Abstract |
Osteoarthritis (OA) is a debilitating chronic condition widely prevalent in ageing populations. Because the pathology of the disease includes cartilage erosion and joint remodelling, OA patients experience a great deal of pain. Despite numerous studies, details of OA are frequently inseparable from other types of chronic pain, and its causes are unknown. In most circumstances in OA, the cartilage lacks afferent innervation, although other joint tissues contain nociceptive neurones. In addition to physical joint damage, there is a strong element of joint inflammation. Genetic studies have identified several associations between ion channels and OA pain, including NaV1.7, P2X7, and TRPV1, but several other channels have also been implicated. Many ion channels involved with OA pain are common to those seen in inflammatory pain. This review considers causes of OA pain and discusses three possible pain-reducing strategies involving ion channel modulation: chondroprotection, innate afferent nerve inhibition, and inhibition of inflammatory hyperalgesia. Future targets for OA pain analgesia could involve a number of ion channels.
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Authors | C A Staunton, R Lewis, R Barrett-Jolley |
Journal | Current pain and headache reports
(Curr Pain Headache Rep)
Vol. 17
Issue 12
Pg. 378
(Dec 2013)
ISSN: 1534-3081 [Electronic] United States |
PMID | 24198035
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
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Chemical References |
- Analgesics
- Anti-Inflammatory Agents, Non-Steroidal
- Ion Channels
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Topics |
- Aged
- Aged, 80 and over
- Analgesics
(therapeutic use)
- Anti-Inflammatory Agents, Non-Steroidal
(therapeutic use)
- Chronic Pain
(drug therapy, etiology, physiopathology)
- Female
- Humans
- Ion Channels
(drug effects)
- Male
- Middle Aged
- Nociceptors
(drug effects)
- Osteoarthritis
(complications, drug therapy, physiopathology)
- Pain
(drug therapy, etiology, physiopathology)
- Pain Measurement
- Treatment Outcome
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