Lifestyle and biomechanical determinants of knee joint structure and symptoms

Osteoarthritis (OA) is the most common form of arthritis and commonly affects weight-bearing joints, such as the knee. With the growing obesity endemic and aging population, the prevalence of knee OA will increase over the coming decades. Since the advent of Magnetic resonance imaging (MRI), OA is now considered a whole-organ disease, affecting multiple articular structures. No cure exists for knee OA and the only definitive management is joint replacement surgery, indicated for painful end-stage disease. There are no disease modifying interventions available, although preventive measures, such as weight loss and exercise, are currently being investigated. Moreover, attempts are being made to better understand the biomechanics of the knee joint, since the aetiology of OA is considered to be predominantly mechanical in nature. This thesis aims to examine both modifiable and non-modifiable risk factors for the development and progression of deleterious knee joint changes and symptoms, in an attempt to identify factors which may expedite and or retard the progression toward clinical knee OA. The initial focus of this thesis is on obesity. Several studies were performed and the most pertinent findings included data demonstrating that as little as 1% weight loss in obese subjects had both a beneficial cartilage and symptom modifying effect at the knee joint. Conversely, as little as 1% weight gain expedited knee cartilage loss and worsened knee symptoms. When a knee joint had pre-existing subclinical damage, as determined by meniscal tears, weight gain accelerated cartilage loss and caused increased knee pain. In body composition studies, increased measures of obesity and adiposity were associated with deleterious cartilage changes at the patella. The second variable to be examined in this thesis was physical activity. Participation in vigorous physical activity was associated with deleterious knee cartilage changes in people with pre-existing bone marrow lesions. At the patellofemoral joint, participation in vigorous physical activity was associated with beneficial cartilage changes in knee joints without pre-existing cartilage defects. Finally, this thesis examined knee joint biomechanics. The main findings were related to knee alignment, whereby static knee alignment was associated with the risk of knee cartilage defects in both healthy and arthritic subjects. A change toward genu valgum was associated with a reduction in the annual rate of medial tibial cartilage volume loss in healthy subjects but also reduced patella cartilage volume. Another determinant of patella cartilage was the congruency of the patellofemoral joint (i.e. the angle of the trochlear groove). A unifying theme of this thesis was the importance of the pre-existing state of the knee joint. When the knee joint has an abnormality such as a bone marrow lesion, meniscal tear, cartilage defect, or even an incongruent joint surface, articular cartilage appears particularly vulnerable to the effects of weight change and physical activity. Although the current works have demonstrated that conservative measures such as weight loss and exercise may benefit the knee joint, the pre-existing health of the joint appears to be a strong determinant that can modify this effect. Finally, biomechanical measures such as knee alignment and joint congruency are also determinants of articular knee joint structures. Whether or not these biomechanical variables can be conservatively modified (e.g. by orthoses) to prevent joint damage requires further attention.