Part of the book: Principles of Osteoarthritis
Part of the book: Osteoarthritis
Targeted therapies including tumour necrosis factor α (TNFα) inhibitors have transformed the management of a number of autoimmune conditions over the past 20 years. One autoimmune rheumatological condition with significant potential for the development of targeted therapies is systemic sclerosis (SSc). In this chapter, we use SSc as an example of how research into the pathogenic processes underlying autoimmune conditions can be translated into novel targeted therapies. We review the evidence base for a range of targeted therapies for SSc identified from a systematic literature search, before highlighting a number of studies currently underway.
Part of the book: Immunopathogenesis and Immune-based Therapy for Selected Autoimmune Disorders
The oral cavity is home to vast populations of commensal microbial organisms which constitute the ‘healthy oral microbiome.’ Periodontitis is a destructive, infectious, inflammatory condition affecting the gums. Initially, a biofilm structure develops, causing localized inflammation. This biofilm is then colonized by certain anaerobic bacteria, including the ‘red complex’ organisms. There is an increasing interest in the communication between these organisms and host immune surveillance, a dialog which may plays an important role in the development of autoimmune diseases. Studies have shown an association between periodontitis and other inflammatory conditions including rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis and systemic lupus. The advent of accessible 16S ribosomal sequencing has led to exciting developments in the characterization of the human microbiome and the ability to study this interaction in more detail. The transmucosal communication between periodontitis and host immunity may provide avenues of discovery regarding the etiology and progression of rheumatic diseases.
Part of the book: Periodontitis
Osteoarthritis (OA) is the most prevalent arthritis worldwide and is a condition affecting the whole joint. Changes in subchondral bone, cartilage integrity and synovitis are recognised during OA progression. Although advances have been made in our understanding of OA pathophysiology, there are no current treatments that delay or halt the progression of the disease. Treatments are largely based upon physical therapies to improve function, anti-inflammatory agents for pain symptoms and joint replacement surgery for late stage disease in large weight bearing joints. There is an urgent need to better understand the pathophysiology of OA that could translate into improved treatments for this condition. In recent years, more advanced imaging techniques including magnetic resonance imaging (MRI) have led to an improved understanding of changes at the bone-cartilage interface in OA, with recognition that loss of integrity at the cartilage-bone junction and development of bone marrow lesions (BMLs) in the subchondral bone are associated with OA pain in large epidemiological studies. In this book chapter, we review the evidence for the role of BMLs and synovitis, particularly in the pathophysiology of hand OA. Based on a systematic review of the literature, we have identified 15 articles reported on BMLs and synovitis in hand OA, which will be discussed in this chapter.
Part of the book: Osteoarthritis Biomarkers and Treatments
Pain is a debilitating feature of rheumatoid arthritis (RA) and is often described by patients as their most important symptom. Rheumatoid arthritis pain has traditionally been attributed solely to joint inflammation, however despite the advent of increasingly effective disease modifying agents, patients continue to report pain at long term follow up. The cause for ongoing pain is multifactorial and includes joint damage and pain sensitisation. In this book chapter, we will describe the mechanisms underlying the distinct components of pain which are manifest in rheumatoid arthritis and discuss why a thorough assessment of pain is vital to target treatments appropriately.
Part of the book: Rheumatoid Arthritis