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Clinical Pharmacology for Prescribing$
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Stevan R. Emmett, Nicola Hill, and Federico Dajas-Bailador

Print publication date: 2019

Print ISBN-13: 9780199694938

Published to Oxford Scholarship Online: November 2020

DOI: 10.1093/oso/9780199694938.001.0001

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PRINTED FROM OXFORD SCHOLARSHIP ONLINE (oxford.universitypressscholarship.com). (c) Copyright Oxford University Press, 2021. All Rights Reserved. An individual user may print out a PDF of a single chapter of a monograph in OSO for personal use. date: 03 March 2021

Musculoskeletal medicine

Musculoskeletal medicine

Chapter:
Chapter 7 Musculoskeletal medicine
Source:
Clinical Pharmacology for Prescribing
Author(s):

Stevan R. Emmett

Nicola Hill

Federico Dajas-Bailador

Publisher:
Oxford University Press
DOI:10.1093/oso/9780199694938.003.0015

Osteoarthritis (OA) is best described as a chronic pain syndrome affecting one, or more frequently, multiple joints. It most commonly affects the knees, hips, hands, neck and lower back, although any joint can be affected. Defining OA by pathological changes is no longer con­sidered best practice, as the correlation between path­ology and symptoms is frequently discordant, i.e. patients with severe structural changes may present with min­imum symptoms and vice versa. For this reason, patients should be assessed using a biopsychosocial model, which takes into consideration impact on social and psycho­logical well- being, alongside pathological changes. OA can create substantial mobility problems and is the most common cause of disability in elderly people in the devel­oped world. Prevalence rises with age such that approxi­mately one- third of people in the UK over 45 have sought treatment for OA compared with 40– 50% of people over the age of 75. In the pathological conditions of OA, there are specific hallmarks of damage that affect load- bearing articular cartilage, the formation of new bone at the joint mar­gins (osteophytosis), subchondral bone changes (scler­osis), thickening of the joint capsule, loss of cartilage, and joint space narrowing (Figure 7.1B). In general, struc­tural changes seen on X- ray or CT do not correlate with the pain of OA, but an association does occur between the presence of synovitis, subchondral bone oedema and osteophytes. In OA the vasculature of the osteochondral junction also expresses higher levels of nerve growth fac­tors (NGF) so pain sensitization associated with inflam­mation is likely to occur. OA is considered by some to be the result of physio­logical processes originally targeted at joint repair that, over time, cause tissue damage resulting in symptomatic OA. In many cases, severe trauma or pathological repair processes may be contributory factors. Other risk factors for OA include genetic and patient factors, such as age and obesity (see Box 7.1). Anti- NGF drugs may be of benefit, primarily via pain modulation, but OA is not considered to be a disease of inflammation and the mainstay of treatment relies on effective analgesia. The presence of synovitis in late disease is controversial and the presence of joint crys­tals may confound inflammation in OA. It is clear that wear, tear, and damage is associated with the break­down of collagen and increased presence of proteo­lytic enzymes called matrix metalloproteinases (MMPs).

Keywords:   abatacept, benzbromarone, canakinumab, denosumab, etidronate, febuxostat, glucosamine, halofantrine

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