Case 9 Osteoarthritis

Description of osteoarthritis

Definition

Osteoarthritis (OA) is a degenerative joint disease characterised by biochemical, cellular and structural changes to the articular cartilage, joint space and subchondral bone. The diarthrodial joints of the body, including the knees, hips and hands, are the most commonly affected. Depending on the aetiology of OA, the condition can be classified as either primary OA (idiopathic aetiology) or secondary OA. Secondary OA can be further defined as traumatic, metabolic, neuropathic, inflammatory or anatomic.¹

Epidemiology

The prevalence of OA increases with advancing age. The prevalence rate of symptomatic OA in people under the age of 45 years, for example, is five per cent. Between the ages of 45 and 64 years, the prevalence rate increases to more than ten per cent, and over 75 years of age, to more than thirty per cent.² In radiological prevalence surveys, the prevalence rate of OA is much higher (i.e. more than fifty per cent of people over 65 years of age),³ and in autopsy studies, even higher again (sixty to seventy per cent of people aged between 70 and 80 years).⁴ The disease is also more prevalent in women than men, particularly radiologically confirmed hand and knee OA, with the female:male ratio varying between 1.5 and 4.0 across studies.⁴

Aetiology and pathophysiology

Many risk factors are associated with the pathogenesis of OA. Increasing age, female sex, ethnicity, congenital joint abnormalities and family history are some of the major non-modifiable risk factors of OA. The modifiable risk factors include obesity, repetitive joint loading (e.g. repetitive squatting, kneeling, lifting), trauma (e.g. fractures, dislocations, joint surgery, meniscal or cruciate ligament tears), diet (e.g. low vitamin D, vitamin C and fruit intake, and elevated omega 6 fatty acid intake), and quadricep weakness.⁴ Several pathological conditions are also associated with the development of OA, including metabolic disease (e.g. haemochromatosis, hypothyroidism, Wilson’s disease), joint inflammation or infection, neuropathy (e.g. Charcot’s arthropathy) and cartilage disorders (e.g. rheumatoid arthritis, chondrocalcinosis).⁵ All of these factors impair the integrity of joint tissue, causing direct damage to joint tissues, impairing repair processes or increasing joint susceptibility to injury.⁴

An initial insult to the joint stimulates chondrocyte activity, but at the same time triggers the release of inflammatory mediators from the synovium into the cartilage.⁵ While the chondrocytes attempt to repair the tissue by increasing the production of proteoglycans and collagen, they do so in opposition to the actions of the inflammatory mediators and proteolytic enzymes, which cause cartilage degradation. When the equilibrium between proteoglycan synthesis and degradation shifts towards net degradation, damage to articular cartilage occurs. Over time, subchondral bone becomes exposed, eburnated, sclerotic and stiff, which results in osseous infarction and subchondral cyst formation. In an attempt to protect the subchondral bone and to stabilise the joint, the body produces osteophytes.⁶ But instead of protecting the tissue, these spurs cause joint immobility and pain, and in some cases, synovitis. Eventually, joint mobility diminishes to such an extent that menisci fissure, supportive muscles weaken and periarticular tendons and ligaments become stressed, resulting in tendinitis and contractures.⁵

Clinical manifestations

OA is a progressive disease and, as such, may not present with any clinical manifestations in the early stages of development. Eventually, the client may begin to experience deep, aching arthralgia in one or several joints, particularly the hips, knees and hands. This pain is often aggravated by exercise, weight-bearing activity and changing weather, and alleviated with rest.⁷ As the disease progresses, joint stiffness develops, which is generally worse in the morning and after prolonged periods of rest. Further loss of articular cartilage results in reduced joint mobility, joint tenderness and crepitus. In the later stages of the disease, the client may experience joint instability and/or locking, muscle contractures and spasms. The structural changes to articular tissue, synovial thickening and joint effusion may also lead to joint enlargement.⁵ The pain and functional impairment associated with this disease also contribute to significant disability and reduced quality of life.²

A 69-year-old woman presents to the clinic complaining of bilateral knee pain, stiffness and reduced mobility secondary to OA. The knee pain is described as a constant deep dull ache of varying intensity. The pain is worse on rising in the morning (pain score = 6/10), after a period of walking (5/10) and in damp weather (5/10), but is alleviated with rest (3/10), ibuprofen (2/10) and cold packs (2/10). Bilateral knee stiffness accompanies the pain, which is worse after prolonged rest. The pain does not radiate and there are no concomitant symptoms. The client began to experience the pain approximately 5–6 years ago, but the pain has now reached the point where the client requires oral ibuprofen 400 mg three times a day. The client is reluctant to continue with this medication long term and is now seeking alternative treatment options.

Diet and fluid intake
Breakfast	Toasted white bread with marmalade, black tea.
Morning tea	Scones, or sweet biscuits or cake, black tea.
Lunch	Braised steak or beef sausages or roast chicken with boiled potato, cabbage and peas, battered butterfish with potato chips.
Afternoon tea	Sweet biscuits, black tea.
Dinner	Sandwich with white bread, ham and/or cheese.
Fluid intake	2–3 cups of water a day, 2–3 cups of tea a day.
Food frequency
Fruit	0–1 serve daily
Vegetables	2–3 serves daily
Dairy	0–1 serve daily
Cereals	6–7 serves daily
Red meat	4 serves a week
Chicken	3 serves a week
Fish	1 serve a week
Takeaway/fast food	0 times a week

Physical examination

Inspection

Client mobilises with a single cane, partially weight-bearing on each leg. Gait is staggered and the expression of discomfort is observed in her face. On closer examination, there is mild swelling and enlargement to both knees, but no evidence of erythema, bruising, deformity, tophi or scarring. Active range of motion is reduced in both knees. Other major articulations (i.e. hips, shoulders, elbows, ankles and wrists) are unremarkable.

Olfaction

There are no abnormal odours present.

Palpation

Palpable tenderness and mild non-pitting oedema is present to both knees. Local skin temperature is unremarkable. Passive range of motion (ROM) is reduced in both knees, with knee flexion reduced to 105° (right) and 100° (left). Bent knee hip flexion is also reduced to 110° bilaterally. Mild bilateral quadricep weakness is also noted. ROM of other major articulations (i.e. shoulders, elbows, ankles and wrists) is unremarkable.

The short form Arthritis Impact Measurement Scale 2 (AIMS2) revealed a score of 68/120 (AIMS2 score ranges from 0, which is high impact, to 120, low impact). This indicates that the client’s arthritis has a moderate impact on physical activity, social function and activities of daily living. The lowest scores (or highest impact) were noted for mobilisation and mood.

Diagnostics

CAM practitioners can request, perform, and/or interpret findings from a range of diagnostic tests in order to add valuable data to the pool of clinical information. While several investigations are pertinent to this case (as described below), the decision to use these tests should be considered alongside factors such as cost, convenience, comfort, turnaround time, access, practitioner competence and scope of practice, and history of previous investigations.

• Bilateral knee arthralgia (actual), secondary to OA, related to genetic predisposition (client has a family history of OA), chronic inflammation (knee pain is relieved by non-steroidal anti-inflammatory drugs and cold packs), elevated omega 6 fatty acid intake (client frequently consumes baked goods and fried foods that are generally high in omega 6 fatty acids; suspicions of high omega 6 fatty acid intake may be supported by plasma/red cell fatty acid analysis), obesity (obesity is a risk factor for OA – the client’s BMI and waist circumference are in the obesity range), low vitamin C and fruit intake (the client typically consumes less than fifty per cent of the recommended daily intake of fruit) and/or proteoglycan degradation (non-steroidal anti-inflammatory drugs inhibit the synthesis of human cartilage matrix in vitro,¹² which is likely to accelerate the rate of degeneration of articular cartilage in OA).

• Bilateral knee stiffness (actual), secondary to OA, related to genetic predisposition, chronic inflammation, elevated omega 6 fatty acid intake, obesity, low vitamin C and fruit intake, and/or proteoglycan degradation.

• Impaired physical mobility (actual), secondary to OA, related to genetic predisposition, chronic inflammation, elevated omega 6 fatty acid intake, obesity, low vitamin C and fruit intake, and/or proteoglycan degradation.

OA is an inflammatory disorder, thus it is conceivable that the consumption of foods and/or nutrients with demonstrable anti-inflammatory activity may play a role in the management of the disease. In a 10-year longitudinal cohort study, a positive association was observed between dietary intake of omega 6 polyunsaturated fatty acids and risk of bone marrow lesions in the non-osteoarthritic knee joint,¹² while an inverse association was reported between dietary intake of vitamin C and fruit, and bone marrow lesions.¹² Neither of these nutrients was found to be associated with statistically significant changes in cartilage volume. In spite of these encouraging results, it is uncertain whether the increased consumption of fruit and foods containing vitamin C, and the reduced intake of omega 6 fatty acid-containing foods, is of any benefit in the secondary prevention of OA.

Dairy and tea consumption (Level III-3, Strength C, Direction +)

There is some evidence to suggest that the consumption of milk and tea could be of benefit to people with joint inflammation. A cross-sectional study of 655 individuals with symptomatic knee OA found lower rates of symptomatic OA among people consuming higher intakes of milk and tea.²⁰ Whether different types of milk (e.g. cow versus goat) and tea (e.g. black versus green) confer different levels of benefit to people with knee OA is an area in need of further research.

Low-calorie diet (Level II, Strength B, Direction +)

Many risk factors are associated with the pathogenesis of OA. One risk factor that is amenable to dietary modification is obesity, which makes effective weight reduction an important goal in OA management. Evidence from two controlled clinical trials shows low-energy diets (with and without exercise) are significantly more effective than control diets at reducing body fat, but more importantly, are significantly more effective than controls in improving functional outcomes in obese individuals with OA.^21,²² These improvements may be attributed to a reduction in joint load, as well as to a decrease in systemic inflammatory activity.²³

Lifestyle

Relaxation therapy (Level II, Strength B, Direction +)

The relaxation response can be induced by a number of behavioural therapies, such as progressive muscle relaxation, guided imagery and autogenic training. Many RCTs have examined the effect of these therapies on pertinent OA outcomes. Results from three small trials have shown progressive muscle relaxation (PMR), hypnosis and guided imagery plus PMR to be significantly more effective than controls at improving OA-related pain,^24,²⁵ immobility,²⁴ quality of life²⁶ and analgesic use²⁵ over 8–12 weeks; there was no statistically significant difference between hypnosis and PMR.²⁵ Further research is needed to examine the comparative effectiveness of other relaxation therapies.

Tai chi (Level I, Strength B, Direction +)

Tai chi is an ancient Chinese therapy generally used as a meditative technique, soft martial art or form of physical exercise. In many ways, the physical and psychological benefits of tai chi are similar to those of exercise.^27,²⁸ Evidence from a systematic review of five RCTs and seven non-randomised controlled clinical trials is not convincing, with tai chi (for 6–24 weeks) failing to demonstrate consistent improvements in pain or physical function in people with OA.²⁹ Findings from recent trials have been more favourable, with 12 weeks of Sun-style tai chi demonstrating significant symptomatic improvements in people with OA when compared with controls.^15,¹⁸ The weight of the evidence seems to be in favour of tai chi, although further investigation is still warranted.

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