Osteoarthritic Joint Pain

Osteoarthritis is a chronic degenerative disease associated with joint pain and loss of joint function. It has an estimated incidence of four in every 100 people and significantly reduces the quality of life in affected individuals. The major symptoms are chronic joint pain, swelling and stiffness; severe pain is often the key factor causing patients to seek medical attention. Within the affected joint there is focal degradation and remodelling of articular cartilage, new bone formation and mild synovitis.
Several mechanisms are thought to contribute to osteoarthritic joint pain, including mild synovial inflammation, bone oedema, ligament stretching, osteophyte formation and cartilage–derived mediators. Changes in joint biomechanics and muscle strength may also affect the severity and duration of the joint pain. From a nervous system perspective, the relative contributions of peripheral afferent nociceptive fibres and central mechanisms remain to be defined. Importantly, there is a clear disconnect between clinical severity, as measured radiographically, and the presence and severity of joint pain. Treatments for osteoarthritic joint pain include non–steroidal anti–inflammatory compounds, exercise and surgical intervention. There remains a critical need for improved control of joint pain in osteoarthritis.
This book covers the clinical presentation of joint pain, the cellular pathways involved, osteoarthritis disease processes and pain, experimental models and pain control. The discussions provide insights into the nature of joint pain, identify key studies needed to advance understanding, highlight possible intervention points and indicate opportunities for better treatment of OA joint pain.

Spis treści:
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 p erspective (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. McCabe, 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.

Okładka tylna:
Osteoarthritis is a chronic degenerative disease associated with joint pain and loss of joint function. It has an estimated incidence of four in every 100 people and significantly reduces the quality of life in affected individuals. The major symptoms are chronic joint pain, swelling and stiffness; severe pain is often the key factor causing patients to seek medical attention. Within the affected joint there is focal degradation and remodelling of articular cartilage, new bone formation and mild synovitis.
Several mechanisms are thought to contribute to osteoarthritic joint pain, including mild synovial inflammation, bone oedema, ligament stretching, osteophyte formation and cartilage–derived mediators. Changes in joint biomechanics and muscle strength may also affect the severity and duration of the joint pain. From a nervous system perspective, the relative contributions of peripheral afferent nociceptive fibres and central mechanisms remain to be defined. Importantly, there is a clear disconnect between clinical severity, as measured radiographically, and the presence and severity of joint pain. Treatments for osteoarthritic joint pain include non–steroidal anti–inflammatory compounds, exercise and surgical intervention. There remains a critical need for improved control of joint pain in osteoarthritis.
This book covers the clinical presentation of joint pain, the cellular pathways involved, osteoarthritis disease processes and pain, experimental models and pain control. The discussions provide insights into the nature of joint pain, identify key studies needed to advance understanding, highlight possible intervention points and indicate opportunities for better treatment of OA joint pain.