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The Science of Inflammation

The most overt characteristic of inflammation is that the body receives a stimulus that it registers as pain. Pain is a nervous system response to a stimulus that the body perceives as harmful. Therefore pain is a perception that the body creates when care need to be taken to a particular tissue or area of the body.

Inflammation causes hypersensitivity in the affected area. A series of receptors, ion channels, and transmitters support this hypersensitivity, as does the interaction of inflammatory mediators and neurons.

There are numerous broad processes associated with pain. They are nociception, pain perception, and various secondary responses such as pain behavior and suffering. Nociception is the body’s detection of harmful stimuli. Once such stimuli are detected, a message is transmitted to the brain. The brain creates perceived pain so as to deliver the message that such stimuli are harmful.

The level of pain experienced is contingent upon several factors, including the timing, intensity, and location of the harmful stimuli. However, in cases of chronic pain, inflamed or injured tissues may experience pain without an immediate trigger hitting the space externally. Different types of stimuli may produce similar pain. In other words, one particular brand of pain experienced is not necessarily indicative of any one stimulus. Therefore the pain experienced as a result of, for example, osteoarthritis and that of herpetic neuralgia may feel the same to a person experiencing them.

There are three major types of receptors involved in the transmission of pain due to inflammation. They are purinergic receptors, acid-sensing receptors, and vanniloid receptors. Recent studies show that this series of ion channel linked receptors are related to the sensory transmission of harmful stimuli. These receptors travel within the nervous system in ion channels. These channels are either sodium or calcium based.

Prosaglandins are mediators of inflammation and also indicate fever and pain. Prosaglandins are created by COX enzymes one and two, also known as cyclo-oxygenase. Peripheral sensitization may be blocked using non-steroidal anti-inflammatory drugs, also known as NSAIDs. Such drugs work to block COX enzymes, thus inhibiting mediation of pain indication from the brain. Opiod compounds may also work to avert pain. Opiates are present in immune cells, and opiod receptors exist in peripheral tissues. During inflammation, receptors in primary afferent neurones increase, blocking spontaneous constrictions of fibers that cause inflamed areas to be hypersensitive. Therefore in opioid compounds there is the potential to relieve pain with topical or systemic application.

The medical and science communities recognize the necessity for new approaches in pain management with regard to inflammation. Research in this field has led to favorable findings by way of medications, particularly those with positive side effects. In the future, scientists hope to discover a pain management drug that will specifically target particular diagnoses, rather than all types of inflammatory pain at once. Such a finding would represent a qualitative difference in signals and pain management.

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