|LETTER TO EDITOR
|Ahead of print publication
Fill in the blanks of fibromyalgia with inflammation!
Ilke Coskun Benlidayi
Department of Physical Medicine and Rehabilitation, Faculty of Medicine, Cukurova University, Adana, Turkey
|Date of Submission||16-Jun-2020|
|Date of Acceptance||17-Jun-2020|
Ilke Coskun Benlidayi,
Department of Physical Medicine and Rehabilitation, Faculty of Medicine, Cukurova University, Adana
Source of Support: None, Conflict of Interest: None
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. 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.
Fibromyalgia is characterized by generalized pain indicating the role of central sensitization and abnormalities in central processing of pain. Inflammation may have place in central modulation of pain in fibromyalgia through neuroinflammation. On the other hand, peripheral neuroimmune interactions may alter peripheral nociception. 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. 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. 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].
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