Where does it hurt? Pain localization in osteoarthritis of the knee

Creamer, Paul; Lethbridge-Çejku, Margaret; Hochberg, Marc C.

doi:10.1053/joca.1998.0130

Cited by 102 publications

(85 citation statements)

References 12 publications

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“…Therefore, the effect of gabapentin on nociception was evaluated by the Knee-Bend and CatWalk tests 22 , that assess movement-and loading-associated nociception, thereby reproducing a hallmark of pain in this pathology 23 . The a2d-1 subunit of voltage-gated calcium channels is a target of gabapentin 24 that has been shown to be overexpressed in DRG neurons after peripheral nerve injury 25 .…”

Section: Introductionmentioning

confidence: 99%

Injury of primary afferent neurons may contribute to osteoarthritis induced pain: an experimental study using the collagenase model in rats

Adães

Ferreira‐Gomes

Mendonça

et al. 2015

Osteoarthritis and Cartilage

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Section: Introductionmentioning

confidence: 99%

Injury of primary afferent neurons may contribute to osteoarthritis induced pain: an experimental study using the collagenase model in rats

Adães

Ferreira‐Gomes

Mendonça

et al. 2015

Osteoarthritis and Cartilage

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“…The mechanisms of pain in knee OA, however, are complex and poorly understood. Moreover, numerous studies have documented that radiographic markers of disease severity are relatively weak correlates of pain severity and disability [7]. Because clinical pain severity is the primary driver of disability, impaired quality of life, and health care burden in OA, investigations aimed at identifying and treating the causes of clinical pain are needed.…”

Section: Introductionmentioning

confidence: 99%

Mechanisms by which sleep disturbance contributes to osteoarthritis pain: A conceptual model

Smith

Quartana²,

Okonkwo³

et al. 2009

Current Science Inc

124

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Sleep disturbance is prevalent in aging and painful rheumatologic populations, but it has largely been a neglected dimension of the routine clinical care of arthritis patients. Pain associated with osteoarthritis (OA) is a leading cause of disability worldwide, and factors that contribute to pain in OA are poorly understood. Sleep disturbance is not only a consequence of pain, it is also likely to play an integral role in pain expression. Emerging research suggests that many patients with OA demonstrate signs of generalized hyperalgesia and faulty central pain modulatory processing similar to other idiopathic pain disorders, such as fibromyalgia. Sleep disruption is increasingly recognized as a direct contributor to both hyperalgesia and impaired endogenous pain modulation. This article reviews the extant literature on sleep disturbance and hyperalgesia in patients with OA. We propose a conceptual working model describing pathways by which sleep disturbance interacts directly with central pain processing mechanisms and inflammatory processes, and indirectly with mood and physical functioning to augment clinical OA pain. The clinical and research implications of the model are discussed.

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“…2). Pain is reported by 10% of subjects with normal radiographs, and 40-79% of patients with the significant radiographic joint abnormalities typical of OA (30). A number of studies indicate that only half of the patients with radiographic OA feel pain, and that there is a weak correlation between pain severity and radiographic changes (31)(32)(33)(34).…”

mentioning

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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Where does it hurt? Pain localization in osteoarthritis of the knee

Cited by 102 publications

References 12 publications

Injury of primary afferent neurons may contribute to osteoarthritis induced pain: an experimental study using the collagenase model in rats

Injury of primary afferent neurons may contribute to osteoarthritis induced pain: an experimental study using the collagenase model in rats

Mechanisms by which sleep disturbance contributes to osteoarthritis pain: A conceptual model

The sources of pain in osteoarthritis: a pathophysiological review

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