9: Osteoarthritis

Michael Doherty and A. Abhishek

Academic Rheumatology, University of Nottingham; Nottingham University Hospitals Trust, Nottingham, UK

Osteoarthritis (OA) is the most common condition to affect synovial joints. It is also the most important cause of locomotor disability and a major challenge for healthcare providers. OA was previously regarded as a degenerative disease due to trauma and ageing (Figure 9.1). However, it is now regarded as a dynamic process characterized by joint tissue injury and attempted joint repair. This may result from either abnormal biomechanical stress on a normal joint or normal stress applied to an inherently compromised joint (Figure 9.2). Frequently, both factors contribute. Therefore, OA is a consequence of a number of interacting processes and risk factors. Risk factors for OA may vary in importance from joint to joint, and risk factors for development of OA may differ from risk factors for its progression (Box 9.1). Often inherent joint repair compensates for the triggering insults, resulting in asymptomatic structural OA. In other cases, however, repair cannot compensate, leading to symptoms and disability.

2 Clustered bar graphs illustrating left-skewed distributions of differences between knee (left) and hip (right) OA in terms of age and sex prevalence, symmetry and likelihood for clinical progression. — **Figure 9.1** Differences between knee and hip OA in terms of age and sex prevalence, symmetry and likelihood for clinical progression, supporting consideration of OA at each site as discrete conditions.

Source: van Sasse *et al*. (1989), reproduced with permission of BMJ Publishing Group Ltd

Flow diagram of pathways to osteoarthritis from abnormal stress and abnormal joint physiology to cell/matrix injury, enzymatic, etc.; to joint damage, pain, and disability; then back to the top. — **Figure 9.2** Pathways to osteoarthritis.

Source: Modified from Poole *et al.* (2007), with permission of Dr Farshid Guilak and Lippincot Williams and Wilkins

Box 9.1 Risk factors of OA

Age	Not a direct consequence of ageing. This association reflects cumulative effects of joint insults and failure of repair mechanisms
Sex	More common in women. More likely to be severe and symptomatic (except hip OA)
Race	Lateral compartment knee OA and hip OA are more common in Chinese and African‐American men respectively compared to Caucasians
Obesity	Important risk factor for knee and hand OA
Genetics	40–65% of OA is heritable. Heritability is stronger for hand and hip OA. Polymorphisms in GDF 5, 7q22 and MCF₂L associate with OA with genome‐wide association significance
Joint injury and use	Major joint injury can cause OA at any site. Recognized occupational hazards include farming, lifting (hip OA); kneeling or squatting, professional soccer (knee OA); heavy manual jobs and frequent pincer movement (hand and thumb base OA)
Joint shape and alignment	Varus or valgus knee alignment (knee OA); excessive medially or laterally placed patella, high‐riding patella (patellofemoral OA); acetabular dysplasia, pistol grip femoral deformity and femoro‐acetabular impingment (hip OA); ≥1 cm lower limb length inequality (lower limb OA)
Bone mineral density (BMD)	High BMD associates with OA but not its progression. Paradoxically, low BMD associates with OA progression

Presentation

Osteoarthritis is traditionally separated into primary and secondary OA. Primary OA typically involves joints in characteristic locations (Figure 9.3) and is likely to result mainly from genetic and other constitutional predisposition. Multiple Heberden’s nodes (bony enlargement of distal interphalangeal joints (DIPJs) of the hand) (Figure 9.4) appear in middle age and are a strong marker for subsequent development of knee OA, and OA at other common target sites (nodal generalized OA). However, OA can occur in any synovial joint. When OA occurs in atypical joints, such as the ankle, the presentation alone should trigger consideration of secondary OA. Typical aetiologies of secondary OA include previous joint trauma, fracture and inflammatory arthritis like gout. Joint injury is the most common of these, and can lead to OA 15–20 years after the joint insult. It is a common cause of young‐onset mono‐ or pauciarticular OA. When abnormal joint stress occurs in those with abnormal joint physiology, the outcome is even more severe. For example, severe knee meniscal damage is more likely to cause eventual knee OA in patients with hand OA (suggesting genetic predisposition to OA) compared to patients without hand OA (Englund and Lohmander, 2004).