Chapter 22 Osteoarthritis
DEFINITION AND AETIOLOGY
Osteoarthritis, also called degenerative joint disease, is primarily a disease of ageing, as 90% of all people have radiographic features of it in the weight-bearing joints by the age of 40 years.1,2,3 It is defined by degeneration of the cartilage and subsequent hypertrophy of the bone surrounding the articulations. There are no systemic signs of disease with this condition. Typically the pain is localised to joints in a non-symmetrical pattern, and is usually relieved by rest and gentle motion. There are hereditary and mechanical risk factors involved in this condition, with obesity and repetitive mechanical loading especially provocative in the lower limb articulations. Degeneration in a joint can be primary by ‘wear and tear’ or secondary to an articular injury, for example a fracture, or metabolic diseases like hyperparathyroidism.2,3
Incidence and cost
In Australia, arthritis and musculoskeletal conditions are large contributors to illness, pain and disability.4 Accounting for more than 4% of the overall disease burden, measured in terms of disability-adjusted life years (DALY), these conditions account for a significant proportion of healthy years of life lost. More than 6.1 million Australians are reported to have arthritis or a musculoskeletal condition. Most commonly reported conditions are back pain and various forms of arthritis. Further, over 1 million Australians are reported to have disability associated with arthritis and related disorders, with mobility limitation the major feature. These conditions are the second most common reason for presentation to a general practitioner,3,5 and the third leading cause of health expenditure.6 In view of this large disease burden—the number of people affected and the high disability impact—arthritis and musculoskeletal conditions were declared a National Health Priority Area (NHPA) in July 2002. 1.3 million Australians (almost 7% of the population) have diagnosed osteoarthritis and females (8%) are more likely than males (5%) to have the disease.3
RISK FACTORS
The risk factors for osteoarthritis have been categorised into a succinct list of modifiable and unmodifiable factors.7
Modifiable
The first and most obvious factor is injury to a joint complex, and this is especially true in men. Trauma to the meniscus and cruciate ligament tears are particularly provocative in the development of osteoarthritis, and this relationship remains despite surgical repair.2,3,7
Obesity is a major risk factor in both the development of weight-bearing joint osteoarthritis and its severity and subsequent disability.3,6–8 Women are particularly susceptible in this factor, and obesity appears to be predisposing to osteoarthritis, and not just secondary to becoming sedentary because of it.
The link between occupational overuse and the development of osteoarthritis has been shown in many different work activities, particularly when the knee is involved in repeated bending, kneeling, squatting or climbing,3,7 and this effect is exacerbated by the addition of heavy-load lifting.9
Unmodifiable
The prevalence of osteoarthritis has an interesting age and gender relationship. Men more commonly have the radiological signs of the condition before the age of 50 years, and conversely women have it after that age. Women are more likely to have bilateral knee osteoarthritis as well as hand osteoarthritis. The disease increases in incidence and severity with age.7
In terms of family history, there is an inherited tendency towards osteoarthritis, with the heritability component estimated in twin studies at 60–65% for hip and hand osteoarthritis, and 40–50% for knee osteoarthritis, although there has been no single gene defect identified.10 There is also evidence that race is involved as a risk factor. For example, there is evidence that Chinese subjects have a lower incidence of hand and hip osteoarthritis.11 These risk factors can compound, as in obesity with occupational bending and twisting. There is some evidence that recreational overuse is a risk, specifically in elite sports.7
DIAGNOSIS
A joint can be defined or diagnosed to have osteoarthritis by symptoms, structural changes, or both (see Figure 22.1). The symptoms of osteoarthritis include:
Radiological changes on X-ray are useful to identify some of the key signs of the osteoarthritic joint: the narrowing of the joint space, marginal osteophyte formation, subchondral sclerosis and the hypertrophy of the periarticular bones. However, radiological changes are not always observed in people with joint symptoms, and people with radiological changes do not always have symptoms. Cartilage is not seen on X-ray as it is not radio-opaque, so ultrasound and magnetic resonance imaging (MRI) and visualisation under arthroscopy might be necessary to clarify the joint changes.2,3
In clinical research studies, the diagnosis and severity of osteoarthritis is commonly measured using the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC).The WOMAC evaluates three clinical domains including pain, stiffness and physical function in people with osteoarthritis of the hip and knee, and assesses change in symptoms of patients who have received therapeutic intervention. Ordinal Likert scales are used to grade the severity of each domain, and the instrument has been extensively evaluated for validity.12,13
The differential diagnosis of osteoarthritis from other forms of arthritide, like rheumatoid arthritis and gout, should include a consideration of the pattern of joint involvement and whether signs of inflammation are present (see Table 22.1 and Figure 22.2). If the patient has a recent history of infection or fever, is less than 40 years old or presents with abnormal routine blood tests, other forms of arthritis (such as rheumatoid or septic) should be considered (see Chapter 28 on autoimmunity). Laboratory tests (for example, ESR, rheumatoid factor and synovial fluid analysis) may be used to rule out alternative diagnoses.2,3,14
| CHARACTERISTIC | STATUS | DISEASE |
|---|---|---|
| Inflammation | Present | Rheumatoid arthritis, systemic lupus erythematosus, gout |
| Absent | Osteoarthritis | |
| Number of involved joints | Monoarticular | Gout, trauma, septic arthritis, Lyme disease, osteoarthritis |
| Oligoarticular (2–4 joints) | Reiter’s disease, psoriatic arthritis, inflammatory bowel disease | |
| Polyarticular (5 or more) | Rheumatoid arthritis, systemic lupus erythematosus | |
| Site of joint involvement | Distal interphalangeal | Osteoarthritis, psoriatic arthritis (not rheumatoid arthritis) |
| Metacarpophalangeal, wrists | Rheumatoid arthritis, systemic lupus erythematosus (not osteoarthritis) | |
| First metatarsophalangeal | Gout, osteoarthritis |
Source: Adapted from 2009 Current Medical Diagnosis and Treatment.2
CONVENTIONAL TREATMENT
The foundations of conventional treatment can be summarised as:2,3,15,16
The exercise program and weight-loss strategies are elements of the self-help management plan that all health practitioners would support—see the discussion below regarding the evidence.
Prescription of NSAIDs is included as the first choice for pain and inflammation control, with the addition of analgesics where necessary. The prescription should be accompanied by an assessment of the presence of risk factors for NSAIDs including age, hypertension, upper gastrointestinal events and cardiovascular, renal or liver disease. Other issues to be considered are aspirin allergy and polypharmacy (for example, concurrent use of diuretics, ACEI and/or anticoagulants).2,3,15,16
In Australia, the percentage of people with osteoarthritis using the common medications are: 8.0% use celecoxib (NSAID), 6.6% paracetamol, 5.3% meloxicam (NSAID), 3.9% diclofenac sodium (NSAID).3
KEY TREATMENT PROTOCOLS
The goals in the naturopathic treatment of people with osteoarthritis are to:
This schedule of therapeutic aims has a large number of individualised permutations based on the many pieces of information that are gleaned from the personal history and lifestyle analysis of each person with osteoarthritis. In naturopathic medicine, this is a vital component of the management of a multifactorial condition such as osteoarthritis. As in any naturopathic approach to case reasoning, the therapeutic order is useful to prioritise management, and to ensure the naturopathic principles are followed.19 The following is a summary of modalities that may be used within naturopathic medicine that have been investigated for this condition.
The naturopathic approach to the management of this condition reflects the evidence-based guidelines of a number of mainstream groups. The Osteoarthritis Research Society International (OARSI) has published practice guidelines for managing hip and knee osteoarthritis.20 The guidelines state that the optimal management requires
TREAT THE WHOLE PATIENT
Qualitative studies of patients with rheumatoid arthritis suggested that fatigue, not pain, was the factor associated with their condition that affected their life the most.17 Similar findings have since been observed in osteoarthritis patients as well.18 Fatigue may be associated with pain, pain medication, poor sleeping patterns or any number of factors. Arthritis may also affect the patient’s ability to perform daily tasks and interact socially or with their partner, and has other psychosocial or emotional ramifications, all of which need to be appropriately addressed in the naturopathic treatment of arthritis.
a combination of non-pharmacological and pharmacological approaches. The first priority is education of the patient about the condition and the importance of changes in lifestyle, exercise and weight reduction in order to unload the damaged joints. The initial focus should be on self-help and patient-driven treatments rather than on passive therapies delivered by health professionals.21 The focus on self-help in obesity and exercise management is also a key element of the guidelines from both the Royal Australian College of General Practitioners22 and the National Arthritis and Musculoskeletal Conditions Advisory Group.14
The approach in naturopathic medicine to ‘address weakened or dysfunctioning systems or organs’ coincides with the clinical approach of looking for the existence of comorbidities that may be linked to the primary problem (see Figure 22.3). This is clear in the management of osteoarthritis, where assessment and treatment may be necessary in the (among others):
Figure 22.3 Integrative treatment of osteoarthritis
Source: Adapted from Dieppe PA, Lohmander LS. Pathogenesis and management of pain in osteoarthritis. Lancet 2005;365(9463):965–973.
Attenuate inflammation
The process of inflammation plays a central role in many disorders, especially those in the musculoskeletal system. Like many processes in the body, there can be positive outcomes from a resolution or there can be uncontrolled and damaging results. The activators of inflammation can include injury, radiation, infection, oxidative stress and certain foods. Tissue injury stimulates the release of inflammatory signalling molecules such as bradykinin, and the release of inflammatory cytokines such as IL-1, TNF and IL-6. Cells that respond to infection or injury include macrophages and mast cells.24 Macrophages and other immune cells secrete chemokines that recruit leukocytes from the circulation to the site of inflammation. Mast cells release histamine, prostaglandins and leukotrienes that act as chemokines, increase vascular permeability and act on the vascular endothelium to increase tissue recruitment of leukocytes.24 Cyclooxygenase (COX) is an enzyme that is responsible for the formation of pro-inflammatory prostaglandins, prostacyclins and thromboxanes from the omega-6 arachidonic acid (see Chapter 28 on autoimmunity for further detail).
Omega-3 essential fatty acids compete with the omega-6, thereby moderating the inflammatory effect. There is evidence that omega-3 oils containing eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) have anti-inflammatory actions,25,26 but clinical data are lacking with regard to the treatment of osteoarthritis.25,27 The most widely available sources of EPA and DHA are cold water oily fish such as salmon, herring, mackerel, anchovies and sardines.
Harpagophytum procumbens, a South African herb, has been reviewed for efficacy and safety in the treatment of osteoarthritis with favourable results, especially in the reduction of pain.28,26 The mechanism of action has not been established, but is thought to be the anti-inflammatory activity of harpagoside.29 An 8-week, single-group, open clinical trial demonstrated statistically significant improvements in patient assessment of global pain, stiffness and function. There were also statistically significant reductions in mean pain scores for hand, wrist, elbow, shoulder, hip, knee and back pain. Quality of life measurements (using the SF-12 health survey) were significantly increased from baseline and 60% of patients either reduced or stopped concomitant pain medication. Adverse effects have been described as no different to placebo.27,30
Figure 22.4 The inflammatory cascade
Source: Pearlman DS. Pathophysiology of the inflammatory response. J Allergy Clin Immunol 1999;104:S132–S137.
in arthritis via a variety of mechanisms. While most of the 43 studies justifying the formulation’s use have focused on pain measures, many have also uncovered various anti-inflammatory mechanisms, with efficacy often comparable to conventional anti-inflammatory medication.31,32
The gum resin extracted from the herb Boswellia serrata has some evidence as a potent anti-inflammatory, anti-arthritic and analgesic agent.33 A recent double-blind, randomised placebo-controlled trial of 75 subjects with osteoarthritis demonstrated that an extract of B. serrata (5-Loxin®) conferred clinically and statistically significant improvements in pain scores and physical function scores, and these changes were recorded in the treatment group as early as 7 days after the start of treatment.34
Salix spp. through the active constituent salicin, has anti-inflammatory and analgesic activity. Standardised preparations of the bark have shown positive effects in a number of trials in musculoskeletal conditions, with an analgesic effect dominant in low back pain.26,35
