Osteoarthritis (OA)-related pain is caused by structural joint changes and other complex factors that affect how the body processes and experiences pain.1 Persistent pain and functional limitations from OA occur predominantly in the knees and hips of middle-aged and elderly individuals.2,3
Key risk factors for developing OA include local factors and systemic factors; local factors are those leading to increased mechanical stress – such as repeated joint trauma, increased body weight, malalignment, weakened muscles around the joint, joint overuse and bone characteristics; systemic factors include age, sex, ethnicity, nutrition and genetics.1,4–7 It has been suggested that the heritability of OA is 50% or more, indicating that half the variation in susceptibility to disease in the population is explained by genetic factors.8
OA will often have a significant ‘knock-on’ effect on a patient’s physical and mental health, and is associated with the development of different comorbidities. OA-related pain limits mobility and causes muscle changes,9 and the resulting restricted physical activity is associated with additional health problems such as cardiovascular disease and hypertension, diabetes mellitus, metabolic syndrome and obesity and depression.10 Obesity is therefore a key risk factor for OA, and it can also contribute to further joint damage and cause additional ‘knock-on’ effects.
Patients with OA across 42 studies from 16 countries have been found to have other comorbidities.11
|Selected comorbidities||Prevalence in OA patients (%)|
|Peptic ulcer disease||16|
Quality of life can decline as the patient experiences increased pain, stiffness, fatigue and functional impairment.12 Rates of OA progression are variable from person to person, and depend on structural, biomechanical and genetic factors.13,14 Structural changes include cartilage and meniscus loss (seen as joint space narrowing) and alterations in underlying bone (indicated by osteophyte formation, sclerosis, cyst formation and changes in bone shape).15 Interestingly, structural changes associated with OA do not necessarily mean that a patient will experience pain – a patient can have significant structural damage without pain, or significant pain despite little structural damage.16 Although progression of OA usually takes decades, in some cases the joint damage may be more rapidly progressive – sometimes referred to as rapidly progressing OA.17
What can I do now?
When communicating with OA sufferers, acknowledge that progression of OA is variable and that several contributing risk factors are outside of patients’ control – and that the progression of joint damage is not inevitable, and not inevitably linked to pain.
1. Rice D, McNair P, Huysmans E, Letzen J, Finan P. Best Evidence Rehabilitation for Chronic Pain Part 5: Osteoarthritis. Journal of Clinical Medicine. 2019;8:1769. 2. Dominick KL, Ahern FM, Gold CH, Heller DA. Health-related quality of life among older adults with arthritis. Health QualLife Outcomes. 2004;2:5. 3. Woolf AD, Pfleger B. Burden of major musculoskeletal conditions. Bull World Health Organ. 2003;81(9):646-656. 4. Srikanth VK, Fryer JL, Zhai G, Winzenberg TM, Hosmer D, Jones G. A meta-analysis of sex differences prevalence, incidence and severity of osteoarthritis. Osteoarthritis Cartilage. 2005;13(9):769-781. 5. Arthritis Foundation. Osteoarthritis causes. https://www.arthritis.org/about-arthritis/types/osteoarthritis/causes.php. Accessed November 15, 2019. 6. Zhang Y, Jordan JM. Epidemiology of osteoarthritis. Clin Geriatr Med. 2010;26(3):355-369. 7. Suri P, Morgenroth DC, Hunter DJ. Epidemiology of osteoarthritis and associated comorbidities. PM R. 2012;4(suppl 5):S10-S19. 8. Spector T, MacGregor A. Risk factors for osteoarthritis: genetics. Osteoarthritis Cartilage. 2004;12:S39-S44. 9. King LK, March L, Anandacoomarasamy A. Obesity & osteoarthritis. Indian J Med Res. 2013;138(2):185-193. 10. Booth FW, Roberts CK, Laye MJ. Lack of exercise is a major cause of chronic diseases. Compr Physiol. 2012;2(2):1143-1211. 11. Swain S, Sarmanova A, Coupland C, Doherty M, Zhang W. Comorbidities in osteoarthritis: a systematic review and meta-analysis of observational studies. Arthritis Care Res. 2019;72(7):991-1000. 12. Bushmakin AG, Cappelleri JC, Taylor-Stokes G, Sayers J, Sadosky A, Carroll D, Gosden T, Emery P. Relationship between patient-reported disease severity and other clinical outcomes in osteoarthritis: a European perspective. J Med Econ. 2011;14(4):381-389. 13. Chen A, Gupte C, Zhao W, Wang T, Han L, Hamilton JL, Im HJ. Osteoarthritis: toward a comprehensive understanding of pathological mechanism. Bone Research. 2017;5:16044. 14. Vincent KR, Conrad BP, Fregly BJ, Vincent HK. The pathophysiology of osteoarthritis: a mechanical perspective on the knee joint. PM R. 2012;4(suppl 5):S3-S9. 15. Sharma AR, Jagga S, Lee SS, Nam JS. Interplay between cartilage and subchondral bone contributing to pathogenesis of osteoarthritis. Int J Mol Sci. 2013;14:19805-19830. 16. Arendt-Nielson L. Joint Pain: More to It Than Just Structural Damage? Pain. 2017;158 (suppl 1):S66-S73. 17. Flemming DJ, Gustas-French CN. Rapidly Progressive Osteoarthritis: a Review of the Clinical and Radiologic Presentation. Curr Rheumatol Rep. 2017; 19:42.
OA will often have a significant ‘knock-on’ effect on a patient’s physical and mental health.9
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PP-INT-GBR-0206 February 2021