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About Arthritis

This section was compiled by Frank M. Painter, D.C.
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The Sympathetic Nervous Response in Inflammation
Arthritis Research & Therapy 2014 (Dec 12);   16 (6):   504 ~ FULL TEXT

Over the past decades evidence has accumulated clearly demonstrating a pivotal role for the sympathetic nervous system (SNS) and its neurotransmitters in regulating inflammation. The first part of this review provides the reader with an overview showing that the interaction of the SNS with the immune system to control inflammation is strongly context-dependent (for example, depending on the activation state of the immune cell or neuro-transmitter concentration). In the second part we focus on autoimmune arthritis as a well investigated example for sympathetically controlled inflammation to show that the SNS and catecholamines play a differential role depending on the time point of ongoing disease.

Sensory and Sympathetic Nerve Fibers Undergo Sprouting
and Neuroma Formation in the Painful Arthritic Joint of Geriatric Mice

Arthritis Research & Therapy 2012 (May 1);   14 (3):   R101 ~ FULL TEXT

Sensory and sympathetic nerve fibers that innervate the aged knee joint clearly maintain the capacity for robust nerve sprouting and formation of neuroma-like structures after inflammation/injury. Understanding the factors that drive this neuroplasticity, whether this pathologic reorganization of nerve fibers contributes to chronic joint pain, and how the phenotype of sensory and sympathetic nerves changes with age may provide pharmacologic insight and targets for better controlling aging-related joint pain.

Editorial:   Osteoarthritis as an Autoinflammatory Disease Caused by
Chondrocyte-mediated Inflammatory Responses

Arthritis & Rheumatism 2012 (Mar);   64 (3):   613616 ~ FULL TEXT

Osteoarthritis (OA) is considered to be primarily a disease of the hyaline articular cartilage, which secondarily affects subchondral bone and synovial membrane. The exact nature and mechanisms of OA, particularly during the early phases of the disease, are unknown. OA per se might in part relate to the poor inherent repair capacity of the articular cartilage, which during the lifetime of modern (long-lived) human beings, is gradually subjected to progressive and accumulative wear and tear. However, the idea of OA as a simple wear-and-tear disease has been widely rejected because various biologic processes, such as inflammation and enzymatic cartilage degradation, are apparently involved in its pathogenesis. Recent findings provide possible new explanatory pathogenic models that intimately link the two phenomena biomechanical wear and tear of the cartilage (osteoarthrosis) and inflammation (osteoarthritis) to each other.

Correlation Between Inflammatory Cytokines Released from
the Lumbar Facet Joint Tissue and Symptoms in
Degenerative Lumbar Spinal Disorders

J Orthop Sci. 2007 (Mar);   12 (2):   154160

Lumbar facet joint tissue has inflammatory cytokines. However, no reports have shown whether inflammatory cytokines in the facet joint leads to pain. This study was designed to characterize the correlation between inflammatory cytokines released from facet joint tissue and symptoms in degenerative lumbar spinal disorders. The purpose of this study was to seek involvement of inflammatory facet joint for radiculopathy in lumbar spinal canal stenosis with clinical and anatomical studies.



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