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Curr Osteoporos Rep. 2018 Oct;16(5):611-616. doi: 10.1007/s11914-018-0477-1.

Mechanisms of Osteoarthritis (OA) Pain.

O'Neill TW1,2,3, Felson DT4,5,6.

Author information

1
Arthritis Research UK Centre for Epidemiology, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, The University of Manchester, The Stopford Building, Oxford Road, Manchester, M13 9PT, UK. terence.o'neill@manchester.ac.uk.
2
NIHR Manchester Biomedical Research Centre, Manchester Academic Health Science Centre, Manchester University NHS Foundation Trust, Manchester, UK. terence.o'neill@manchester.ac.uk.
3
Salford Royal NHS Foundation Trust, Salford, UK. terence.o'neill@manchester.ac.uk.
4
Arthritis Research UK Centre for Epidemiology, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, The University of Manchester, The Stopford Building, Oxford Road, Manchester, M13 9PT, UK.
5
NIHR Manchester Biomedical Research Centre, Manchester Academic Health Science Centre, Manchester University NHS Foundation Trust, Manchester, UK.
6
Boston University School of Medicine, Boston, MA, USA.

Abstract

PURPOSE OF REVIEW:

Osteoarthritis (OA) is a major cause of pain and disability worldwide. There is, however, a relatively poor correlation between the severity of OA based on plain radiograph changes and symptoms. In this review, we consider the mechanisms of pain in OA.

RECENT FINDINGS:

It is now widely recognised that OA is a disease of the whole joint. Data from large observational studies which have used magnetic resonance imaging (MRI) suggest that pain in OA is associated with a number of structural factors including the presence of bone marrow lesions (BMLs) and also synovitis. There is evidence also of alterations in nerve processing and that both peripheral and central nerve sensitisation may contribute to pain in OA. Identification of the causes of pain in an individual patient may be of benefit in helping to better target with appropriate therapy to help reduce their symptoms and improve function.

KEYWORDS:

Bone marrow lesions; Central sensitisation; Osteoarthritis; Pain; Peripheral sensitisation; Synovitis

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