Understanding the Mechanisms of Pain in Rheumatoid Arthritis

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.

The Role of Estrogens in Rheumatoid Arthritis Physiopathology

Rheumatoid arthritis (RA) is a chronic, inflammatory joint disease that can lead to irreversible disability. It affects women in a higher proportion than men (3:1 cases). Several reports suggest a link between female sexual hormones (estrogens) and RA features. It’s been described that biological processes where basal estrogen levels are altered like in menstruation, pregnancy, and menopause modifies RA onset, flare, disease severity, and inflammation. Estrogens have a direct action upon the immune system though ERα and ERβ receptors, which have distinct affinity to estrogen concentrations and modifications and have effects upon RA in a dose and receptor dependent manner. The studies focused on dose dependent response at experimental settings reveal a wide (from 25 pg/L to several μg/L) and even contradictory spectrum of effects in patients and cells. This chapter summarizes the contributions and effects of estrogens in RA physiopathology, clinical features, and discusses the possible contributions of estrogen administration and concentration of hormone replacement therapy (HRT) to improve the quality of life and reduce the symptoms of RA patients based on the knowledge of the biology of these hormones.

Myopenia and Musculoskeletal Aging in Rheumatoid Arthritis

Rheumatoid arthritis (RA), the commonest inflammatory arthritis, is a debilitating disease leading to decreased functional capacity, social disability and reduced quality of life. RA affects multisystems with chronic inflammatory disease characterized by destructive synovitis and muscular dysfunction leading to premature musculoskeletal aging, which has been coined with many terms including myopenia, sarcopenia, cachexia, muscle failure and muscle wasting. Myopenia is described as the presence of clinically relevant muscle wasting due to any illness at any age, associated with impaired muscle function, increased morbidity and mortality. RA myopenia has significantly less muscle mass compared to the general population muscle loss showing preservation or slight increase in fat mass. RA myopenia is unique compared to chronic disease-related myopenia in cancer, chronic heart failure, kidney disease and chronic infection as it is rarely accompanied by a net weight loss. RA myopenia has younger-age onset compared to elderly primary sarcopenia, while higher-grade inflammation has been considered as the pathophysiology of muscle wasting. Research, however, indicates that inflammation itself cannot fully explain the high prevalence of muscle wasting in RA. This chapter aims to review the literature on the casual relationships among RA myopenia, premature musculoskeletal aging and management strategies to delay musculoskeletal aging.

Vascular Involvement in Rheumatoid Arthritis

Rheumatoid arthritis (RA) represents the one of the most common inflammatory rheumatic diseases, which generates disability and significantly reduces the quality of life. RA can affect the vascular system, in addition to joint involvement. Vascular involvement increases the morbidity and mortality among these patients. Macrovascular disease, related to accelerated atherosclerosis, has a high prevalence among RA patients, in the form of carotid artery disease, ischemic heart disease, and peripheral arterial obstructive disease. Microvascular disease, studied in recent years by means of nailfold capillaroscopy, is present even in the early stage of RA evolution. Rheumatoid vasculitis can occur in severe forms of RA.

Self-Management in Patients with Rheumatoid Arthritis

Despite the effective pharmacological management of the disease over the last two decades, many individuals with RA continue to have psychological distress, and this is associated with poor outcomes. Addressing psychological issues hand in hand with pharmacological treatment will help to maximize outcomes for people with RA. Self-management (SM) is of utmost importance for people with rheumatoid arthritis to minimize their complaints, reduce clinic visits, and reduce disability. Considering the continuous update on the guidelines for disease management, non-pharmacological management remains a poorly addressed need of importance. In this chapter, we will introduce the current and progress of self-management in patients with rheumatoid arthritis.

Diagnostic Challenges and Management Update in Rheumatoid Arthritis

Rheumatoid arthritis is a chronic, systemic inflammatory disease, with certain evidence of multiple factors involved, but also with the strong autoimmune component, leading to a high potential for disability, through synovial inflammation and joint destruction. Diagnostic methods and management possibilities have recently improved, thus leading to a better outcome, based on the treat to target recommendation. Although biologic agents represent efficient therapeutic agents, in the last few years, the advances in understanding the mediators involved in rheumatoid arthritis pathogenesis have provided new targeted therapies, represented by small molecule inhibitors against the Janus kinases that contribute in the signaling pathways of various cytokine receptors.