Phenotypic alterations of neurons that innervate osteoarthritic joints in rats

Ferreira‐Gomes, Joana; Adães, Sara; Sarkander, Jana; Castro-Lopes, José Manuel

doi:10.1002/art.27713

Cited by 63 publications

(95 citation statements)

References 47 publications

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“…CGRP-positive neuron areas were measured in the same IR cells randomly selected for cell counting (n = 5 rats for controls and the 4d MA; n = 4 rats for each of the other experimental groups). IR cells with visible nuclei were manually outlined using a computer mouse and the cross-sectional area was determined using the ImageJ version 1.37 (free access software) [29,30] . Cell areas were grouped into three categories: small ( !…”

Section: Cell Size Distributionmentioning

confidence: 99%

Neuronal Injury Marker ATF-3 Is Induced in Primary Afferent Neurons of Monoarthritic Rats

et al. 2011

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Activating transcription factor 3 (ATF-3) expression has been associated with several signaling pathways implicated in cellular stress response in many cell types and is usually regarded as a neuronal damage marker in dorsal root ganglia (DRG). We investigated ATF-3 expression in primary afferents in the monoarthritic (MA) model of chronic inflammatory joint pain. Immunohistochemistry revealed that ATF-3 is highly induced mainly in small and medium neurons, especially at 2 and 4 days of MA in L₅ DRGs. Colocalization with calcitonin gene-related peptide (CGRP) and isolectin B4 (IB4) demonstrated that ATF-3-immunoreactive cells are mainly peptidergic. The lack of significant differences in ATF-3 and pAkt colocalization indicated that ATF-3 is probably not involved in a pAkt-mediated survival pathway. Anti-inflammatory (ketoprofen) administration failed to reverse ATF-3 induction in MA rats, but significantly increased CGRP expression. These data suggest that ATF-3 expression is definitely involved in MA, actually marking injured neurons. Some degree of neuronal damage seems to occur right from the first days of disease, mainly affecting small-to-medium peptidergic neurons. The intra-articular injection of complete Freund’s adjuvant and the generation of a neuroinflammatory environment seem to be the plausible explanation for the local nerve damage.

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Section: Cell Size Distributionmentioning

confidence: 99%

Neuronal Injury Marker ATF-3 Is Induced in Primary Afferent Neurons of Monoarthritic Rats

et al. 2011

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“…The decrease in number of mechanoreceptors within ligaments, reported in animals [12] and humans [2,6,13], is presumably one of the underlying mechanisms. In addition, total number of knee joint aVerents decreases with aging [14] and OA changes [15,16] in rodents. Taken together, the decrease in the number of mechanoreceptors at least partially accounts for the age-related loss of joint innervation and progression of OA changes.…”

Section: Discussionmentioning

confidence: 99%

“…Therefore, our results indicate that nociceptive inputs selectively remain in the PCL of OA knees, while the total innervation decreases. One possible reason for this Wnding is that OA and arthritic changes in knee cause an up-regulation of CGRP in rodent dorsal root ganglia [16,23], These Wndings will give new insights to the PCL issue in TKA and should be taken into account.…”

Section: Discussionmentioning

confidence: 99%

Nociceptive sensory innervation of the posterior cruciate ligament in osteoarthritic knees

Ikeuchi

Wang

Izumi

et al. 2012

Arch Orthop Trauma Surg

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Our results showed that, in spite of a significant decrease in total innervation in OA knees, the PCLs have constant nociceptive sensory innervation. Although the relationship between the decrease in total innervations in the PCL and OA pathophysiology is still unclear, the PCL is the possible source of OA knee pain. Our results should be taken into account when examining the pain source of the OA knees and handling the PCL during total knee arthroplasty.

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“…Animal model studies have demonstrated potent facilitation of the joint Group II afferents following induced joint inflammation [39] and induced monoarthritis [40,41]. Indirect evidence in patient populations may provide further support.…”

Section: Spinal Hyperexcitabilitymentioning

confidence: 94%

Neuromuscular Function in Painful Knee Osteoarthritis

Courtney

O’Hearn

Hornby

2012

Curr Pain Headache Rep

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Pain is a major cause of impaired mobility in elderly patients with chronic osteoarthritis (OA) of the knee. Central sensitization and impaired nociceptive inhibitory mechanisms have both been identified as contributing factors to heightened pain in this patient population. While central sensitization has been shown to produce enhanced pain responses and spread of pain to adjacent and remote body regions, conditioned pain modulation has also been shown to be adversely affected, and may be characteristic of those patients with chronic pain. Alterations of quantitative sensory testing measures have been demonstrated in patients with knee OA, and may serve as a clinical means of staging chronic musculoskeletal pain, including assessment of hyperalgesia and hypoesthesia. In addition, pain and altered somatosensation commonly associated with OA may be correlated with functional deficits.

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Phenotypic alterations of neurons that innervate osteoarthritic joints in rats

Cited by 63 publications

References 47 publications

Neuronal Injury Marker ATF-3 Is Induced in Primary Afferent Neurons of Monoarthritic Rats

Neuronal Injury Marker ATF-3 Is Induced in Primary Afferent Neurons of Monoarthritic Rats

Nociceptive sensory innervation of the posterior cruciate ligament in osteoarthritic knees

Neuromuscular Function in Painful Knee Osteoarthritis

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