Nociception (pain perception) and inflammation are two responses of an organisms defence system towards external noxious stimuli. Although different in nature, pain and inflammation are strongly associated with each other. An important sign of inflammation - besides local redness, swelling, heat, and loss of function -  is in fact pain. The events of inflammation that underlie these symptoms are induced and regulated by a large number of chemical mediators that are also found to mediate the mechanisms of pain perception. These mediators include eicosanoids, kinins, complement proteins, neurotransmitters (e.g. histamine), protons, NO, prostaglandins, leukotrienes, neurotrophins, and monokines[1].
Inflammation is a major protective response of the immune system to tissue damage and infection, and ranges from the acute inflammation associated with infection of the skin, through to chronic inflammatory processes in atherosclerosis, asthma and chronic bronchitis, and rheumatoid arthritis, among many others. Acute inflammation is knows for its rapid onset and short duration. It is mediated by tissue-resident macrophages and mast cells, and characterized by the exudation of fluids and plasma proteins, and the migration of leukocytes (mainly neutrophils) into the injured area. In contrast, chronic inflammation is of a more prolonged duration and manifests histologically by the presence of lymphocytes and macrophages, resulting in fibrosis and tissue necrosis[2].
Similar to Inflammation, pain may also be divided into two main categories: acute and chronic pain. Acute or nociceptive pain is part of a rapid warning relay instructing the motor neurons of the central nervous system to minimize detected physical harm. It is mediated by nocicepters: free nerve endings that terminate just below the skin, in tendons, joints, and in body organs.  Nociceptors are extremely heterogeneous, differing in the neurotransmitters they contain, the receptors and ion channels they express, their speed of conduction, their response properties to noxious stimuli, and their capacity to be sensitized during inflammation, injury, and disease. Nociception can be associated with nerve damage caused by trauma, diseases such as diabetes, shingles, irritable bowel syndrome, late-stage cancer or the toxic effects of chemotherapy. It typically responds well to treatment with opioids and NSAIDs. Chronic pain, however, serves no biologic function as it is not a symptom of a disease process but is a disease process itself[3],[4].