Osteoarthritis (OA) is the most common joint disease in the world and the single largest cause of disability for those over 18 years. It affects more than twice as many people as does cardiac disease, and increases in incidence and prevalence with age. Animal and human studies have shown no evidence of increased risk of hip or knee OA with moderate exercise and in the absence of traumatic injury, sporting activity has a protective effect. One age-matched case control study found recreational runners who ran 12–14 miles per week for up to 40 years had no increase in radiological or symptomatic hip or knee OA. However, higher rates of hip OA occur in contact sports than in age-matched controls, with the highest rate in professional players. Soccer players with torn anterior cruciate ligaments (ACL) are more likely to develop knee OA than those with intact ACL. Early ACL repair reduces the risk of knee OA, but does not prevent it. Established injury prevention programmes have been refined to prevent injuries such as ACL rupture.
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Osteoarthritis is a disease entity involving all joint components including cartilage, synovial membrane and subchondral bone. Initially it was thought that synovitis was secondary to cartilage injuries, but recent information suggests that synovial inflammation occurs early in the process and plays a role in the progression of the damage. Recent research has concentrated on identifying whether cartilage or bone is primarily involved in the pathogenesis of osteoarthritis. This is an important topic, as we know that cartilage degeneration is well advanced at the clinical stage of the disease.
Aetiology and incidence of osteoarthritis
Siblings of patients undergoing hip and knee replacement surgery have a two to three times increased risk of osteoarthritis with the heritability rate of severe osteoarthritis of 27%.1 To date, the lack of a clear genetic linkage for most families suggests a multifactorial aetiology with primary osteoarthritis in rare cases with evidence of direct linkage. The data, however, are unclear as to how genes influence the incidence, progression and disability associated with osteoarthritis.
Mechanically abnormal joints, typically due to malalignment or milder congenital and developmental disorders of the hip are relatively common (congenital acetabular dysplasia, Legg–Calvé–Perthes disease and slipped upper femoral epiphysis) and may account for a portion of idiopathic hip osteoarthritis. Critically, these are modifiable if diagnosed early. Acetabular dysplasia is a common independent predictor of hip osteoarthritis.2 Patients with this condition present early with painful hips if involved in contact sports. Surgery can improve the symptoms but return to contact sports in particular can increase the onset of osteoarthritis in the joint. Repetitive excessive joint loading of a ‘normal’ joint, is associated with osteoarthritis—be it occupational (including miners, dock workers, farmers)3,–,6 or exercise related.
Sport and recreational activity
Regular physical activity does not appear to increase the risk or progression of hip or knee osteoarthritis, for example, recreational runners showed no increase in incident radiographic hip osteoarthritis compared with non-runners over a 9-year period.7 The combination of improved muscle strength and proprioception, and reduced body mass index (BMI) are joint protective. This may be due to the maintenance of physiological joint loading. This balance is lost in elite non-contact athletes,8,–,10 and especially so in contact sports. In professional or elite athletes involved in contact sports there is a higher incidence of significant joint injuries and a greater motivation to continue playing despite pain, potentially adding further insult to the joint. The impact of anterior cruciate ligament (ACL) rupture has been well studied. Soccer players with a ruptured ACL are more likely to develop knee osteoarthritis than those players whose ACL is intact.11 ACL-deficient knees may be at a significantly increased risk of subsequent osteoarthritis regardless of whether the ACL is surgically repaired.7 12 However, ACL reconstruction appears to decrease the rates of subsequent meniscal and cartilage injuries in young healthy adults,13 and other studies suggest that early ACL repair does minimise the risk of knee osteoarthritis.7 In summary, these findings and many retrospective and prospective studies of non-athletes confirm that joint injuries significantly increase the future risk of osteoarthritis.14,–,16
Muscles and alignment
A painful joint may result in less use of the joint, with secondary muscle atrophy and weakness. Quadriceps weakness occurs in both acute and chronic knee injury,17 and has been shown to predate the symptoms of osteoarthritis.23 It may further accelerate the process, due to reduced joint stability. This effect may vary between the normal and malaligned joint. Further research is required to clarify the impact of both to give a clear picture of the importance of muscular activity in relation to osteoarthritis. It has also been established that valgus and varus alignment result in a threefold increased risk of tibiofemoral osteoarthritis progression while allowing for age, sex and BMI.18 Patients with bilaterally malaligned knees are more than two times more likely to have deterioration in their physical function over 18 months compared with those without malalignment.19
Body mass index
Obesity is a long recognised risk factor for osteoarthritis. A high BMI (weight in kilograms/(height in metres)2) greatly increases the risk of developing symptomatic and radiographic knee osteoarthritis20 21 and hip osteoarthritis.22 This is especially so for women, with a closer relationship to bilateral than unilateral osteoarthritis.23 24 Men with a BMI of between 23 and 25 have four times the risk of osteoarthritis compared with men with a BMI of less than 23.25 The risk of knee osteoarthritis increases approximately 15% for each additional kg/m2 above 27.24 Longitudinal studies show that high BMI increases the risk of progression of radiographic knee osteoarthritis.20 Weight loss on the other hand, by reducing the loading across the knee joint, reduces the risk of developing symptomatic knee osteoarthritis.23
Management and prevention
Injury prevention is key in all sporting activity. Education should focus on increased awareness of risk and the introduction of appropriate prevention programmes. Non-modifiable risk factors such as inherited traits and hypermobility (box 1) cannot by definition be changed, but awareness of their presence can allow for some adaptation and reduced exposure to high-risk sports. Particular attention should be paid to modifiable factors in children and adolescents, including the assessment of an individual's size and weight relative to their age group in underage competition (box 1). Skill development is critical to prevent injury and the introduction of a carefully supervised strength training programme, optimally following the growth spurt (aged 14.1 years in young men).
Box 1 Prevention of injury and osteoarthritis in contact sports
Leg length discrepancy
Modifiable factors (eg, children and adolescents in rugby football):
Selection—size/weight versus age
Formal prevention programmes have been developed in individual sports. For example, the rugby union injury prevention programme emphasises that all players should be registered with a club and complete an education programme involving advice on risk management and injury prevention. Rugby Ready has been developed for players, coaches and referees in the sport, and provides advice on pre-participation screening, fitness, skill training, injury awareness and prevention. In addition, specific coaching is necessary to minimise injury risk in the high impact areas of the scrum, tackle and ruck and maul.
Should an injury occur or surgery be required, a carefully planned and monitored rehabilitation programme is critical to returning to train and to play. Returning to contact and play should occur when the player has recovered full function in the joint and has reached his or her pre-accident fitness level.
Treatment: non-pharmacological and pharmacological
Treatment for osteoarthritis is mostly symptomatic with no medications yet influencing progression. Non-pharmacological modalities include self-management programmes, weight loss and other physical therapies (box 2). The pharmacological management of osteoarthritis is comprehensively described by the American College of Rheumatology, as outlined in box 3. The role of non-steroidal anti-inflammatory drugs (NSAID) warrants comment as at present a number of these cyclo-oxygenase 2 selective inhibitors have been withdrawn from the market. They should be used with great caution in osteoarthritis because of the adverse events associated with their use, particularly in elderly patients in whom the risk of complications is greatest. The use of the non-selective cyclo-oxygenase 1 drugs requires medication such as proton pump inhibitors to reduce the risk of gastrointestinal complications.
Box 2 Non-pharmacological therapy for patients with osteoarthritis
American College of Rheumatology (ACR) guidelines for the management of osteoarthritis, 200026
Self-management programmes (eg, Arthritis Foundation self-management programme)
Personalised social support through telephone contact
Weight loss (if overweight)
Aerobic exercise programmes
Physical therapy range-of-motion exercises
Assistive devices for ambulation
Lateral-wedged insoles (for genu varum)
Joint protection and energy conservation
Assistive devices for activities of daily living
Box 3 Pharmacological therapy for patients with osteoarthritis*
ACR guidelines on the management of osteoarthritis, 200026
Cyclo-oxygenase 2-specific inhibitor
Non-selective NSAID plus misoprostol or a proton pump inhibitor†
Other pure analgesics
ACR guidelines on pharmacological management of osteoarthritis (2000) involve the analgesic ladder from simple analgesia with infrequent use of NSAID and other topical and intra-articular therapies.
However, as the pathophysiology of the disease is being clarified, new disease-modifying drugs are being developed.
Following knee injury in sport, MRI or arthroscopic confirmation of meniscal injury may lead to repair or grafting of the lesion. A ruptured ACL will require surgical repair, which gives stability to the joint followed by a carefully structured rehabilitation programme. It usually takes 6–8 months before the player returns to contact sports and performance at the highest level. The use of cartilage graft for small articular lesions has found some success, but the long-term outcomes are as yet unclear.27 Matrix-induced chondrocyte implantation knee surgery has also been carried out; however, the long-term outcomes from this need careful follow-up using randomised controlled trials.
What is already known on this topic
▶ Moderate levels of exercise are beneficial for joints
▶ Increased joint loading and joint trauma increase the risk of developing osteoarthritis
▶ Injury prevention programs have proven successful in reducing joint injury and therefore osteoarthritis, e.g. anterior cruciate injury prevention.
Exercise is good for the joint; however, too much exercise or injury to the joint can result in osteoarthritis. Injury resulting in joint damage is the single greatest risk factor for osteoarthritis. Increased awareness of risk with appropriate injury prevention programmes is essential for all sports at all levels.
Competing interests None.
Provenance and peer review Not commissioned; externally peer reviewed.
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