Pain is the main manifestation of many rheumatic diseases (be they overtly inflammatory such as rheumatoid arthritis or dysfunctional such as fibromyalgia) but, at least initially, the mechanisms involved in the genesis, amplification and chronicisation of the persistent pain characterising the various conditions can be very different. The main peripheral mechanism underlying acute nociceptive pain is a change in the activity of the nociceptors located in the affected anatomical structures (joints, tendons and ligaments), which makes them more sensitive to normally painful stimuli (hyperalgesia) or normally non-painful stimuli (allodynia). This physiopathological mechanism of peripheral sensitisation plays a primary role in rheumatic diseases characterised by acute inflammation, such as the arthritides due to microcrystals. In the case of chronic rheumatic diseases that do not regress spontaneously, functional and structural central nervous system changes cause a generalised reduction in the pain threshold that is not limited to the anatomical structures involved, thus leading to the appearance of hyperalgesia and allodynia in many, if not all body districts. This is the physiopathological basis of chronic, widespread musculoskeletal pain.

Physiopathology of pain in rheumatology / M. Cazzola, F. Atzeni, L. Boccassini, G. Cassisi, P. Sarzi-Puttini. - In: REUMATISMO. - ISSN 0048-7449. - 66:1(2014 Jun), pp. 4-13. [10.4081/reumatismo.2014.758]

Physiopathology of pain in rheumatology

F. Atzeni;P. Sarzi-Puttini
2014-06

Abstract

Pain is the main manifestation of many rheumatic diseases (be they overtly inflammatory such as rheumatoid arthritis or dysfunctional such as fibromyalgia) but, at least initially, the mechanisms involved in the genesis, amplification and chronicisation of the persistent pain characterising the various conditions can be very different. The main peripheral mechanism underlying acute nociceptive pain is a change in the activity of the nociceptors located in the affected anatomical structures (joints, tendons and ligaments), which makes them more sensitive to normally painful stimuli (hyperalgesia) or normally non-painful stimuli (allodynia). This physiopathological mechanism of peripheral sensitisation plays a primary role in rheumatic diseases characterised by acute inflammation, such as the arthritides due to microcrystals. In the case of chronic rheumatic diseases that do not regress spontaneously, functional and structural central nervous system changes cause a generalised reduction in the pain threshold that is not limited to the anatomical structures involved, thus leading to the appearance of hyperalgesia and allodynia in many, if not all body districts. This is the physiopathological basis of chronic, widespread musculoskeletal pain.
Allodynia; Chronic rheumatic diseases; Hyperalgesia; Peripheral mechanisms; Adaptation, Psychological; Autonomic Nervous System; Central Nervous System Sensitization; Chronic Pain; Depression; Humans; Hyperalgesia; Musculoskeletal Pain; Nerve Growth Factors; Neuroimmunomodulation; Neurotransmitter Agents; Nociceptors; Pain Management; Pain Perception; Peripheral Nervous System; Posterior Horn Cells; Rheumatic Diseases; Rheumatology
Settore MED/16 - Reumatologia
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/2434/643198
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