Osteoarthritis is a chronic degenerative disease associated with
joint pain and loss of joint function. It has an estimated
incidence of 4 out of every 100 people and significantly reduces
the quality of life in affected individuals. The major symptoms are
chronic pain, swelling and stiffness; severe, chronic joint pain is
often the central factor that causes patients to seek medical
attention. Within the affected joint, there is focal degradation
and remodelling of articular cartilage, new bone formation
(osteophytes) and mild synovitis.
Several mechanisms are thought to contribute to osteoarthritic
joint pain. These include mild synovial inflammation, bone oedema,
ligament stretching, osteophyte formation and cartilage-derived
mediators. Changes in joint biomechanics and muscle strength also
influence the severity and duration of joint pain in
osteoarthritis. Within the nervous system, the relative
contributions of peripheral afferent nociceptive fibres and central
mechanisms remain to be defined, and there is limited information
on the phenotype of sensory neurons in the OA joint. Importantly,
there is no relation between clinical severity, as measured by
radiographic changes, and the presence and severity of joint pain.
Patients with severe joint pain may have normal joint architecture
as determined by X-ray, whereas patients with considerable evidence
of joint remodelling may not have significant joint pain.
Treatments for osteoarthritic joint pain include non-steroidal
anti-inflammatory compounds, exercise, corrective shoes and
surgical intervention. There remains a critical need for improved
control of joint pain in osteoarthritis.
This book brings together contributions from key investigators
in the area of osteoarthritic joint pain. It covers the
clinical presentation of joint pain, the pathways involved in joint
pain, osteoarthritis disease processes and pain, experimental
models and pain control. The discussions provide insights into
the nature of osteoarthritic joint pain, identify key studies
needed to advance understanding of the problem, highlight possible
intervention points and indicate future pathways towards a better
treatment of osteoarthritic joint pain.
Tabla de materias
Chair’s Introduction (D. Felson).
Spinal mechanisms contributing to joint pain (H. Schaible).
Activation of sensory neurons in the arthritic joint (B.
Grubb).
Neuromuscular aspects of osteoarthritis: a perspective (K.
Brandt).
Current perspectives on the clinical presentation of joint pain
in human osteoarthritis (P. Creamer).
Joint mechanics in osteoarthritis (W. Herzog, et
al.).
General discussion I Developing animal models of RA.
Characterization of joint pain in human osteoarthritis (G.
Ordeberg).
The role of inflammatory mediators on nociception and pain in
arthritis (B. Kidd, et al.).
Molecular events of chronic pain: from neurone to whole animal
in an animal model of osteoarthritis (J. Henry).
Phantoms of rheumatology (C. Mc Cabe, et al.).
Bone pain and pressure in osteoarthritic joints (P. Simkin).
Structural associations of osteoarthritis pain: lessons from
magnetic resonance imaging (P. Conaghan & D. Felson).
The role of TRP channels in sensory neurons (M. Koltenberg)
Mechanisms that generate and maintain bone cancer pain (P.
Mantyh & S. Hunt).
Symmetry, T cells and neurogenic arthritis (N. Shenker, et
al.).
Lessons from fibromyalgia: abnormal pain sensitivity in knee
ostheoarthritis (L. Bradley, et al.).
Chair’s summing up (D. Felson).
Index of contributors.
Subject index.
Sobre el autor
Derek J. Chadwick and Jamie A. Goode are editors for Osteoarthritic Joint Pain and other scientific titles.
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