Joint pain

Schaible, Hans‐Georg; Richter, Frank; Ebersberger, Andrea; Boettger, Michael Karl; Vanegas, Horacio; Natura, Gabriel; Vázquez, Enrique; Banchet, Gisela Segond von

doi:10.1007/s00221-009-1782-9

Cited by 174 publications

(148 citation statements)

References 90 publications

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“…Pain is certainly the most important symptom of OA, but also the least well understood [39]. Recent models imply that OA pain consists of a nociceptive stimulation of the joint and of peripheral sensitization, which can be accompanied by spinal and central sensitization [2,[40][41][42][43]. Leptin may affect the OA pain response in at least two possible ways.…”

Section: Discussionmentioning

confidence: 99%

Do synovial leptin levels correlate with pain in end stage arthritis?

Lübbeke

Finckh

Puskás

et al. 2013

International Orthopaedics (SICOT)

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Purpose We evaluated whether synovial fluid (SF) leptin concentrations correlate with pain severity in patients with hip or knee endstage osteoarthritis (OA) and whether they mediate the association between increased joint pain and (1) female gender and (2) obesity. Methods We conducted a cross-sectional study including patients with primary hip and knee OA undergoing joint replacement between January and December 2010. SF leptin concentrations obtained on the day of surgery were assessed. Main outcome was pain severity measured pre-operatively using WOMAC and VAS pain scales. Results A total of 219 patients were included, 123 hip and 96 knee arthroplasties. Mean age was 72 years, 59 % were women. Mean SF leptin levels were 22.9 (±25.6) ng/ml in women and 5.4 (±5.9) ng/ml in men. Levels >19.6 ng/ml (highest quartile) were significantly associated with increased pain on both WOMAC (mean difference −9.6, 95 % CI −15.1 to −4.0) and VAS scale (mean difference 0.8, 95 % CI 0.2-1.3). Associations remained unchanged after adjusting for age, co-morbidities, contra-lateral arthritic joint, OA site, and disability. The associations observed between increased pain and female gender or obesity were substantially reduced after adjusting for SF leptin. Conclusion Joint pain is associated with SF leptin concentrations. Increased pre-operative pain observed in women and obese may be related to high intra-articular leptin levels.

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Section: Discussionmentioning

confidence: 99%

Do synovial leptin levels correlate with pain in end stage arthritis?

Lübbeke

Finckh

Puskás

et al. 2013

International Orthopaedics (SICOT)

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“…Sensitization is often accompanied by an increase in the sensitive area (Mense, 1993). In addition, other alterations of the nociceptors, including activation of silent nociceptors, hav e b e e n f o u n d a s t h e r e s u l t o f i n j u r y o r inflammation (Schaible et al, 2009). When persistent alterations in the nociceptors as the result of induced gene transcription and protein synthesis drive pain in the absence of noxious stimuli these alterations represent a pathological condition (Woolf & Ma, 2007).…”

Section: Muscle Nociception and Peripheral Sensitizationmentioning

confidence: 99%

Potential Muscle Biomarkers of Chronic Myalgia in Humans - A Systematic Review of Microdialysis Studies

Gerdle¹,

Larsson²

2012

Biomarker

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“…Although OA-related pain is mainly considered to be a combination of nociceptive pain and local inflammatory processes, neuropathic mechanisms may also contribute to the pain experience. This is especially true when the local joint damage leads to the involvement of peripheral nerves and, consequently, neuropathic pain (28).…”

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confidence: 99%

The sources of pain in osteoarthritis: a pathophysiological review

2014

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summaryThe pain of osteoarthritis (OA) has multifaceted etiologies within and outside the joint. It is believed to be driven by both nociceptive and neuropathic mechanisms, as well as abnormal excitability in the pain pathways of the peripheral and central nervous system. Inflammation in the joint triggers a cascade of events that leads to peripheral sensitization, increased sensitivity of nociceptive primary afferent neurons, and hyperexcitability of the nociceptive neurons in the central nervous system. Pain receptors have been found in the synovium, ligaments, capsule, subchondral bone and surrounding tissues, with the exception of articular cartilage. The bone-related causes of pain in OA include subchondral microfractures, bone stretching with elevation of the periosteum due to osteophyte growth, bone remodeling and repair, bone marrow lesions, and bone angina caused by decreased blood flow and increased intra-osseous pressure. Central factors alter pain processing by setting the gain in such a way that, when a peripheral input is present, it is processed against a background of central factors that can enhance or diminish the experience of pain. As a complex phenomenon with a strong subjective component, pain can also be influenced by the nature of the underlying disease, personal predisposition (biological and psychological), and environmental and psychosocial factors. This review examines the current literature regarding the sources and mechanisms of pain in OA.

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Joint pain

Cited by 174 publications

References 90 publications

Do synovial leptin levels correlate with pain in end stage arthritis?

Do synovial leptin levels correlate with pain in end stage arthritis?

Potential Muscle Biomarkers of Chronic Myalgia in Humans - A Systematic Review of Microdialysis Studies

The sources of pain in osteoarthritis: a pathophysiological review

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