Volume 8 Issue 7, July 2012

Systems level analysis using stimulus–response modelling could increase our understanding of the interplay between biochemical, structural and functional variables that influence the development and manifestation of osteoarthritis. Furthermore, surrogate markers of clinical responses identified might enable early diagnosis, improve therapy, and facilitate development of new treatments and end points.

Coronary artery aneurysms affect a substantial proportion of patients with Kawasaki disease, especially when standard therapy fails. Adjunctive primary corticosteroid treatment reduces inflammation and might reduce the incidence of coronary artery disease in a subset of patients at high risk of this comorbidity, but reliably identifying such individuals is a challenge.

Accumulating data from clinical practice hint that an alternative class of biologic agent may be the best choice when anti-TNF therapy for rheumatoid arthritis fails to produce the desired effect. Furthermore, evidence suggests that non-anti-TNF biologic agents should perhaps also be considered as the initial choice of biologic agent.

A new multinational guideline for treating pain in the setting of inflammatory arthritis highlights the absence of well-designed studies to answer the myriad questions faced by clinicians. To use the recommendations as a starting point for alleviating this common condition, clinicians will need to read between the lines.

Analyzing bone turnover markers—an approach boosted by the advent of automated analysis—can guide clinical decision making and the development of new therapies in osteoporosis. How such markers are, ought to be, and might be, used to understand osteoporosis and to optimize its treatment form the focus of this Review.

Angiogenesis facilitates inflammation and contributes to structural disease progression in osteoarthritis (OA). As new blood vessel growth is coupled with innervation, inappropriate vascularization might sensitize tissues that are usually impervious to pain. In this article, the authors describe sites of angiogenesis and mechanisms of nerve and new blood vessel growth in the synovial joint. They discuss the neurovascular interactions that might contribute to pain in OA, as well as potential targets for new therapies.

Both sicca and systemic symptoms affect quality of life in patient with Sjögren's syndrome, and their management is complicated by the low level of evidence supporting the available therapeutic options. Here, the authors comprehensively review the data on the efficacy of treatments for the glandular and extraglandular manifestations of this disease. Ramos-Casals and colleagues also recommend treatment approaches tailored to different clinical scenarios that patients with Sjögren's syndrome can present.

Loss of meniscal function is one of the strongest identified risk factors for knee osteoarthritis (OA). However, the best therapeutic strategy for patients with meniscus damage remains controversial. The authors explain the role of meniscus pathology in OA and discuss the current options for treatment of degenerative and traumatic meniscal tears.

Alphaviruses can cause rheumatic manifestations (usually polyarthralgia and/or polyarthritis) in humans. Arthritogenic alphaviruses are distributed globally and include chikungunya virus, Ross River virus, Barmah Forest virus, Sindbis virus, o'nyong nyong virus and Mayaro virus. In this Review, the authors provide an overview of these viruses, describing epidemiology, pathogenesis, disease manifestations, diagnosis and interventions.

In the past decade, the introduction of targeted biologic therapies has revolutionized the treatment of rheumatic diseases. Patents for many of these key biologic agents will soon expire, and the introduction of biosimilar versions is likely to lead to substantial cost savings. Focusing on targeted therapies for rheumatic diseases, the authors describe biosimilar agent manufacture, safety and efficacy concerns, and the current worldwide status of regulations for the approval of biosimilar drugs.