoimmune disorders. Many additional questions remain open. The most important of these is which markers identify clinical responders to therapy. Attempts to correlate clinical response to the level of T cell depletion, modulation of the target antigens or in vitro functional assays so far have not yielded significant results. Other questions relate to the frequency of antibody administration and the amounts needed to permanently suppress disease activity. The initial hope based on animal experiments of inducing a permanent tolerance to certain antigens by anti-CD4 treatment has been clearly shown not to apply to rheumatoid arthritis. Even though there are individual variations, the efficacy of anti-T cell treatment tends to wear off after 3 or even 1 month, necessitating retreatment. Protocols will have to be designed for either longer treatment periods, repeated courses or more frequent single administrations.(ABSTRACT TRUNCATED AT 400 WORDS)

Inflammatory arthritis has the potential to cause irreversible erosive damage to cartilage and bone. This may occur very early in the course of the disease. At present it is not possible at diagnosis to identify those patients who will develop erosive damage. If this were possible, it would enable aggressive therapy to be targeted to those patients at greatest risk. There is therefore a need for sensitive markers to detect and quantify joint damage at as early a stage as possible. In this chapter we review potential biochemical markers of such damage and assess their clinical usefulness.

In this chapter, we investigate the use of non-toxic 'probe drugs' to give information about basic biochemical pathways. We have examined the hypothesis that a major factor in RA is defective metabolism of sulphur-containing compounds. At least two pathways have been shown to be abnormal in RA. Generally, patients have reduced capacity to metabolize and detoxify thiol compounds by methylation, and have increased levels of plasma cysteine. They also have a lower capacity for S-oxidation of cysteine and its derivatives, with reduced amounts of plasma sulphate. The raised cysteine resulting from less effective metabolism may lead to reduced clearance of immune complexes and a raised inflammatory response in RA patients. Lower plasma sulphate, however, leads to defective tissue synthesis, and makes adequate repair of damaged joints less feasible. The co-existence of defects in these two interacting endogenous pathways serves to perpetuate the disease process, leading to chronic inflammation and tissue destruction. These enzyme defects have been shown to be predictive of persistent disease.

For more than 100 years it has been suspected that bacteria or products derived from them are deposited in joints and cause arthritis without suppuration. Over this time a vast amount of evidence, much of which is still unchallenged, has accumulated to demonstrate that whole bacteria and subcellular bacterial elements do pass, under certain circumstances, from sites of mucosal colonization or infection into the circulation and thence into joints. Similarly, experimental studies have demonstrated that the deposition of both inert material and bacterial components within synovium is sometimes, but not always, associated with the development and persistence of synovitis. In human reactive arthritis aseptic synovitis follows localized bacterial infection in the gut or genitourinary tract. A genetic predisposition, associated with the HLA B27 antigen, is recognized, and interaction between class I HLA determinants and bacteria-derived antigens may underlie the development of arthritis. Although much remains to be learned about the dissemination of antigens from the primary site of infection in reactive arthritis, strong evidence implicates the deposition of antigenic elements of Chlamydia, Yersinia, Salmonella and perhaps other micro-organisms within the synovium. Immunological findings support the notion that such antigens are being presented within the joint and participating in the induction and/or maintenance of synovitis. It is not yet clear whether such bacteria are complete or viable or whether persistence at an extra-articular site is important to the persistence of arthritis. The possibility that reactive arthritis, and perhaps other forms of seronegative arthritis also, is caused and perpetuated by bacterial antigens within the joint poses new questions about the role of HLA B27 in pathogenesis. It also raises important and exciting issues regarding treatment. Already, studies of antimicrobial therapy have yielded encouraging initial findings, and it is now possible to design and evaluate therapies aimed at blocking specific antigen recognition within the joint.