Rheumatoid arthritis (RA) is a complex disease that despite decades of research still remains of unknown aetiology [1-3]. Key factors of the pathology are: the mechanism of induction of inflammation and the immunological network leading to disease perpetuation and development into a chronic severe disabling and painful disease. If answers to the fundamental complex molecular events that leads to the development of RA could be precisely dissected and analysed like an exact multi dimensional puzzle, this would enable academic scientists and pharmaceutical companies to identify new important targets for treatment of this disorder. To reach this goal, it is crucial to identify and quantify the gene expression of cells in the tissues that are involved in the initiation and development of chronic inflammatory arthritis. Although an approach focused on understanding the relevance of individual genes is important. There must also be efforts to understand the complete patho-genesis of RA. Hence, a real effort has to be made to avoid a too restrictive vision. Since articular diseases like RA are multifactorial disorders, a variety of unbiased possibilities of molecular mechanisms must be taken into account during identification of possible pharmaceutical drugs against RA.
In this chapter we will attempt to describe molecular genetic tools that can be used to identify novel genes that are involved in disease regulation and could be potential targets for drug development. The use of animal models for identification of new disease mechanism will be highlighted as a potential way to circumvent the heterogeneous complexity of the human population. We will also describe the potential to use the accumulating information of the human genome that can be used to individualise treatments against RA to increase treatment efficacy and avoid serious adverse effects of treatment in susceptible individuals.
Was this article helpful?