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 Table of Contents  
Year : 2020  |  Volume : 15  |  Issue : 3  |  Page : 253-254

Fill in the blanks of fibromyalgia with inflammation!

Department of Physical Medicine and Rehabilitation, Faculty of Medicine, Cukurova University, Adana, Turkey

Date of Submission16-Jun-2020
Date of Acceptance17-Jun-2020
Date of Web Publication3-Sep-2020

Correspondence Address:
Dr. Ilke Coskun Benlidayi
Department of Physical Medicine and Rehabilitation, Faculty of Medicine, Cukurova University, Adana
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/injr.injr_152_20

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How to cite this article:
Benlidayi IC. Fill in the blanks of fibromyalgia with inflammation!. Indian J Rheumatol 2020;15:253-4

How to cite this URL:
Benlidayi IC. Fill in the blanks of fibromyalgia with inflammation!. Indian J Rheumatol [serial online] 2020 [cited 2021 Dec 2];15:253-4. Available from:

The pathophysiology of fibromyalgia is complex and related to several factors such as hormonal, psychological, neural, genetic, and environmental issues. On the other hand, still, there are unsolved or poorly understood points.[1] Inflammation is a defense given by the organism toward any stimulus and may be a potential factor that can fill the blanks in fibromyalgia pathogenesis.[2]

Fibromyalgia is characterized by generalized pain indicating the role of central sensitization and abnormalities in central processing of pain.[3] Inflammation may have place in central modulation of pain in fibromyalgia through neuroinflammation. On the other hand, peripheral neuroimmune interactions may alter peripheral nociception.[2] Cytokines/chemokines, lipid mediators, and free radicals/reactive oxygen species interfere with the inflammatory cascade. Some of the pro-inflammatory molecules were found to be at high concentrations in patients with fibromyalgia.[4] There is also growing evidence regarding the involvement of mast cells in fibromyalgia. Thalamic mast cells can modulate neuroinflammation by releasing neurosensitizing molecules including interleukin (IL)-6, IL-1β, tumor necrosis factor-α, histamine, calcitonin gene-related peptide, and substance P in fibromyalgia.[5] Still, there is not much known about the potential involvement of inflammation in the pathogenesis of fibromyalgia. Therefore, generating and testing future hypotheses would increase our understanding on this particular topic [Figure 1].
Figure 1: Cartoon

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  References Top

Bradley LA. Pathophysiology of fibromyalgia. Am J Med 2009;122 12 Suppl: S22-30.  Back to cited text no. 1
Coskun Benlidayi I. Role of inflammation in the pathogenesis and treatment of fibromyalgia. Rheumatol Int 2019;39:781-91.  Back to cited text no. 2
Staud R, Smitherman ML. Peripheral and central sensitization in fibromyalgia: Pathogenetic role. Curr Pain Headache Rep 2002;6:259-66.  Back to cited text no. 3
Mendieta D, De la Cruz-Aguilera DL, Barrera-Villalpando MI, Becerril-Villanueva E, Arreola R, Hernández-Ferreira E, et al. IL-8 and IL-6 primarily mediate the inflammatory response in fibromyalgia patients. J Neuroimmunol 2016;290:22-5.  Back to cited text no. 4
Theoharides TC, Tsilioni I, Bawazeer M. Mast cells, neuroinflammation and pain in fibromyalgia syndrome. Front Cell Neurosci 2019;13:353.  Back to cited text no. 5


  [Figure 1]


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